install lanyon-plus theme

This commit is contained in:
shelley 2017-08-08 21:53:28 +02:00
parent bf138a54e3
commit 50d45cd462
86 changed files with 3548 additions and 133 deletions

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CNAME.sample Normal file
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dyndna.github.io/lanyon-plus

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Gemfile
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source "https://rubygems.org"
source 'https://rubygems.org'
# Hello! This is where you manage which Jekyll version is used to run.
# When you want to use a different version, change it below, save the
# file and run `bundle install`. Run Jekyll with `bundle exec`, like so:
#
# bundle exec jekyll serve
#
# This will help ensure the proper Jekyll version is running.
# Happy Jekylling!
gem "jekyll", "3.5.1"
# This is the default theme for new Jekyll sites. You may change this to anything you like.
gem "minima", "~> 2.0"
# If you want to use GitHub Pages, remove the "gem "jekyll"" above and
# uncomment the line below. To upgrade, run `bundle update github-pages`.
# gem "github-pages", group: :jekyll_plugins
# If you have any plugins, put them here!
group :jekyll_plugins do
gem "jekyll-feed", "~> 0.6"
gem 'jekyll'
gem 'jekyll-sitemap'
gem 'jemoji'
gem 'jekyll-redirect-from'
gem 'jekyll-paginate'
gem 'jekyll-compose'
end
# Windows does not include zoneinfo files, so bundle the tzinfo-data gem
gem 'tzinfo-data', platforms: [:mingw, :mswin, :x64_mingw, :jruby]
gem 'font-awesome-sass'
gem 'kramdown'
gem 'rouge'

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GEM
remote: https://rubygems.org/
specs:
addressable (2.5.1)
public_suffix (~> 2.0, >= 2.0.2)
colorator (1.1.0)
ffi (1.9.18)
forwardable-extended (2.6.0)
jekyll (3.5.1)
addressable (~> 2.4)
colorator (~> 1.0)
activesupport (4.2.5)
i18n (~> 0.7)
json (~> 1.7, >= 1.7.7)
minitest (~> 5.1)
thread_safe (~> 0.3, >= 0.3.4)
tzinfo (~> 1.1)
colorator (0.1)
ffi (1.9.10)
font-awesome-sass (4.5.0)
sass (>= 3.2)
gemoji (2.1.0)
html-pipeline (2.2.2)
activesupport (>= 2, < 5)
nokogiri (>= 1.4)
i18n (0.7.0)
jekyll (3.0.1)
colorator (~> 0.1)
jekyll-sass-converter (~> 1.0)
jekyll-watch (~> 1.1)
kramdown (~> 1.3)
liquid (~> 4.0)
liquid (~> 3.0)
mercenary (~> 0.3.3)
pathutil (~> 0.9)
rouge (~> 1.7)
safe_yaml (~> 1.0)
jekyll-feed (0.9.2)
jekyll (~> 3.3)
jekyll-sass-converter (1.5.0)
jekyll-compose (0.4.1)
jekyll (>= 2.5.0)
jekyll-paginate (1.1.0)
jekyll-redirect-from (0.9.1)
jekyll (>= 2.0)
jekyll-sass-converter (1.4.0)
sass (~> 3.4)
jekyll-watch (1.5.0)
listen (~> 3.0, < 3.1)
kramdown (1.14.0)
liquid (4.0.0)
listen (3.0.8)
rb-fsevent (~> 0.9, >= 0.9.4)
rb-inotify (~> 0.9, >= 0.9.7)
mercenary (0.3.6)
minima (2.1.1)
jekyll (~> 3.3)
pathutil (0.14.0)
forwardable-extended (~> 2.6)
public_suffix (2.0.5)
rb-fsevent (0.10.2)
rb-inotify (0.9.10)
ffi (>= 0.5.0, < 2)
rouge (1.11.1)
jekyll-sitemap (0.9.0)
jekyll-watch (1.3.0)
listen (~> 3.0)
jemoji (0.5.1)
gemoji (~> 2.0)
html-pipeline (~> 2.2)
jekyll (>= 2.0)
json (1.8.3)
kramdown (1.9.0)
liquid (3.0.6)
listen (3.0.5)
rb-fsevent (>= 0.9.3)
rb-inotify (>= 0.9)
mercenary (0.3.5)
mini_portile2 (2.0.0)
minitest (5.8.3)
nokogiri (1.6.7.1)
mini_portile2 (~> 2.0.0.rc2)
rb-fsevent (0.9.7)
rb-inotify (0.9.5)
ffi (>= 0.5.0)
rouge (1.10.1)
safe_yaml (1.0.4)
sass (3.5.1)
sass-listen (~> 4.0.0)
sass-listen (4.0.0)
rb-fsevent (~> 0.9, >= 0.9.4)
rb-inotify (~> 0.9, >= 0.9.7)
sass (3.4.21)
thread_safe (0.3.5)
tzinfo (1.2.2)
thread_safe (~> 0.1)
PLATFORMS
ruby
DEPENDENCIES
jekyll (= 3.5.1)
jekyll-feed (~> 0.6)
minima (~> 2.0)
tzinfo-data
BUNDLED WITH
1.15.3
font-awesome-sass
jekyll
jekyll-compose
jekyll-paginate
jekyll-redirect-from
jekyll-sitemap
jemoji
kramdown
rouge

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# Released under MIT License
Copyright (c) 2014 Mark Otto.
Permission is hereby granted, free of charge, to any person obtaining a copy of this software and associated documentation files (the "Software"), to deal in the Software without restriction, including without limitation the rights to use, copy, modify, merge, publish, distribute, sublicense, and/or sell copies of the Software, and to permit persons to whom the Software is furnished to do so, subject to the following conditions:
The above copyright notice and this permission notice shall be included in all copies or substantial portions of the Software.
THE SOFTWARE IS PROVIDED "AS IS", WITHOUT WARRANTY OF ANY KIND, EXPRESS OR IMPLIED, INCLUDING BUT NOT LIMITED TO THE WARRANTIES OF MERCHANTABILITY, FITNESS FOR A PARTICULAR PURPOSE AND NONINFRINGEMENT. IN NO EVENT SHALL THE AUTHORS OR COPYRIGHT HOLDERS BE LIABLE FOR ANY CLAIM, DAMAGES OR OTHER LIABILITY, WHETHER IN AN ACTION OF CONTRACT, TORT OR OTHERWISE, ARISING FROM, OUT OF OR IN CONNECTION WITH THE SOFTWARE OR THE USE OR OTHER DEALINGS IN THE SOFTWARE.

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# Welcome to Jekyll!
# Permalinks
#
# This config file is meant for settings that affect your whole blog, values
# which you are expected to set up once and rarely edit after that. If you find
# yourself editing this file very often, consider using Jekyll's data files
# feature for the data you need to update frequently.
#
# For technical reasons, this file is *NOT* reloaded automatically when you use
# 'bundle exec jekyll serve'. If you change this file, please restart the server process.
# Use of `relative_permalinks` ensures post links from the index work properly.
#permalink: pretty
permalink: /blog/:year/:month/:day/:title/
relative_permalinks: false
# Site settings
# These are used to personalize your new site. If you look in the HTML files,
# you will see them accessed via {{ site.title }}, {{ site.email }}, and so on.
# You can create any custom variable you would like, and they will be accessible
# in the templates via {{ site.myvariable }}.
title: Wild Toad
email: your-email@example.com
description: > # this means to ignore newlines until "baseurl:"
Write an awesome description for your new site here. You can edit this
line in _config.yml. It will appear in your document head meta (for
Google search results) and in your feed.xml site description.
baseurl: "" # the subpath of your site, e.g. /blog
url: "" # the base hostname & protocol for your site, e.g. http://example.com
twitter_username: jekyllrb
github_username: jekyll
# Build settings
# Setup
title: foo
#tagline: 'foo's website
description: Foo's blog...
url: https://dyndna.github.io/lanyon-plus
baseurl: "/lanyon-plus"
urlimg: https://dyndna.github.io/lanyon-plus/images/
markdown: kramdown
theme: minima
plugins:
- jekyll-feed
paginate: 5
paginate_path: "/blog/page:num"
excerpt_separator: <!--more-->
default_bg: sitelogo.png
safe: false
#timezone: America/Chicago
future: true
# Exclude from processing.
# The following items will not be processed, by default. Create a custom list
# to override the default setting.
exclude:
- Gemfile
- Gemfile.lock
- node_modules
# - vendor/bundle/
# - vendor/cache/
# - vendor/gems/
- vendor/ruby/
gems:
- jekyll-paginate
- jemoji
- font-awesome-sass
- kramdown
- rouge
include: [".htaccess"]
exclude: ["lib", "config.rb", "Gemfile", "Capfile", "Gemfile.lock", "config", "log", "Rakefile", "Rakefile.rb", "rakefile", "README.md", "tmp", "less", "*.sublime-project", "*.sublime-workspace", "test", "spec", "Gruntfile.js", "package.json", "node_modules", "LICENSE", "vendor", "assets", "_plugins", "public/dormant"]
# About/contact
author:
name: Foo Boo
url: https://twitter.com/abcd
avatar: foo.png
#email:
# Owner/author information
owner:
name: Foo Boo
avatar: foo.png
#email:
# Use the coder's toolbox at http://coderstoolbox.net/string/#!encoding=xml&action=encode&charset=us_ascii to encode your description into XML string
description:
# Social networking links used in footer. Update and remove as you like.
twitter: abcd
facebook:
github: xyz123abc
stackexchange:
linkedin: https://www.linkedin.com/in/foo
instagram:
flickr:
tumblr:
google_plus: https://plus.google.com/+foo
# orcid and google scholar IDs are different than standard username.
orcid: xyz123abc
gscholar: xyz123abc
## sidebar links:
# For external links add external: true
links:
- title: <i class="iconside iconm-home"></i> Home
url: /
- title: <i class="iconside iconm-user"></i> About
url: /about/
- title: <i class="iconside iconm-quill"></i> Blog
url: /blog/
- title: <i class="fa fa-tags"></i> Tags
url: /tags/
- title: <i class="fa fa-archive"></i> Archive
url: /archive/
- title: <i class="iconside iconm-wordpress"></i> Old Blog
url: https://foo.wordpress.com
external: true
- title: <i class="iconside iconm-envelop"></i> Contact
url: /contact/
- title: <i class="iconside iconm-twitter"></i> Twitter
url: https://twitter.com/abcd
external: true
- title: <i class="iconside iconm-feed2"></i> Feed
url: /feed.xml
# Google Custom Search:
#google_search: xyz123abc
# Twitter stream widget:
# Replace xyz123abc with your twitter widget id from https://twitter.com/settings/widgets
#twitter_widget_id: xyz123abc
# Add disqus username for Disqus comment board:
disqus_shortname: foo
# Analytics and webmaster tools stuff goes here
#google_analytics: xyz123abc
#### For dummy website only - remove if you wish ####
github_repo: https://github.com/dyndna/lanyon-plus
version: 1.1.0
## END ##

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- name: Twitter
url: https://twitter.com/abcd
class: fa fa-twitter-square
title: "Follow me @foo"
- name: Google Plus
url: https://plus.google.com/+foo
class: fa fa-google-plus-square
title: "Follow me +foo"
- name: GitHub
url: https://github.com/xyz123abc
class: fa fa-github-square
title: Code repository
- name: Contact
url: "/contact/"
class: fa fa-envelope-square
title: "Reach Us"
- name: RSS
url: "/feed.xml"
class: fa fa-rss-square
title: "Subscribe to RSS"

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# Permalinks
#
# Use of `relative_permalinks` ensures post links from the index work properly.
#permalink: pretty
permalink: /blog/:year/:month/:day/:title/
relative_permalinks: false
# Setup
title: foo
#tagline: 'foo's website
description: Foo's blog...
url: http://localhost:4000
baseurl: ""
urlimg: http://localhost:4000/images/
markdown: kramdown
paginate: 5
paginate_path: "/blog/page:num"
excerpt_separator: <!--more-->
default_bg: sitelogo.png
safe: false
#timezone: America/Chicago
future: true
gems:
- jekyll-paginate
- jemoji
- font-awesome-sass
- kramdown
- rouge
include: [".htaccess"]
exclude: ["lib", "config.rb", "Gemfile", "Capfile", "Gemfile.lock", "config", "log", "Rakefile", "Rakefile.rb", "rakefile", "README.md", "tmp", "less", "*.sublime-project", "*.sublime-workspace", "test", "spec", "Gruntfile.js", "package.json", "node_modules", "LICENSE", "vendor", "assets", "_plugins", "public/dormant"]
# About/contact
author:
name: Foo Boo
url: https://twitter.com/abcd
avatar: foo.png
#email:
# Owner/author information
owner:
name: Foo Boo
avatar: foo.png
#email:
# Use the coder's toolbox at http://coderstoolbox.net/string/#!encoding=xml&action=encode&charset=us_ascii to encode your description into XML string
description:
# Social networking links used in footer. Update and remove as you like.
twitter: abcd
facebook:
github: xyz123abc
stackexchange:
linkedin: https://www.linkedin.com/in/foo
instagram:
flickr:
tumblr:
google_plus: https://plus.google.com/+foo
# orcid and google scholar IDs are different than standard username.
orcid: xyz123abc
gscholar: xyz123abc
## sidebar links:
# For external links add external: true
links:
- title: <i class="iconside iconm-home"></i> Home
url: /
- title: <i class="iconside iconm-user"></i> About
url: /about/
- title: <i class="iconside iconm-quill"></i> Blog
url: /blog/
- title: <i class="fa fa-tags"></i> Tags
url: /tags/
- title: <i class="fa fa-archive"></i> Archive
url: /archive/
- title: <i class="iconside iconm-wordpress"></i> Old Blog
url: https://foo.wordpress.com
external: true
- title: <i class="iconside iconm-envelop"></i> Contact
url: /contact/
- title: <i class="iconside iconm-twitter"></i> Twitter
url: https://twitter.com/abcd
external: true
- title: <i class="iconside iconm-feed2"></i> Feed
url: /feed.xml
# Google Custom Search:
#google_search: xyz123abc
# Twitter stream widget:
# Replace xyz123abc with your twitter widget id from https://twitter.com/settings/widgets
#twitter_widget_id: xyz123abc
# Add disqus username for Disqus comment board:
disqus_shortname: foo
# Analytics and webmaster tools stuff goes here
#google_analytics: xyz123abc
#### For dummy website only - remove if you wish ####
github_repo: https://github.com/dyndna/lanyon-plus
version: 1.1.0
## END ##

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---
layout: post
title: Introducing Lanyon
---
Lanyon is an unassuming [Jekyll](http://jekyllrb.com) theme that places content first by tucking away navigation in a hidden drawer. It's based on [Poole](http://getpoole.com), the Jekyll butler.
<!--more-->
### Built on Poole
Poole is the Jekyll Butler, serving as an upstanding and effective foundation for Jekyll themes by [@mdo](https://twitter.com/mdo). Poole, and every theme built on it (like Lanyon here) includes the following:
* Complete Jekyll setup included (layouts, config, [404](/404), [RSS feed](/atom.xml), posts, and [example page](/about))
* Mobile friendly design and development
* Easily scalable text and component sizing with `rem` units in the CSS
* Support for a wide gamut of HTML elements
* Related posts (time-based, because Jekyll) below each post
* Syntax highlighting, courtesy Pygments (the Python-based code snippet highlighter)
### Lanyon features
In addition to the features of Poole, Lanyon adds the following:
* Toggleable sliding sidebar (built with only CSS) via **☰** link in top corner
* Sidebar includes support for textual modules and a dynamically generated navigation with active link support
* Two orientations for content and sidebar, default (left sidebar) and [reverse](https://github.com/poole/lanyon#reverse-layout) (right sidebar), available via `<body>` classes
* [Eight optional color schemes](https://github.com/poole/lanyon#themes), available via `<body>` classes
[Head to the readme](https://github.com/poole/lanyon#readme) to learn more.
### Browser support
Lanyon is by preference a forward-thinking project. In addition to the latest versions of Chrome, Safari (mobile and desktop), and Firefox, it is only compatible with Internet Explorer 9 and above.
### Download
Lanyon is developed on and hosted with GitHub. Head to the <a href="https://github.com/poole/lanyon">GitHub repository</a> for downloads, bug reports, and features requests.
Thanks!

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&lt;hr&gt;&lt;a href=&quot;https://twitter.com/share?text={{ post.title }}&amp;url={{ post.url | prepend: site.baseurl | prepend: site.url }}&amp;via={{ site.owner.twitter }} @rbloggers&quot; target=&quot;_blank&quot; title=&quot;tweet author @{{ site.owner.twitter }}&quot;&gt;tweet author&lt;/a&gt; | &lt;a href=&quot;https://plus.google.com/share?url={{ post.url | prepend: site.baseurl | prepend: site.url }}&quot; target=&quot;_blank&quot; title=&quot;Share on Google+&quot;&gt;share on Google+&lt;/a&gt;{% if page.comments %} | &lt;a href=&quot;{{ post.url | prepend: site.baseurl | prepend: site.url }}#disqus_thread&quot; title=&quot;Comment at author&apos;s website&quot;&gt;Comments&lt;/a&gt;{% endif %}

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<script type="text/javascript">
/* * * CONFIGURATION VARIABLES: EDIT BEFORE PASTING INTO YOUR WEBPAGE * * */
var disqus_shortname = '{{ site.disqus_shortname }}';
var disqus_identifier = '{{ site.url }}{{ page.url }}';
/* * * DON'T EDIT BELOW THIS LINE * * */
(function() {
var dsq = document.createElement('script'); dsq.type = 'text/javascript'; dsq.async = true;
dsq.src = '//' + disqus_shortname + '.disqus.com/embed.js';
(document.getElementsByTagName('head')[0] || document.getElementsByTagName('body')[0]).appendChild(dsq);
})();
</script>
<noscript>Please enable JavaScript to view the <a href="https://disqus.com/?ref_noscript">comments powered by Disqus.</a></noscript>

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&lt;hr&gt;&lt;a href=&quot;https://twitter.com/share?text={{ post.title }}&amp;url={{ post.url | prepend: site.baseurl | prepend: site.url }}&amp;via={{ site.owner.twitter }}&quot; target=&quot;_blank&quot; title=&quot;tweet author @{{ site.owner.twitter }}&quot;&gt;tweet author&lt;/a&gt; | &lt;a href=&quot;https://plus.google.com/share?url={{ post.url | prepend: site.baseurl | prepend: site.url }}&quot; target=&quot;_blank&quot; title=&quot;Share on Google+&quot;&gt;share on Google+&lt;/a&gt;{% if page.comments %} | &lt;a href=&quot;{{ post.url | prepend: site.baseurl | prepend: site.url }}#disqus_thread&quot; title=&quot;Comment at author&apos;s website&quot;&gt;Comments&lt;/a&gt;{% endif %}

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<div class="custom-footer" style="display: block;">
<div class="footer-social-icons">
<ul class="social-icons">
{% for social_item in site.data.socialmedia %}
{% if social_item.url contains 'http' %}
{% assign domain = '' %}
{% else %}
{% assign domain = site.url %}
{% endif %}
<li><a href="{{ domain }}{{ social_item.url }}" rel="me" {% if social_item.url contains 'http' %} target="_blank" {% endif %} class="social-icons" title="{{ social_item.title }}"> <i class="{{ social_item.class }} fa-2x"></i></a></li>
{% endfor %}
</ul>
</div>
<h6 class="text-footer"><a rel="license" href="{{ site.url }}/disclosure/" title="CC BY-NC-SA 4.0 License, link to site disclosure" class="social-icon"><i class="fa fa-creative-commons"></i></a> <a rel="license" href="{{ site.url }}/disclosure/" title="CC BY-NC-SA 4.0 License, link to site disclosure">2015-{{ site.time | date: '%Y' }}</a>: <a href="{{ site.url }}" title="Home">example.com</a> | <a href="{{ site.url }}/about/" rel="me">About</a></h6>
</div>

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<!--Gist embed -->
<script type="text/javascript" src="https://ajax.googleapis.com/ajax/libs/jquery/1.9.1/jquery.min.js"></script>
<script type="text/javascript" src="https://cdnjs.cloudflare.com/ajax/libs/gist-embed/2.4/gist-embed.min.js"></script>

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<head prefix="og: http://ogp.me/ns# fb: http://ogp.me/ns/fb#">
<!-- link href="http://gmpg.org/xfn/11" rel="profile" -->
<meta http-equiv="X-UA-Compatible" content="IE=edge">
<meta http-equiv="content-type" content="text/html; charset=utf-8">
<!-- Enable responsiveness on mobile devices-->
<meta name="HandheldFriendly" content="True">
<meta name="viewport" content="width=device-width, initial-scale=1.0, maximum-scale=1">
<title>
{% if page.title == "Home" %}
{{ site.title }} &middot; {{ site.tagline }}
{% else %}
{{ page.title }} &middot; {{ site.title }}
{% endif %}
</title>
<!-- Search Engine Optimization -->
<meta name="description" content="{% if page.description %}{{ page.description }}{% elsif page.content %}{{ page.content | strip_html | truncatewords: 50 }}{% else %}{{ site.description }}{% endif %}">
{% if page.tags %}<meta name="keywords" content="{{ page.tags | join: ', ' }}">{% endif %}
{% if page.noindex == true %}<meta name="robots" content="noindex">{% endif %}
{% if page.nofollow == true %}<meta name="robots" content="nofollow">{% endif %}
{% if site.google_verify %}<meta name="google-site-verification" content="{{ site.google_verify }}">{% endif %}
{% if site.owner.twitter %}<!-- Twitter Cards -->
{% include twitter_card.html %}
{% endif %}
<meta name="twitter:title" content="{% if page.title %}{{ page.title }}{% else %}{{ site.title }}{% endif %}">
<meta name="twitter:description" content="{% if page.description %}{{ page.description }}{% elsif page.content %}{{ page.content | strip_html | truncatewords: 50 }}{% else %}{{ site.description }}{% endif %}">
<meta name="twitter:creator" content="@{{ site.owner.twitter }}">
<!-- End Twitter Cards -->
<!-- Open Graph -->
<meta property="og:locale" content="en_US">
<meta property="og:type" content="article">
<meta property="og:title" content="{% if page.title %}{{ page.title }}{% else %}{{ site.title }}{% endif %}">
<meta property="og:description" content="{% if page.description %}{{ page.description }}{% elsif page.content %}{{ page.content | strip_html | truncatewords: 50 }}{% else %}{{ site.description }}{% endif %}">
<meta property="og:url" content="{{ site.url }}{{ page.url }}">
<meta property="og:site_name" content="{{ site.title }}">
{% if page.imagefeature %}
{% if page.imagefeature contains 'http' %}
{% assign domain = '' %}
{% else %}
{% assign domain = site.urlimg %}
{% endif %}
<meta property="og:image" content="{{ domain }}{{ page.imagefeature }}">{% else %}
<meta property="og:image" content="{% if page.imagesummary %}{{ site.urlimg }}{{ page.imagesummary }}{% else %}{{ site.urlimg }}{{ site.default_bg }}{% endif %}">{% endif %}
{% if page.videofeature %}<meta property="og:video" content="{{ page.videofeature }}">{% endif %}
<meta property="fb:app_id" content="1003108156422006">
<meta property="fb:admins" content="817465054">
<!-- Fonts -->
<link rel="stylesheet" href="https://fonts.googleapis.com/css?family=PT+Serif:400,400italic,700%7CPT+Sans:400|Tangerine|Inconsolata">
<link rel="stylesheet" href="https://maxcdn.bootstrapcdn.com/font-awesome/4.5.0/css/font-awesome.min.css">
<link rel="stylesheet" href="{{ site.baseurl }}/public/css/iconmoon.css">
<!-- CSS -->
<link rel="stylesheet" href="{{ site.baseurl }}/public/css/style.min.css">
{% if page.category contains 'mypubs' or page.category contains 'myaoi' %}
<link rel="stylesheet" href="{{ site.baseurl }}/public/css/publ.css">
<script src="{{ site.baseurl }}/public/js/jquery.min.js"></script>
{% endif %}
<!-- Add-on CSS to override system-wide defaults -->
<link rel="stylesheet" href="{{ site.baseurl }}/public/css/addon.css">
<!-- CSS override per page -->
{% if page.style %}
<style type="text/css">
{{ page.style }}
</style>
{% endif %}
<!-- Java scripts -->
<!-- <script src="{{ site.baseurl }}/public/js/jquery.min.js"></script> -->
<!-- Icons -->
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<div class="full-bib-section"><div class="bib-item"><div class="csl-entry">Beerenwinkel, N., Greenman, C. D., &amp; Lagergren, J. (2016). <a class="doctitle" href="http://dx.doi.org/10.1371/journal.pcbi.1004717">Computational Cancer Biology: An Evolutionary Perspective.</a> <i>PLoS Comput Biol</i>, <i>12</i>(2), e1004717. http://doi.org/10.1371/journal.pcbi.1004717</div><div class="blink"><a href="javascript:show(this);" onclick="show(this);">bib</a><div class="bibshowhide"><div class="bib">@article{beerenwinkel_computational_2016,
title = {Computational {Cancer} {Biology}: {An} {Evolutionary} {Perspective}},
volume = {12},
shorttitle = {Computational {Cancer} {Biology}},
url = {http://dx.doi.org/10.1371/journal.pcbi.1004717},
doi = {10.1371/journal.pcbi.1004717},
number = {2},
urldate = {2016-02-05TZ},
journal = {PLoS Comput Biol},
author = {Beerenwinkel, Niko and Greenman, Chris D. and Lagergren, Jens},
month = feb,
year = {2016},
keywords = {cancer, concepts, darwinian, epigenetics, evolution, mathematical modeling, review, statistics, variant},
pages = {e1004717}
}</div></div></div><div class="blink"><a title="Download EndNote record" href="javascript:downloadFile(this);" onclick="downloadFile(this);">ris</a><div class="bibshowhide"><div class="ris">TY - JOUR
TI - Computational Cancer Biology: An Evolutionary Perspective
AU - Beerenwinkel, Niko
AU - Greenman, Chris D.
AU - Lagergren, Jens
T2 - PLoS Comput Biol
DA - 2016/02/04/
PY - 2016
DO - 10.1371/journal.pcbi.1004717
DP - PLoS Journals
VL - 12
IS - 2
SP - e1004717
J2 - PLoS Comput Biol
ST - Computational Cancer Biology
UR - http://dx.doi.org/10.1371/journal.pcbi.1004717
Y2 - 2016/02/05/T20:21:50Z
KW - cancer
KW - concepts
KW - darwinian
KW - epigenetics
KW - evolution
KW - mathematical modeling
KW - review
KW - statistics
KW - variant
ER -</div></div></div></div><div class="bib-item"><div class="csl-entry">Kaufman, C. K., Mosimann, C., Fan, Z. P., Yang, S., Thomas, A. J., Ablain, J., … Zon, L. I. (2016). <a class="doctitle" href="http://science.sciencemag.org/content/351/6272/aad2197">A zebrafish melanoma model reveals emergence of neural crest identity during melanoma initiation.</a> <i>Science</i>, <i>351</i>(6272), aad2197. http://doi.org/10.1126/science.aad2197</div><div class="blink"><a href="javascript:show(this);" onclick="show(this);">abstract</a><div class="bibshowhide"><div class="abstract">Visualizing the beginnings of melanoma
In cancer biology a tumor begins from a single cell within a group of precancerous cells that share genetic mutations. Kaufman et al. used a zebrafish melanoma model to visualize cancer initiation (see the Perspective by Boumahdi and Blanpain). They used a fluorescent reporter that specifically lit up neural crest progenitors that are only present during embryogenesis or during adult melanoma tumor formation. The appearance of this tumor correlated with a set of gene regulatory elements called super-enhancers whose identification and manipulation may prove beneficial in detecting and preventing melanoma initiation.
Science this issue p. 10.1126/science.aad3867; see also p. 453
Structured Abstract
INTRODUCTIONThe “cancerized field” concept posits that cells in a given tissue sharing an oncogenic mutation are cancer-prone yet only discreet clones within the field initiate tumors. Studying the process of cancer initiation has remained challenging because of (i) the rarity of these events (ii) the difficulty of visiualizing initiating clones in living organisms and (iii) the transient nature of a newly transformed clone emerging before it expands to form an early tumor. A more complete understanding of the molecular processes that regulate cancer initiation could provide important prognostic information about which precancerous lesions are most prone to becoming cancer and also implicate druggable molecular pathways that when inhibited may prevent the cancer from ever starting.
RATIONALEThe majority of benign nevi carry oncogenic BRAFV600E mutations and can be considered a cancerized field of melanocytes but they only rarely convert to melanoma. In an effort to define events that initiate cancer we used a melanoma model in the zebrafish in which the human BRAFV600E oncogene is driven by the melanocyte-specific mitfa promoter. When bred into a p53 mutant background these fish develop melanoma tumors over the course of many months. The zebrafish crestin gene is expressed embryonically in neural crest progenitors (NCPs) and is specifically reexpressed only in melanoma tumors making it an ideal candidate for tracking melanoma from initiation onward.
RESULTSWe developed a crestin:EGFP reporter that recapitulates the embryonic neural crest expression pattern of crestin and its expression in melanoma tumors. We show through live imaging of transgenic zebrafish crestin reporters that within a cancerized field (BRAFV600E-mutant; p53-deficient) a single melanocyte reactivates the NCP state and this establishes that a fate change occurs at melanoma initiation in this model. Early crestin+ patches of cells expand and are transplantable in a manner consistent with their possessing tumorigenic activity and they exhibit a gene expression pattern consistent with the NCP identity readout by the crestin reporter. The crestin element is regulated by NCP transcription factors including sox10. Forced sox10 overexpression in melanocytes accelerated melanoma formation whereas CRISPR/Cas9 targeting of sox10 delayed melanoma onset. We show activation of super-enhancers at NCP genes in both zebrafish and human melanomas identifying an epigenetic mechanism for control of this NCP signature leading to melanoma.
CONCLUSIONThis work using our zebrafish melanoma model and in vivo reporter of NCP identity allows us to see cancer from its birth as a single cell and shows the importance of NCP-state reemergence as a key event in melanoma initiation from a field of cancer-prone melanocytes. Thus in addition to the typical fixed genetic alterations in oncogenes and tumor supressors that are required for cancer development the reemergence of progenitor identity may be an additional rate-limiting step in the formation of melanoma. Preventing NCP reemergence in a field of cancer-prone melanocytes may thus prove therapeutically useful and the association of NCP genes with super-enhancer regulatory elements implicates the associated druggable epigenetic machinery in this process. Download high-res image Open in new tab Download Powerpoint Neural crest reporter expression in melanoma.The crestin:EGFP transgene is specifically expressed in melanoma in BRAFV600E/p53 mutant melanoma-prone zebrafish. (Top) A single cell expressing crestin:EGFP expands into a small patch of cells over the course of 2 weeks capturing the initiation of melanoma formation (bracket). (Bottom) A fully formed melanoma specifically expresses crestin:EGFP whereas the rest of the fish remains EGFP-negative.
The “cancerized field” concept posits that cancer-prone cells in a given tissue share an oncogenic mutation but only discreet clones within the field initiate tumors. Most benign nevi carry oncogenic BRAFV600E mutations but rarely become melanoma. The zebrafish crestin gene is expressed embryonically in neural crest progenitors (NCPs) and specifically reexpressed in melanoma. Live imaging of transgenic zebrafish crestin reporters shows that within a cancerized field (BRAFV600E-mutant; p53-deficient) a single melanocyte reactivates the NCP state revealing a fate change at melanoma initiation in this model. NCP transcription factors including sox10 regulate crestin expression. Forced sox10 overexpression in melanocytes accelerated melanoma formation which is consistent with activation of NCP genes and super-enhancers leading to melanoma. Our work highlights NCP state reemergence as a key event in melanoma initiation.
Melanocytes with oncogenic or tumor suppressor mutations revert to expressing the crestin gene early in melanoma formation. [Also see Perspective by Boumahdi and Blanpain]
Melanocytes with oncogenic or tumor suppressor mutations revert to expressing the crestin gene early in melanoma formation. [Also see Perspective by Boumahdi and Blanpain]</div></div></div><div class="blink"><a href="javascript:show(this);" onclick="show(this);">bib</a><div class="bibshowhide"><div class="bib">@article{kaufman_zebrafish_2016,
title = {A zebrafish melanoma model reveals emergence of neural crest identity during melanoma initiation},
volume = {351},
copyright = {Copyright © 2016, American Association for the Advancement of Science},
issn = {0036-8075, 1095-9203},
url = {http://science.sciencemag.org/content/351/6272/aad2197},
doi = {10.1126/science.aad2197},
language = {en},
number = {6272},
urldate = {2016-01-29TZ},
journal = {Science},
author = {Kaufman, Charles K. and Mosimann, Christian and Fan, Zi Peng and Yang, Song and Thomas, Andrew J. and Ablain, Julien and Tan, Justin L. and Fogley, Rachel D. and Rooijen, Ellen van and Hagedorn, Elliott J. and Ciarlo, Christie and White, Richard M. and Matos, Dominick A. and Puller, Ann-Christin and Santoriello, Cristina and Liao, Eric C. and Young, Richard A. and Zon, Leonard I.},
month = jan,
year = {2016},
keywords = {Development, SKCM, classics, epigenetics, evolution, melanoma, super\_enhancer, zebrafish},
pages = {aad2197}
}</div></div></div><div class="blink"><a title="Download EndNote record" href="javascript:downloadFile(this);" onclick="downloadFile(this);">ris</a><div class="bibshowhide"><div class="ris">TY - JOUR
TI - A zebrafish melanoma model reveals emergence of neural crest identity during melanoma initiation
AU - Kaufman, Charles K.
AU - Mosimann, Christian
AU - Fan, Zi Peng
AU - Yang, Song
AU - Thomas, Andrew J.
AU - Ablain, Julien
AU - Tan, Justin L.
AU - Fogley, Rachel D.
AU - Rooijen, Ellen van
AU - Hagedorn, Elliott J.
AU - Ciarlo, Christie
AU - White, Richard M.
AU - Matos, Dominick A.
AU - Puller, Ann-Christin
AU - Santoriello, Cristina
AU - Liao, Eric C.
AU - Young, Richard A.
AU - Zon, Leonard I.
T2 - Science
AB - Visualizing the beginnings of melanoma
In cancer biology, a tumor begins from a single cell within a group of precancerous cells that share genetic mutations. Kaufman et al. used a zebrafish melanoma model to visualize cancer initiation (see the Perspective by Boumahdi and Blanpain). They used a fluorescent reporter that specifically lit up neural crest progenitors that are only present during embryogenesis or during adult melanoma tumor formation. The appearance of this tumor correlated with a set of gene regulatory elements, called super-enhancers, whose identification and manipulation may prove beneficial in detecting and preventing melanoma initiation.
Science, this issue p. 10.1126/science.aad3867; see also p. 453
Structured Abstract
INTRODUCTIONThe “cancerized field” concept posits that cells in a given tissue sharing an oncogenic mutation are cancer-prone, yet only discreet clones within the field initiate tumors. Studying the process of cancer initiation has remained challenging because of (i) the rarity of these events, (ii) the difficulty of visiualizing initiating clones in living organisms, and (iii) the transient nature of a newly transformed clone emerging before it expands to form an early tumor. A more complete understanding of the molecular processes that regulate cancer initiation could provide important prognostic information about which precancerous lesions are most prone to becoming cancer and also implicate druggable molecular pathways that, when inhibited, may prevent the cancer from ever starting.
RATIONALEThe majority of benign nevi carry oncogenic BRAFV600E mutations and can be considered a cancerized field of melanocytes, but they only rarely convert to melanoma. In an effort to define events that initiate cancer, we used a melanoma model in the zebrafish in which the human BRAFV600E oncogene is driven by the melanocyte-specific mitfa promoter. When bred into a p53 mutant background, these fish develop melanoma tumors over the course of many months. The zebrafish crestin gene is expressed embryonically in neural crest progenitors (NCPs) and is specifically reexpressed only in melanoma tumors, making it an ideal candidate for tracking melanoma from initiation onward.
RESULTSWe developed a crestin:EGFP reporter that recapitulates the embryonic neural crest expression pattern of crestin and its expression in melanoma tumors. We show through live imaging of transgenic zebrafish crestin reporters that within a cancerized field (BRAFV600E-mutant; p53-deficient), a single melanocyte reactivates the NCP state, and this establishes that a fate change occurs at melanoma initiation in this model. Early crestin+ patches of cells expand and are transplantable in a manner consistent with their possessing tumorigenic activity, and they exhibit a gene expression pattern consistent with the NCP identity readout by the crestin reporter. The crestin element is regulated by NCP transcription factors, including sox10. Forced sox10 overexpression in melanocytes accelerated melanoma formation, whereas CRISPR/Cas9 targeting of sox10 delayed melanoma onset. We show activation of super-enhancers at NCP genes in both zebrafish and human melanomas, identifying an epigenetic mechanism for control of this NCP signature leading to melanoma.
CONCLUSIONThis work using our zebrafish melanoma model and in vivo reporter of NCP identity allows us to see cancer from its birth as a single cell and shows the importance of NCP-state reemergence as a key event in melanoma initiation from a field of cancer-prone melanocytes. Thus, in addition to the typical fixed genetic alterations in oncogenes and tumor supressors that are required for cancer development, the reemergence of progenitor identity may be an additional rate-limiting step in the formation of melanoma. Preventing NCP reemergence in a field of cancer-prone melanocytes may thus prove therapeutically useful, and the association of NCP genes with super-enhancer regulatory elements implicates the associated druggable epigenetic machinery in this process. Download high-res image Open in new tab Download Powerpoint Neural crest reporter expression in melanoma.The crestin:EGFP transgene is specifically expressed in melanoma in BRAFV600E/p53 mutant melanoma-prone zebrafish. (Top) A single cell expressing crestin:EGFP expands into a small patch of cells over the course of 2 weeks, capturing the initiation of melanoma formation (bracket). (Bottom) A fully formed melanoma specifically expresses crestin:EGFP, whereas the rest of the fish remains EGFP-negative.
The “cancerized field” concept posits that cancer-prone cells in a given tissue share an oncogenic mutation, but only discreet clones within the field initiate tumors. Most benign nevi carry oncogenic BRAFV600E mutations but rarely become melanoma. The zebrafish crestin gene is expressed embryonically in neural crest progenitors (NCPs) and specifically reexpressed in melanoma. Live imaging of transgenic zebrafish crestin reporters shows that within a cancerized field (BRAFV600E-mutant; p53-deficient), a single melanocyte reactivates the NCP state, revealing a fate change at melanoma initiation in this model. NCP transcription factors, including sox10, regulate crestin expression. Forced sox10 overexpression in melanocytes accelerated melanoma formation, which is consistent with activation of NCP genes and super-enhancers leading to melanoma. Our work highlights NCP state reemergence as a key event in melanoma initiation.
Melanocytes with oncogenic or tumor suppressor mutations revert to expressing the crestin gene early in melanoma formation. [Also see Perspective by Boumahdi and Blanpain]
Melanocytes with oncogenic or tumor suppressor mutations revert to expressing the crestin gene early in melanoma formation. [Also see Perspective by Boumahdi and Blanpain]
DA - 2016/01/29/
PY - 2016
DO - 10.1126/science.aad2197
DP - science.sciencemag.org
VL - 351
IS - 6272
SP - aad2197
LA - en
SN - 0036-8075, 1095-9203
UR - http://science.sciencemag.org/content/351/6272/aad2197
Y2 - 2016/01/29/T14:40:26Z
KW - Development
KW - SKCM
KW - classics
KW - epigenetics
KW - evolution
KW - melanoma
KW - super_enhancer
KW - zebrafish
ER -</div></div></div></div><div class="bib-item"><div class="csl-entry">Lipinski, K. A., Barber, L. J., Davies, M. N., Ashenden, M., Sottoriva, A., &amp; Gerlinger, M. (2016). <a class="doctitle" href="http://www.sciencedirect.com/science/article/pii/S2405803315000692">Cancer Evolution and the Limits of Predictability in Precision Cancer Medicine.</a> <i>Trends in Cancer</i>, <i>2</i>(1), 4963. http://doi.org/10.1016/j.trecan.2015.11.003</div><div class="blink"><a href="javascript:show(this);" onclick="show(this);">abstract</a><div class="bibshowhide"><div class="abstract">The ability to predict the future behavior of an individual cancer is crucial for precision cancer medicine. The discovery of extensive intratumor heterogeneity and ongoing clonal adaptation in human tumors substantiated the notion of cancer as an evolutionary process. Random events are inherent in evolution and tumor spatial structures hinder the efficacy of selection which is the only deterministic evolutionary force. This review outlines how the interaction of these stochastic and deterministic processes which have been extensively studied in evolutionary biology limits cancer predictability and develops evolutionary strategies to improve predictions. Understanding and advancing the cancer predictability horizon is crucial to improve precision medicine outcomes.</div></div></div><div class="blink"><a href="javascript:show(this);" onclick="show(this);">bib</a><div class="bibshowhide"><div class="bib">@article{lipinski_cancer_2016,
title = {Cancer {Evolution} and the {Limits} of {Predictability} in {Precision} {Cancer} {Medicine}},
volume = {2},
issn = {2405-8033},
url = {http://www.sciencedirect.com/science/article/pii/S2405803315000692},
doi = {10.1016/j.trecan.2015.11.003},
number = {1},
urldate = {2016-01-30TZ},
journal = {Trends in Cancer},
author = {Lipinski, Kamil A. and Barber, Louise J. and Davies, Matthew N. and Ashenden, Matthew and Sottoriva, Andrea and Gerlinger, Marco},
month = jan,
year = {2016},
keywords = {classics, evolution, heterogeneity, resistance, review},
pages = {49--63}
}</div></div></div><div class="blink"><a title="Download EndNote record" href="javascript:downloadFile(this);" onclick="downloadFile(this);">ris</a><div class="bibshowhide"><div class="ris">TY - JOUR
TI - Cancer Evolution and the Limits of Predictability in Precision Cancer Medicine
AU - Lipinski, Kamil A.
AU - Barber, Louise J.
AU - Davies, Matthew N.
AU - Ashenden, Matthew
AU - Sottoriva, Andrea
AU - Gerlinger, Marco
T2 - Trends in Cancer
AB - The ability to predict the future behavior of an individual cancer is crucial for precision cancer medicine. The discovery of extensive intratumor heterogeneity and ongoing clonal adaptation in human tumors substantiated the notion of cancer as an evolutionary process. Random events are inherent in evolution and tumor spatial structures hinder the efficacy of selection, which is the only deterministic evolutionary force. This review outlines how the interaction of these stochastic and deterministic processes, which have been extensively studied in evolutionary biology, limits cancer predictability and develops evolutionary strategies to improve predictions. Understanding and advancing the cancer predictability horizon is crucial to improve precision medicine outcomes.
DA - 2016/01//
PY - 2016
DO - 10.1016/j.trecan.2015.11.003
DP - ScienceDirect
VL - 2
IS - 1
SP - 49
EP - 63
J2 - Trends in Cancer
SN - 2405-8033
UR - http://www.sciencedirect.com/science/article/pii/S2405803315000692
Y2 - 2016/01/30/T22:58:32Z
KW - classics
KW - evolution
KW - heterogeneity
KW - resistance
KW - review
ER -</div></div></div></div><div class="bib-item"><div class="csl-entry">Trapnell, C. (2015). <a class="doctitle" href="http://genome.cshlp.org/content/25/10/1491">Defining cell types and states with single-cell genomics.</a> <i>Genome Research</i>, <i>25</i>(10), 14911498. http://doi.org/10.1101/gr.190595.115</div><div class="blink"><a href="javascript:show(this);" onclick="show(this);">abstract</a><div class="bibshowhide"><div class="abstract">A revolution in cellular measurement technology is under way: For the first time we have the ability to monitor global gene regulation in thousands of individual cells in a single experiment. Such experiments will allow us to discover new cell types and states and trace their developmental origins. They overcome fundamental limitations inherent in measurements of bulk cell population that have frustrated efforts to resolve cellular states. Single-cell genomics and proteomics enable not only precise characterization of cell state but also provide a stunningly high-resolution view of transitions between states. These measurements may finally make explicit the metaphor that C.H. Waddington posed nearly 60 years ago to explain cellular plasticity: Cells are residents of a vast “landscape” of possible states over which they travel during development and in disease. Single-cell technology helps not only locate cells on this landscape but illuminates the molecular mechanisms that shape the landscape itself. However single-cell genomics is a field in its infancy with many experimental and computational advances needed to fully realize its full potential.</div></div></div><div class="blink"><a href="javascript:show(this);" onclick="show(this);">bib</a><div class="bibshowhide"><div class="bib">@article{trapnell_defining_2015,
title = {Defining cell types and states with single-cell genomics},
volume = {25},
issn = {1088-9051, 1549-5469},
url = {http://genome.cshlp.org/content/25/10/1491},
doi = {10.1101/gr.190595.115},
language = {en},
number = {10},
urldate = {2015-10-14TZ},
journal = {Genome Research},
author = {Trapnell, Cole},
month = oct,
year = {2015},
pmid = {26430159},
keywords = {Waddington, capacitance, chromatin, classics, epigenetics, evolution, genomics, ideas, oped, review, single-cell},
pages = {1491--1498}
}</div></div></div><div class="blink"><a title="Download EndNote record" href="javascript:downloadFile(this);" onclick="downloadFile(this);">ris</a><div class="bibshowhide"><div class="ris">TY - JOUR
TI - Defining cell types and states with single-cell genomics
AU - Trapnell, Cole
T2 - Genome Research
AB - A revolution in cellular measurement technology is under way: For the first time, we have the ability to monitor global gene regulation in thousands of individual cells in a single experiment. Such experiments will allow us to discover new cell types and states and trace their developmental origins. They overcome fundamental limitations inherent in measurements of bulk cell population that have frustrated efforts to resolve cellular states. Single-cell genomics and proteomics enable not only precise characterization of cell state, but also provide a stunningly high-resolution view of transitions between states. These measurements may finally make explicit the metaphor that C.H. Waddington posed nearly 60 years ago to explain cellular plasticity: Cells are residents of a vast “landscape” of possible states, over which they travel during development and in disease. Single-cell technology helps not only locate cells on this landscape, but illuminates the molecular mechanisms that shape the landscape itself. However, single-cell genomics is a field in its infancy, with many experimental and computational advances needed to fully realize its full potential.
DA - 2015/10/01/
PY - 2015
DO - 10.1101/gr.190595.115
DP - genome.cshlp.org
VL - 25
IS - 10
SP - 1491
EP - 1498
J2 - Genome Res.
LA - en
SN - 1088-9051, 1549-5469
UR - http://genome.cshlp.org/content/25/10/1491
Y2 - 2015/10/14/T06:07:23Z
KW - Waddington
KW - capacitance
KW - chromatin
KW - classics
KW - epigenetics
KW - evolution
KW - genomics
KW - ideas
KW - oped
KW - review
KW - single-cell
ER -</div></div></div></div><div class="bib-item"><div class="csl-entry">Jacobs, F. M. J., Greenberg, D., Nguyen, N., Haeussler, M., Ewing, A. D., Katzman, S., … Haussler, D. (2014). <a class="doctitle" href="http://www.nature.com/nature/journal/v516/n7530/full/nature13760.html">An evolutionary arms race between KRAB zinc-finger genes ZNF91/93 and SVA/L1 retrotransposons.</a> <i>Nature</i>, <i>516</i>(7530), 242245. http://doi.org/10.1038/nature13760</div><div class="blink"><a href="javascript:show(this);" onclick="show(this);">abstract</a><div class="bibshowhide"><div class="abstract">Throughout evolution primate genomes have been modified by waves of retrotransposon insertions. For each wave the host eventually finds a way to repress retrotransposon transcription and prevent further insertions. In mouse embryonic stem cells transcriptional silencing of retrotransposons requires KAP1 (also known as TRIM28) and its repressive complex which can be recruited to target sites by KRAB zinc-finger (KZNF) proteins such as murine-specific ZFP809 which binds to integrated murine leukaemia virus DNA elements and recruits KAP1 to repress them. KZNF genes are one of the fastest growing gene families in primates and this expansion is hypothesized to enable primates to respond to newly emerged retrotransposons. However the identity of KZNF genes battling retrotransposons currently active in the human genome such as SINE-VNTR-Alu (SVA) and long interspersed nuclear element 1 (L1) is unknown. Here we show that two primate-specific KZNF genes rapidly evolved to repress these two distinct retrotransposon families shortly after they began to spread in our ancestral genome. ZNF91 underwent a series of structural changes 8-12 million years ago that enabled it to repress SVA elements. ZNF93 evolved earlier to repress the primate L1 lineage until [sim]12.5 million years ago when the L1PA3-subfamily of retrotransposons escaped ZNF93/s restriction through the removal of the ZNF93-binding site. Our data support a model where KZNF gene expansion limits the activity of newly emerged retrotransposon classes and this is followed by mutations in these retrotransposons to evade repression a cycle of events that could explain the rapid expansion of lineage-specific KZNF genes.</div></div></div><div class="blink"><a href="javascript:show(this);" onclick="show(this);">bib</a><div class="bibshowhide"><div class="bib">@article{jacobs_evolutionary_2014,
title = {An evolutionary arms race between {KRAB} zinc-finger genes {ZNF}91/93 and {SVA}/{L}1 retrotransposons},
volume = {516},
copyright = {© 2014 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.},
issn = {0028-0836},
url = {http://www.nature.com/nature/journal/v516/n7530/full/nature13760.html},
doi = {10.1038/nature13760},
language = {en},
number = {7530},
urldate = {2015-10-12TZ},
journal = {Nature},
author = {Jacobs, Frank M. J. and Greenberg, David and Nguyen, Ngan and Haeussler, Maximilian and Ewing, Adam D. and Katzman, Sol and Paten, Benedict and Salama, Sofie R. and Haussler, David},
month = dec,
year = {2014},
keywords = {classics, genereg, ideas, interactions, lncrna, network, transposon},
pages = {242--245}
}</div></div></div><div class="blink"><a title="Download EndNote record" href="javascript:downloadFile(this);" onclick="downloadFile(this);">ris</a><div class="bibshowhide"><div class="ris">TY - JOUR
TI - An evolutionary arms race between KRAB zinc-finger genes ZNF91/93 and SVA/L1 retrotransposons
AU - Jacobs, Frank M. J.
AU - Greenberg, David
AU - Nguyen, Ngan
AU - Haeussler, Maximilian
AU - Ewing, Adam D.
AU - Katzman, Sol
AU - Paten, Benedict
AU - Salama, Sofie R.
AU - Haussler, David
T2 - Nature
AB - Throughout evolution primate genomes have been modified by waves of retrotransposon insertions. For each wave, the host eventually finds a way to repress retrotransposon transcription and prevent further insertions. In mouse embryonic stem cells, transcriptional silencing of retrotransposons requires KAP1 (also known as TRIM28) and its repressive complex, which can be recruited to target sites by KRAB zinc-finger (KZNF) proteins such as murine-specific ZFP809 which binds to integrated murine leukaemia virus DNA elements and recruits KAP1 to repress them. KZNF genes are one of the fastest growing gene families in primates and this expansion is hypothesized to enable primates to respond to newly emerged retrotransposons. However, the identity of KZNF genes battling retrotransposons currently active in the human genome, such as SINE-VNTR-Alu (SVA) and long interspersed nuclear element 1 (L1), is unknown. Here we show that two primate-specific KZNF genes rapidly evolved to repress these two distinct retrotransposon families shortly after they began to spread in our ancestral genome. ZNF91 underwent a series of structural changes 8-12 million years ago that enabled it to repress SVA elements. ZNF93 evolved earlier to repress the primate L1 lineage until [sim]12.5 million years ago when the L1PA3-subfamily of retrotransposons escaped ZNF93/'s restriction through the removal of the ZNF93-binding site. Our data support a model where KZNF gene expansion limits the activity of newly emerged retrotransposon classes, and this is followed by mutations in these retrotransposons to evade repression, a cycle of events that could explain the rapid expansion of lineage-specific KZNF genes.
DA - 2014/12/11/
PY - 2014
DO - 10.1038/nature13760
DP - www.nature.com
VL - 516
IS - 7530
SP - 242
EP - 245
J2 - Nature
LA - en
SN - 0028-0836
UR - http://www.nature.com/nature/journal/v516/n7530/full/nature13760.html
Y2 - 2015/10/12/T21:07:51Z
KW - classics
KW - genereg
KW - ideas
KW - interactions
KW - lncrna
KW - network
KW - transposon
ER -</div></div></div></div></div></div>

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<div class="full-bib-section"><div class="bib-item"><div class="csl-entry">Beerenwinkel, N., Greenman, C. D., &amp; Lagergren, J. (2016). <a class="doctitle" href="http://dx.doi.org/10.1371/journal.pcbi.1004717">Computational Cancer Biology: An Evolutionary Perspective.</a> <i>PLoS Comput Biol</i>, <i>12</i>(2), e1004717. http://doi.org/10.1371/journal.pcbi.1004717</div><div class="blink"><a href="javascript:show(this);" onclick="show(this);">bib</a><div class="bibshowhide"><div class="bib">@article{beerenwinkel_computational_2016,
title = {Computational {Cancer} {Biology}: {An} {Evolutionary} {Perspective}},
volume = {12},
shorttitle = {Computational {Cancer} {Biology}},
url = {http://dx.doi.org/10.1371/journal.pcbi.1004717},
doi = {10.1371/journal.pcbi.1004717},
number = {2},
urldate = {2016-02-05TZ},
journal = {PLoS Comput Biol},
author = {Beerenwinkel, Niko and Greenman, Chris D. and Lagergren, Jens},
month = feb,
year = {2016},
keywords = {cancer, concepts, darwinian, epigenetics, evolution, mathematical modeling, review, statistics, variant},
pages = {e1004717}
}</div></div></div><div class="blink"><a title="Download EndNote record" href="javascript:downloadFile(this);" onclick="downloadFile(this);">ris</a><div class="bibshowhide"><div class="ris">TY - JOUR
TI - Computational Cancer Biology: An Evolutionary Perspective
AU - Beerenwinkel, Niko
AU - Greenman, Chris D.
AU - Lagergren, Jens
T2 - PLoS Comput Biol
DA - 2016/02/04/
PY - 2016
DO - 10.1371/journal.pcbi.1004717
DP - PLoS Journals
VL - 12
IS - 2
SP - e1004717
J2 - PLoS Comput Biol
ST - Computational Cancer Biology
UR - http://dx.doi.org/10.1371/journal.pcbi.1004717
Y2 - 2016/02/05/T20:21:50Z
KW - cancer
KW - concepts
KW - darwinian
KW - epigenetics
KW - evolution
KW - mathematical modeling
KW - review
KW - statistics
KW - variant
ER -</div></div></div></div><div class="bib-item"><div class="csl-entry">Kaufman, C. K., Mosimann, C., Fan, Z. P., Yang, S., Thomas, A. J., Ablain, J., … Zon, L. I. (2016). <a class="doctitle" href="http://science.sciencemag.org/content/351/6272/aad2197">A zebrafish melanoma model reveals emergence of neural crest identity during melanoma initiation.</a> <i>Science</i>, <i>351</i>(6272), aad2197. http://doi.org/10.1126/science.aad2197</div><div class="blink"><a href="javascript:show(this);" onclick="show(this);">abstract</a><div class="bibshowhide"><div class="abstract">Visualizing the beginnings of melanoma
In cancer biology a tumor begins from a single cell within a group of precancerous cells that share genetic mutations. Kaufman et al. used a zebrafish melanoma model to visualize cancer initiation (see the Perspective by Boumahdi and Blanpain). They used a fluorescent reporter that specifically lit up neural crest progenitors that are only present during embryogenesis or during adult melanoma tumor formation. The appearance of this tumor correlated with a set of gene regulatory elements called super-enhancers whose identification and manipulation may prove beneficial in detecting and preventing melanoma initiation.
Science this issue p. 10.1126/science.aad3867; see also p. 453
Structured Abstract
INTRODUCTIONThe “cancerized field” concept posits that cells in a given tissue sharing an oncogenic mutation are cancer-prone yet only discreet clones within the field initiate tumors. Studying the process of cancer initiation has remained challenging because of (i) the rarity of these events (ii) the difficulty of visiualizing initiating clones in living organisms and (iii) the transient nature of a newly transformed clone emerging before it expands to form an early tumor. A more complete understanding of the molecular processes that regulate cancer initiation could provide important prognostic information about which precancerous lesions are most prone to becoming cancer and also implicate druggable molecular pathways that when inhibited may prevent the cancer from ever starting.
RATIONALEThe majority of benign nevi carry oncogenic BRAFV600E mutations and can be considered a cancerized field of melanocytes but they only rarely convert to melanoma. In an effort to define events that initiate cancer we used a melanoma model in the zebrafish in which the human BRAFV600E oncogene is driven by the melanocyte-specific mitfa promoter. When bred into a p53 mutant background these fish develop melanoma tumors over the course of many months. The zebrafish crestin gene is expressed embryonically in neural crest progenitors (NCPs) and is specifically reexpressed only in melanoma tumors making it an ideal candidate for tracking melanoma from initiation onward.
RESULTSWe developed a crestin:EGFP reporter that recapitulates the embryonic neural crest expression pattern of crestin and its expression in melanoma tumors. We show through live imaging of transgenic zebrafish crestin reporters that within a cancerized field (BRAFV600E-mutant; p53-deficient) a single melanocyte reactivates the NCP state and this establishes that a fate change occurs at melanoma initiation in this model. Early crestin+ patches of cells expand and are transplantable in a manner consistent with their possessing tumorigenic activity and they exhibit a gene expression pattern consistent with the NCP identity readout by the crestin reporter. The crestin element is regulated by NCP transcription factors including sox10. Forced sox10 overexpression in melanocytes accelerated melanoma formation whereas CRISPR/Cas9 targeting of sox10 delayed melanoma onset. We show activation of super-enhancers at NCP genes in both zebrafish and human melanomas identifying an epigenetic mechanism for control of this NCP signature leading to melanoma.
CONCLUSIONThis work using our zebrafish melanoma model and in vivo reporter of NCP identity allows us to see cancer from its birth as a single cell and shows the importance of NCP-state reemergence as a key event in melanoma initiation from a field of cancer-prone melanocytes. Thus in addition to the typical fixed genetic alterations in oncogenes and tumor supressors that are required for cancer development the reemergence of progenitor identity may be an additional rate-limiting step in the formation of melanoma. Preventing NCP reemergence in a field of cancer-prone melanocytes may thus prove therapeutically useful and the association of NCP genes with super-enhancer regulatory elements implicates the associated druggable epigenetic machinery in this process. Download high-res image Open in new tab Download Powerpoint Neural crest reporter expression in melanoma.The crestin:EGFP transgene is specifically expressed in melanoma in BRAFV600E/p53 mutant melanoma-prone zebrafish. (Top) A single cell expressing crestin:EGFP expands into a small patch of cells over the course of 2 weeks capturing the initiation of melanoma formation (bracket). (Bottom) A fully formed melanoma specifically expresses crestin:EGFP whereas the rest of the fish remains EGFP-negative.
The “cancerized field” concept posits that cancer-prone cells in a given tissue share an oncogenic mutation but only discreet clones within the field initiate tumors. Most benign nevi carry oncogenic BRAFV600E mutations but rarely become melanoma. The zebrafish crestin gene is expressed embryonically in neural crest progenitors (NCPs) and specifically reexpressed in melanoma. Live imaging of transgenic zebrafish crestin reporters shows that within a cancerized field (BRAFV600E-mutant; p53-deficient) a single melanocyte reactivates the NCP state revealing a fate change at melanoma initiation in this model. NCP transcription factors including sox10 regulate crestin expression. Forced sox10 overexpression in melanocytes accelerated melanoma formation which is consistent with activation of NCP genes and super-enhancers leading to melanoma. Our work highlights NCP state reemergence as a key event in melanoma initiation.
Melanocytes with oncogenic or tumor suppressor mutations revert to expressing the crestin gene early in melanoma formation. [Also see Perspective by Boumahdi and Blanpain]
Melanocytes with oncogenic or tumor suppressor mutations revert to expressing the crestin gene early in melanoma formation. [Also see Perspective by Boumahdi and Blanpain]</div></div></div><div class="blink"><a href="javascript:show(this);" onclick="show(this);">bib</a><div class="bibshowhide"><div class="bib">@article{kaufman_zebrafish_2016,
title = {A zebrafish melanoma model reveals emergence of neural crest identity during melanoma initiation},
volume = {351},
copyright = {Copyright © 2016, American Association for the Advancement of Science},
issn = {0036-8075, 1095-9203},
url = {http://science.sciencemag.org/content/351/6272/aad2197},
doi = {10.1126/science.aad2197},
language = {en},
number = {6272},
urldate = {2016-01-29TZ},
journal = {Science},
author = {Kaufman, Charles K. and Mosimann, Christian and Fan, Zi Peng and Yang, Song and Thomas, Andrew J. and Ablain, Julien and Tan, Justin L. and Fogley, Rachel D. and Rooijen, Ellen van and Hagedorn, Elliott J. and Ciarlo, Christie and White, Richard M. and Matos, Dominick A. and Puller, Ann-Christin and Santoriello, Cristina and Liao, Eric C. and Young, Richard A. and Zon, Leonard I.},
month = jan,
year = {2016},
keywords = {Development, SKCM, classics, epigenetics, evolution, melanoma, super\_enhancer, zebrafish},
pages = {aad2197}
}</div></div></div><div class="blink"><a title="Download EndNote record" href="javascript:downloadFile(this);" onclick="downloadFile(this);">ris</a><div class="bibshowhide"><div class="ris">TY - JOUR
TI - A zebrafish melanoma model reveals emergence of neural crest identity during melanoma initiation
AU - Kaufman, Charles K.
AU - Mosimann, Christian
AU - Fan, Zi Peng
AU - Yang, Song
AU - Thomas, Andrew J.
AU - Ablain, Julien
AU - Tan, Justin L.
AU - Fogley, Rachel D.
AU - Rooijen, Ellen van
AU - Hagedorn, Elliott J.
AU - Ciarlo, Christie
AU - White, Richard M.
AU - Matos, Dominick A.
AU - Puller, Ann-Christin
AU - Santoriello, Cristina
AU - Liao, Eric C.
AU - Young, Richard A.
AU - Zon, Leonard I.
T2 - Science
AB - Visualizing the beginnings of melanoma
In cancer biology, a tumor begins from a single cell within a group of precancerous cells that share genetic mutations. Kaufman et al. used a zebrafish melanoma model to visualize cancer initiation (see the Perspective by Boumahdi and Blanpain). They used a fluorescent reporter that specifically lit up neural crest progenitors that are only present during embryogenesis or during adult melanoma tumor formation. The appearance of this tumor correlated with a set of gene regulatory elements, called super-enhancers, whose identification and manipulation may prove beneficial in detecting and preventing melanoma initiation.
Science, this issue p. 10.1126/science.aad3867; see also p. 453
Structured Abstract
INTRODUCTIONThe “cancerized field” concept posits that cells in a given tissue sharing an oncogenic mutation are cancer-prone, yet only discreet clones within the field initiate tumors. Studying the process of cancer initiation has remained challenging because of (i) the rarity of these events, (ii) the difficulty of visiualizing initiating clones in living organisms, and (iii) the transient nature of a newly transformed clone emerging before it expands to form an early tumor. A more complete understanding of the molecular processes that regulate cancer initiation could provide important prognostic information about which precancerous lesions are most prone to becoming cancer and also implicate druggable molecular pathways that, when inhibited, may prevent the cancer from ever starting.
RATIONALEThe majority of benign nevi carry oncogenic BRAFV600E mutations and can be considered a cancerized field of melanocytes, but they only rarely convert to melanoma. In an effort to define events that initiate cancer, we used a melanoma model in the zebrafish in which the human BRAFV600E oncogene is driven by the melanocyte-specific mitfa promoter. When bred into a p53 mutant background, these fish develop melanoma tumors over the course of many months. The zebrafish crestin gene is expressed embryonically in neural crest progenitors (NCPs) and is specifically reexpressed only in melanoma tumors, making it an ideal candidate for tracking melanoma from initiation onward.
RESULTSWe developed a crestin:EGFP reporter that recapitulates the embryonic neural crest expression pattern of crestin and its expression in melanoma tumors. We show through live imaging of transgenic zebrafish crestin reporters that within a cancerized field (BRAFV600E-mutant; p53-deficient), a single melanocyte reactivates the NCP state, and this establishes that a fate change occurs at melanoma initiation in this model. Early crestin+ patches of cells expand and are transplantable in a manner consistent with their possessing tumorigenic activity, and they exhibit a gene expression pattern consistent with the NCP identity readout by the crestin reporter. The crestin element is regulated by NCP transcription factors, including sox10. Forced sox10 overexpression in melanocytes accelerated melanoma formation, whereas CRISPR/Cas9 targeting of sox10 delayed melanoma onset. We show activation of super-enhancers at NCP genes in both zebrafish and human melanomas, identifying an epigenetic mechanism for control of this NCP signature leading to melanoma.
CONCLUSIONThis work using our zebrafish melanoma model and in vivo reporter of NCP identity allows us to see cancer from its birth as a single cell and shows the importance of NCP-state reemergence as a key event in melanoma initiation from a field of cancer-prone melanocytes. Thus, in addition to the typical fixed genetic alterations in oncogenes and tumor supressors that are required for cancer development, the reemergence of progenitor identity may be an additional rate-limiting step in the formation of melanoma. Preventing NCP reemergence in a field of cancer-prone melanocytes may thus prove therapeutically useful, and the association of NCP genes with super-enhancer regulatory elements implicates the associated druggable epigenetic machinery in this process. Download high-res image Open in new tab Download Powerpoint Neural crest reporter expression in melanoma.The crestin:EGFP transgene is specifically expressed in melanoma in BRAFV600E/p53 mutant melanoma-prone zebrafish. (Top) A single cell expressing crestin:EGFP expands into a small patch of cells over the course of 2 weeks, capturing the initiation of melanoma formation (bracket). (Bottom) A fully formed melanoma specifically expresses crestin:EGFP, whereas the rest of the fish remains EGFP-negative.
The “cancerized field” concept posits that cancer-prone cells in a given tissue share an oncogenic mutation, but only discreet clones within the field initiate tumors. Most benign nevi carry oncogenic BRAFV600E mutations but rarely become melanoma. The zebrafish crestin gene is expressed embryonically in neural crest progenitors (NCPs) and specifically reexpressed in melanoma. Live imaging of transgenic zebrafish crestin reporters shows that within a cancerized field (BRAFV600E-mutant; p53-deficient), a single melanocyte reactivates the NCP state, revealing a fate change at melanoma initiation in this model. NCP transcription factors, including sox10, regulate crestin expression. Forced sox10 overexpression in melanocytes accelerated melanoma formation, which is consistent with activation of NCP genes and super-enhancers leading to melanoma. Our work highlights NCP state reemergence as a key event in melanoma initiation.
Melanocytes with oncogenic or tumor suppressor mutations revert to expressing the crestin gene early in melanoma formation. [Also see Perspective by Boumahdi and Blanpain]
Melanocytes with oncogenic or tumor suppressor mutations revert to expressing the crestin gene early in melanoma formation. [Also see Perspective by Boumahdi and Blanpain]
DA - 2016/01/29/
PY - 2016
DO - 10.1126/science.aad2197
DP - science.sciencemag.org
VL - 351
IS - 6272
SP - aad2197
LA - en
SN - 0036-8075, 1095-9203
UR - http://science.sciencemag.org/content/351/6272/aad2197
Y2 - 2016/01/29/T14:40:26Z
KW - Development
KW - SKCM
KW - classics
KW - epigenetics
KW - evolution
KW - melanoma
KW - super_enhancer
KW - zebrafish
ER -</div></div></div></div><div class="bib-item"><div class="csl-entry">Lipinski, K. A., Barber, L. J., Davies, M. N., Ashenden, M., Sottoriva, A., &amp; Gerlinger, M. (2016). <a class="doctitle" href="http://www.sciencedirect.com/science/article/pii/S2405803315000692">Cancer Evolution and the Limits of Predictability in Precision Cancer Medicine.</a> <i>Trends in Cancer</i>, <i>2</i>(1), 4963. http://doi.org/10.1016/j.trecan.2015.11.003</div><div class="blink"><a href="javascript:show(this);" onclick="show(this);">abstract</a><div class="bibshowhide"><div class="abstract">The ability to predict the future behavior of an individual cancer is crucial for precision cancer medicine. The discovery of extensive intratumor heterogeneity and ongoing clonal adaptation in human tumors substantiated the notion of cancer as an evolutionary process. Random events are inherent in evolution and tumor spatial structures hinder the efficacy of selection which is the only deterministic evolutionary force. This review outlines how the interaction of these stochastic and deterministic processes which have been extensively studied in evolutionary biology limits cancer predictability and develops evolutionary strategies to improve predictions. Understanding and advancing the cancer predictability horizon is crucial to improve precision medicine outcomes.</div></div></div><div class="blink"><a href="javascript:show(this);" onclick="show(this);">bib</a><div class="bibshowhide"><div class="bib">@article{lipinski_cancer_2016,
title = {Cancer {Evolution} and the {Limits} of {Predictability} in {Precision} {Cancer} {Medicine}},
volume = {2},
issn = {2405-8033},
url = {http://www.sciencedirect.com/science/article/pii/S2405803315000692},
doi = {10.1016/j.trecan.2015.11.003},
number = {1},
urldate = {2016-01-30TZ},
journal = {Trends in Cancer},
author = {Lipinski, Kamil A. and Barber, Louise J. and Davies, Matthew N. and Ashenden, Matthew and Sottoriva, Andrea and Gerlinger, Marco},
month = jan,
year = {2016},
keywords = {classics, evolution, heterogeneity, resistance, review},
pages = {49--63}
}</div></div></div><div class="blink"><a title="Download EndNote record" href="javascript:downloadFile(this);" onclick="downloadFile(this);">ris</a><div class="bibshowhide"><div class="ris">TY - JOUR
TI - Cancer Evolution and the Limits of Predictability in Precision Cancer Medicine
AU - Lipinski, Kamil A.
AU - Barber, Louise J.
AU - Davies, Matthew N.
AU - Ashenden, Matthew
AU - Sottoriva, Andrea
AU - Gerlinger, Marco
T2 - Trends in Cancer
AB - The ability to predict the future behavior of an individual cancer is crucial for precision cancer medicine. The discovery of extensive intratumor heterogeneity and ongoing clonal adaptation in human tumors substantiated the notion of cancer as an evolutionary process. Random events are inherent in evolution and tumor spatial structures hinder the efficacy of selection, which is the only deterministic evolutionary force. This review outlines how the interaction of these stochastic and deterministic processes, which have been extensively studied in evolutionary biology, limits cancer predictability and develops evolutionary strategies to improve predictions. Understanding and advancing the cancer predictability horizon is crucial to improve precision medicine outcomes.
DA - 2016/01//
PY - 2016
DO - 10.1016/j.trecan.2015.11.003
DP - ScienceDirect
VL - 2
IS - 1
SP - 49
EP - 63
J2 - Trends in Cancer
SN - 2405-8033
UR - http://www.sciencedirect.com/science/article/pii/S2405803315000692
Y2 - 2016/01/30/T22:58:32Z
KW - classics
KW - evolution
KW - heterogeneity
KW - resistance
KW - review
ER -</div></div></div></div><div class="bib-item"><div class="csl-entry">Trapnell, C. (2015). <a class="doctitle" href="http://genome.cshlp.org/content/25/10/1491">Defining cell types and states with single-cell genomics.</a> <i>Genome Research</i>, <i>25</i>(10), 14911498. http://doi.org/10.1101/gr.190595.115</div><div class="blink"><a href="javascript:show(this);" onclick="show(this);">abstract</a><div class="bibshowhide"><div class="abstract">A revolution in cellular measurement technology is under way: For the first time we have the ability to monitor global gene regulation in thousands of individual cells in a single experiment. Such experiments will allow us to discover new cell types and states and trace their developmental origins. They overcome fundamental limitations inherent in measurements of bulk cell population that have frustrated efforts to resolve cellular states. Single-cell genomics and proteomics enable not only precise characterization of cell state but also provide a stunningly high-resolution view of transitions between states. These measurements may finally make explicit the metaphor that C.H. Waddington posed nearly 60 years ago to explain cellular plasticity: Cells are residents of a vast “landscape” of possible states over which they travel during development and in disease. Single-cell technology helps not only locate cells on this landscape but illuminates the molecular mechanisms that shape the landscape itself. However single-cell genomics is a field in its infancy with many experimental and computational advances needed to fully realize its full potential.</div></div></div><div class="blink"><a href="javascript:show(this);" onclick="show(this);">bib</a><div class="bibshowhide"><div class="bib">@article{trapnell_defining_2015,
title = {Defining cell types and states with single-cell genomics},
volume = {25},
issn = {1088-9051, 1549-5469},
url = {http://genome.cshlp.org/content/25/10/1491},
doi = {10.1101/gr.190595.115},
language = {en},
number = {10},
urldate = {2015-10-14TZ},
journal = {Genome Research},
author = {Trapnell, Cole},
month = oct,
year = {2015},
pmid = {26430159},
keywords = {Waddington, capacitance, chromatin, classics, epigenetics, evolution, genomics, ideas, oped, review, single-cell},
pages = {1491--1498}
}</div></div></div><div class="blink"><a title="Download EndNote record" href="javascript:downloadFile(this);" onclick="downloadFile(this);">ris</a><div class="bibshowhide"><div class="ris">TY - JOUR
TI - Defining cell types and states with single-cell genomics
AU - Trapnell, Cole
T2 - Genome Research
AB - A revolution in cellular measurement technology is under way: For the first time, we have the ability to monitor global gene regulation in thousands of individual cells in a single experiment. Such experiments will allow us to discover new cell types and states and trace their developmental origins. They overcome fundamental limitations inherent in measurements of bulk cell population that have frustrated efforts to resolve cellular states. Single-cell genomics and proteomics enable not only precise characterization of cell state, but also provide a stunningly high-resolution view of transitions between states. These measurements may finally make explicit the metaphor that C.H. Waddington posed nearly 60 years ago to explain cellular plasticity: Cells are residents of a vast “landscape” of possible states, over which they travel during development and in disease. Single-cell technology helps not only locate cells on this landscape, but illuminates the molecular mechanisms that shape the landscape itself. However, single-cell genomics is a field in its infancy, with many experimental and computational advances needed to fully realize its full potential.
DA - 2015/10/01/
PY - 2015
DO - 10.1101/gr.190595.115
DP - genome.cshlp.org
VL - 25
IS - 10
SP - 1491
EP - 1498
J2 - Genome Res.
LA - en
SN - 1088-9051, 1549-5469
UR - http://genome.cshlp.org/content/25/10/1491
Y2 - 2015/10/14/T06:07:23Z
KW - Waddington
KW - capacitance
KW - chromatin
KW - classics
KW - epigenetics
KW - evolution
KW - genomics
KW - ideas
KW - oped
KW - review
KW - single-cell
ER -</div></div></div></div><div class="bib-item"><div class="csl-entry">Jacobs, F. M. J., Greenberg, D., Nguyen, N., Haeussler, M., Ewing, A. D., Katzman, S., … Haussler, D. (2014). <a class="doctitle" href="http://www.nature.com/nature/journal/v516/n7530/full/nature13760.html">An evolutionary arms race between KRAB zinc-finger genes ZNF91/93 and SVA/L1 retrotransposons.</a> <i>Nature</i>, <i>516</i>(7530), 242245. http://doi.org/10.1038/nature13760</div><div class="blink"><a href="javascript:show(this);" onclick="show(this);">abstract</a><div class="bibshowhide"><div class="abstract">Throughout evolution primate genomes have been modified by waves of retrotransposon insertions. For each wave the host eventually finds a way to repress retrotransposon transcription and prevent further insertions. In mouse embryonic stem cells transcriptional silencing of retrotransposons requires KAP1 (also known as TRIM28) and its repressive complex which can be recruited to target sites by KRAB zinc-finger (KZNF) proteins such as murine-specific ZFP809 which binds to integrated murine leukaemia virus DNA elements and recruits KAP1 to repress them. KZNF genes are one of the fastest growing gene families in primates and this expansion is hypothesized to enable primates to respond to newly emerged retrotransposons. However the identity of KZNF genes battling retrotransposons currently active in the human genome such as SINE-VNTR-Alu (SVA) and long interspersed nuclear element 1 (L1) is unknown. Here we show that two primate-specific KZNF genes rapidly evolved to repress these two distinct retrotransposon families shortly after they began to spread in our ancestral genome. ZNF91 underwent a series of structural changes 8-12 million years ago that enabled it to repress SVA elements. ZNF93 evolved earlier to repress the primate L1 lineage until [sim]12.5 million years ago when the L1PA3-subfamily of retrotransposons escaped ZNF93/s restriction through the removal of the ZNF93-binding site. Our data support a model where KZNF gene expansion limits the activity of newly emerged retrotransposon classes and this is followed by mutations in these retrotransposons to evade repression a cycle of events that could explain the rapid expansion of lineage-specific KZNF genes.</div></div></div><div class="blink"><a href="javascript:show(this);" onclick="show(this);">bib</a><div class="bibshowhide"><div class="bib">@article{jacobs_evolutionary_2014,
title = {An evolutionary arms race between {KRAB} zinc-finger genes {ZNF}91/93 and {SVA}/{L}1 retrotransposons},
volume = {516},
copyright = {© 2014 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.},
issn = {0028-0836},
url = {http://www.nature.com/nature/journal/v516/n7530/full/nature13760.html},
doi = {10.1038/nature13760},
language = {en},
number = {7530},
urldate = {2015-10-12TZ},
journal = {Nature},
author = {Jacobs, Frank M. J. and Greenberg, David and Nguyen, Ngan and Haeussler, Maximilian and Ewing, Adam D. and Katzman, Sol and Paten, Benedict and Salama, Sofie R. and Haussler, David},
month = dec,
year = {2014},
keywords = {classics, genereg, ideas, interactions, lncrna, network, transposon},
pages = {242--245}
}</div></div></div><div class="blink"><a title="Download EndNote record" href="javascript:downloadFile(this);" onclick="downloadFile(this);">ris</a><div class="bibshowhide"><div class="ris">TY - JOUR
TI - An evolutionary arms race between KRAB zinc-finger genes ZNF91/93 and SVA/L1 retrotransposons
AU - Jacobs, Frank M. J.
AU - Greenberg, David
AU - Nguyen, Ngan
AU - Haeussler, Maximilian
AU - Ewing, Adam D.
AU - Katzman, Sol
AU - Paten, Benedict
AU - Salama, Sofie R.
AU - Haussler, David
T2 - Nature
AB - Throughout evolution primate genomes have been modified by waves of retrotransposon insertions. For each wave, the host eventually finds a way to repress retrotransposon transcription and prevent further insertions. In mouse embryonic stem cells, transcriptional silencing of retrotransposons requires KAP1 (also known as TRIM28) and its repressive complex, which can be recruited to target sites by KRAB zinc-finger (KZNF) proteins such as murine-specific ZFP809 which binds to integrated murine leukaemia virus DNA elements and recruits KAP1 to repress them. KZNF genes are one of the fastest growing gene families in primates and this expansion is hypothesized to enable primates to respond to newly emerged retrotransposons. However, the identity of KZNF genes battling retrotransposons currently active in the human genome, such as SINE-VNTR-Alu (SVA) and long interspersed nuclear element 1 (L1), is unknown. Here we show that two primate-specific KZNF genes rapidly evolved to repress these two distinct retrotransposon families shortly after they began to spread in our ancestral genome. ZNF91 underwent a series of structural changes 8-12 million years ago that enabled it to repress SVA elements. ZNF93 evolved earlier to repress the primate L1 lineage until [sim]12.5 million years ago when the L1PA3-subfamily of retrotransposons escaped ZNF93/'s restriction through the removal of the ZNF93-binding site. Our data support a model where KZNF gene expansion limits the activity of newly emerged retrotransposon classes, and this is followed by mutations in these retrotransposons to evade repression, a cycle of events that could explain the rapid expansion of lineage-specific KZNF genes.
DA - 2014/12/11/
PY - 2014
DO - 10.1038/nature13760
DP - www.nature.com
VL - 516
IS - 7530
SP - 242
EP - 245
J2 - Nature
LA - en
SN - 0028-0836
UR - http://www.nature.com/nature/journal/v516/n7530/full/nature13760.html
Y2 - 2015/10/12/T21:07:51Z
KW - classics
KW - genereg
KW - ideas
KW - interactions
KW - lncrna
KW - network
KW - transposon
ER -</div></div></div></div></div></div>

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{% if site.google_analytics %}
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<!-- Target for toggling the sidebar `.sidebar-checkbox` is for regular
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<p>{{ site.description }}</p>
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<nav class="sidebar-nav">
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{% comment %}
The code below dynamically generates a sidebar nav of pages with
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{% comment %}
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<!DOCTYPE html>
<html lang="en-us">
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<body>
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<small><a href="{{ site.url }}/blog" rel="me" title="Blog"><i class="iconm iconm-quill"></i></a></small>
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{% include scripts.html %}
</body>
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---
layout: default
---
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---
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{% include meta_info.html %}
{% endunless %}
{{ content }}
<hr>
{% if page.tags contains 'R' %}
{% include rblogger.html %}
{% endif %}
<span class="post-date metafoot" itemprop="datePublished" content="{{ page.date | date: "%Y-%m-%d" }}"><i class="fa fa-calendar" title="Date published"> <a class="permalink" href="{{ site.url }}{{ page.url }}" itemprop="url" title="Permanent link to this post">{{ page.date | date_to_string }}</a> </i></span>
{% if page.modified.size > 2 %}{% assign moddate = page.modified | date_to_string %}{% assign pgdate = page.date | date_to_string %}{% unless moddate == pgdate | date_to_string %}<span class="post-date metafoot" itemprop="dateModified" content="{{ page.modified | date: "%Y-%m-%d" }}"><i class="fa fa-edit" title="Last updated"> {{ page.modified | date_to_string }}</i></span>{% endunless %}{% endif %}
<span class="post-tags" itemprop="keywords" content="{{ page.tags | array_to_sentence_string }}">{% for tag in page.tags %}{% if forloop.first %}<i class="fa fa-tags" title="page tags"></i>{% endif %} <a href="{{ site.url }}/tags/#{{ tag | cgi_escape }}" title="Pages tagged {{ tag }}" rel="tag">{{ tag }}</a>{% unless forloop.last %} &bull; {% endunless %}{% endfor %}</span>
{% unless page.show_meta == false %}
{% include meta_info.html %}
{% endunless %}
</div>
{% unless page.hide_printmsg == true %}
{% include printmsgposts.html %}
{% endunless %}
<div class="page-break"></div>
<div class="related">
<h2>Related Posts</h2>
<ul>
{% for post in site.posts %}
{% if post.url != page.url %}
{% for tag in page.tags %}
{% if post.tags contains tag %}
<li><a href="{{ site.url }}{{ post.url }}">{{ post.title }}</a><br /></li>
{% break %}
{% endif %}
{% endfor %}
{% endif %}
{% endfor %}
</ul>
</div>
<div class="prevnext">
{% if page.previous.url %}
<a class="prevnext-item older" href="{{ site.url }}{{page.previous.url}}" title="{{ page.previous.title }}">Older</a>
{% else %}
<span class="prevnext-item older">Older</span>
{% endif %}
{% if page.next.url %}
<a class="prevnext-item older" href="{{ site.url }}{{page.next.url}}" title="{{ page.next.title }}">Newer</a>
{% else %}
<span class="prevnext-item older">Newer</span>
{% endif %}
</div>
<div class="page-break"></div>
{% if site.disqus_shortname and page.comments == true %}<div id="disqus_thread"></div><!-- /#disqus_thread -->{% endif %}

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---
layout: default
---
<div class="page">
<h1 class="page-title">{{ page.title }}</h1>
{% if page.show_meta == true %}
{% include meta_info.html %}
{% endif %}
{{ content }}
{% if page.category contains "mypubs" %}
{% include mypubs.html %}
{% elsif page.category contains "myaoi" %}
{% include myaoi.html %}
{% endif %}
{% if page.show_meta == true %}
{% include meta_info.html %}
{% endif %}
</div>
{% unless page.hide_printmsg == true %}
{% include printmsgpages.html %}
{% endunless %}
<div class="page-break"></div>
{% if site.disqus_shortname and page.comments == true %}<div id="disqus_thread"></div><!-- /#disqus_thread -->{% endif %}

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---
# This layout is used to redirect pages, if you moved them.
# Use the following settings in front matter:
#
# layout: redirect
# sitemap: false
# permalink: /old-location/
# redirect_to: /new-location/
#
# Idea and Code by: http://codingtips.kanishkkunal.in/about/
---
<!DOCTYPE html>
<html>
<head>
{% if page.redirect_to contains 'http' %}
{% assign domain = '' %}
{% else %}
{% assign domain = site.url %}
{% endif %}
<link rel="canonical" href="{{ domain }}{{ page.redirect_to }}"/>
<meta http-equiv="content-type" content="text/html; charset=utf-8" />
<meta http-equiv="refresh" content="1;url={{ domain }}{{ page.redirect_to }}" />
</head>
<body>
<h1>Redirecting...</h1>
{% if page.redirect_to contains 'http' %}
{% assign domain = '' %}
{% else %}
{% assign domain = site.url %}
{% endif %}
If you are not redirected automatically, visit <a href="{{ domain }}{{ page.redirect_to }}">{{ domain }}{{ page.redirect_to }}<a>.
<script>location='{{ domain }}{{ page.redirect_to }}'</script>
</body>
</html>

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---
layout: post
title: "Example content"
date: "2013-01-01"
slug: "example_content"
description: "Example content from lanyon. If page description is more than 140 words, it will be shown as post summary on home page and blog index else post excerpt will be shown. Same rule is for html meta description: >140 words in description or first 50 words of posts will be shown as summary. Page excerpt supports markdown formatted summary."
category:
- views
- featured
# tags will also be used as html meta keywords.
tags:
- examples
- common_tag
show_meta: true
comments: true
mathjax: true
gistembed: true
published: true
noindex: false
nofollow: false
# hide QR code, permalink block while printing.
hide_printmsg: false
# show post summary or full post in RSS feed.
summaryfeed: false
## for twitter summary card with squared image and page description or page excerpt:
# imagesummary: foo.png
## for twitter card with large image:
# imagefeature: "http://img.youtube.com/vi/VEIrQUXm_hY/0.jpg"
## for twitter video card: (active for this page)
videofeature: "https://www.youtube.com/embed/iG9CE55wbtY"
imagefeature: "http://img.youtube.com/vi/iG9CE55wbtY/0.jpg"
videocredit: tedtalks
---
Howdy! This is an example blog post that shows features supported in **lanyon-plus** theme. See [raw post](https://raw.githubusercontent.com/dyndna/lanyon-plus/master/_posts/2013-01-01-example-content.md) for required YAML header and liquid tag specifications.
<!--more-->
* TOC
{:toc}
### Heading
# H1
{:.no_toc}
## H2
{:.no_toc}
### H3
{:.no_toc}
#### H4
{:.no_toc}
##### H5
{:.no_toc}
###### H6
{:.no_toc}
Vivamus sagittis lacus vel augue rutrum faucibus dolor auctor. Duis mollis, est non commodo luctus, nisi erat porttitor ligula, eget lacinia odio sem nec elit. Morbi leo risus, porta ac consectetur ac, vestibulum at eros.
### Inline HTML elements
HTML defines a long list of available inline tags, a complete list of which can be found on the [Mozilla Developer Network](https://developer.mozilla.org/en-US/docs/Web/HTML/Element).
- **To bold text**, use `<strong>`.
- *To italicize text*, use `<em>`.
- Abbreviations, like <abbr title="HyperText Markup Langage">HTML</abbr> should use `<abbr>`, with an optional `title` attribute for the full phrase.
- Citations, like <cite>&mdash; Mark otto</cite>, should use `<cite>`.
- <del>Deleted</del> text should use `<del>` and <ins>inserted</ins> text should use `<ins>`.
- Superscript <sup>text</sup> uses `<sup>` and subscript <sub>text</sub> uses `<sub>`.
Most of these elements are styled by browsers with few modifications on our part.
### Code
Cum sociis natoque penatibus et magnis dis `code element` montes, nascetur ridiculus mus.
{% highlight js %}
// Example can be run directly in your JavaScript console
// Create a function that takes two arguments and returns the sum of those arguments
var adder = new Function("a", "b", "return a + b");
// Call the function
adder(2, 6);
// > 8
{% endhighlight %}
Aenean lacinia bibendum nulla sed consectetur. Etiam porta sem malesuada magna mollis euismod. Fusce dapibus, tellus ac cursus commodo, tortor mauris condimentum nibh, ut fermentum massa.
#### Alternate code block:
~~~r
library(uuid)
library(stringr)
library(parallel)
library(data.table)
~~~
#### `pygments` based highlighting (deprecated)
{% highlight bash %}
library(uuid)
library(stringr)
library(parallel)
library(data.table)
{% endhighlight %}
### Lists
Cum sociis natoque penatibus et magnis dis parturient montes, nascetur ridiculus mus. Aenean lacinia bibendum nulla sed consectetur. Etiam porta sem malesuada magna mollis euismod. Fusce dapibus, tellus ac cursus commodo, tortor mauris condimentum nibh, ut fermentum massa justo sit amet risus.
* Praesent commodo cursus magna, vel scelerisque nisl consectetur et.
* Donec id elit non mi porta gravida at eget metus.
* Nulla vitae elit libero, a pharetra augue.
Donec ullamcorper nulla non metus auctor fringilla. Nulla vitae elit libero, a pharetra augue.
1. Vestibulum id ligula porta felis euismod semper.
2. Cum sociis natoque penatibus et magnis dis parturient montes, nascetur ridiculus mus.
3. Maecenas sed diam eget risus varius blandit sit amet non magna.
Cras mattis consectetur purus sit amet fermentum. Sed posuere consectetur est at lobortis.
<dl>
<dt>HyperText Markup Language (HTML)</dt>
<dd>The language used to describe and define the content of a Web page</dd>
<dt>Cascading Style Sheets (CSS)</dt>
<dd>Used to describe the appearance of Web content</dd>
<dt>JavaScript (JS)</dt>
<dd>The programming language used to build advanced Web sites and applications</dd>
</dl>
Integer posuere erat a ante venenatis dapibus posuere velit aliquet. Morbi leo risus, porta ac consectetur ac, vestibulum at eros. Nullam quis risus eget urna mollis ornare vel eu leo.
### Tables
#### markdown formatted:
| Heading 1 | Heading 2 | Heading 3 |
| :--- | --- | ---: |
| Hello | World | <i class="fa fa-twitter"> @foo</i> |
Aenean lacinia bibendum nulla sed consectetur. Lorem ipsum dolor sit amet, consectetur adipiscing elit.
#### html table:
<table>
<thead>
<tr>
<th>Name</th>
<th>Upvotes</th>
<th>Downvotes</th>
</tr>
</thead>
<tfoot>
<tr>
<td>Totals</td>
<td>21</td>
<td>23</td>
</tr>
</tfoot>
<tbody>
<tr>
<td>Alice</td>
<td>10</td>
<td>11</td>
</tr>
<tr>
<td>Bob</td>
<td>4</td>
<td>3</td>
</tr>
<tr>
<td>Charlie</td>
<td>7</td>
<td>9</td>
</tr>
</tbody>
</table>
### Text highlight:
Nullam id dolor id nibh ultricies vehicula ut id elit. Sed posuere consectetur est at lobortis. Nullam quis risus eget urna mollis ornare vel eu leo. `Nullam id dolor id nibh ultricies vehicula ut id elit. Highlighted color will be removed during prinintg and replaced with underline.`{:.yelhglt}
### Blockquotes
#### stylized
<blockquote class="style1">
Aenean lacinia bibendum nulla sed consectetur. Etiam porta sem malesuada magna mollis euismod.
</blockquote>
#### regular
>When you bring new things into a society, you can either, it's like the balance of the force. You can either use it for good or you can use it for evil. And what happens when something new: People have a tendency to overdo it; they abuse it.
### Embed video
{% include youtube.html %}
### Embed picture
{:.text-center img}
![Toy example]({{ site.urlimg }}/media/apple-icon.png "Toy example")
### Inline css attributes
[MahJax source - link open in new window](http://haixing-hu.github.io/programming/2013/09/20/how-to-use-mathjax-in-jekyll-generated-github-pages/){:target="_blank"}
### MathJax
Let's test some inline math $x$, $y$, $x_1$, $y_1$.
Now a inline math with special character: $\|\psi\rangle$, $x'$, $x^\*$ and $\|\psi_1\rangle = a\|0\rangle + b\|1\rangle$
Test a display math:
$$
|\psi_1\rangle = a|0\rangle + b|1\rangle
$$
Is it O.K.?
Test a display math with equation number:
\begin{equation}
|\psi_1\rangle = a|0\rangle + b|1\rangle
\end{equation}
Is it O.K.?
Test a display math with equation number:
$$
\begin{align}
|\psi_1\rangle &= a|0\rangle + b|1\rangle \\
|\psi_2\rangle &= c|0\rangle + d|1\rangle
\end{align}
$$
Is it O.K.?
And test a display math without equaltion number:
$$
\begin{align*}
|\psi_1\rangle &= a|0\rangle + b|1\rangle \\
|\psi_2\rangle &= c|0\rangle + d|1\rangle
\end{align*}
$$
Is it O.K.?
Test a display math with equation number:
$$
\begin{align}
|\psi_1\rangle &= a|0\rangle + b|1\rangle \\
|\psi_2\rangle &= c|0\rangle + d|1\rangle
\end{align}
$$
Is it O.K.?
And test a display math without equaltion number:
$$
\begin{align*}
|\psi_1\rangle &= a|0\rangle + b|1\rangle \\
|\psi_2\rangle &= c|0\rangle + d|1\rangle
\end{align*}
$$
### gist embed
Below is a partial code showing main steps of merge function.
<code data-gist-id="0fe211678316cc53370c" data-gist-file="merge_tables_datatable.R" data-gist-line="50-52,57,65-69,80,88-90,100-106"></code>
### References
Multiple[^1]<sup>,</sup>[^3] and with comments[^2]
Want to see something else added? <a href="https://github.com/dyndna/lanyon-plus/issues/new">Open an issue.</a>
[^1]: [lanyon theme](http://lanyon.getpoole.com)
[^2]:
[lanyon-plus theme](https://github.com/dyndna/lanyon-plus "accessed on {{ page.date | date: '%B %d, %Y' }}")
>Excerpt: Sample post showing enabled features for post: `inline code`, `text highlight`{:.yelhglt}, code block with syntax highlights, embed gist, stylized blockquotes, video and image cards for twitter, markdown tables, inline and code bocks having mathjax support, references, print format, disqus comments, related posts, tags.
[^3]: [About]({{ site.url }}/about)

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---
layout: post
title: What's Jekyll?
# date element overrides date in title format.
date: 2015-1-31
tag:
- common_tag
- other_tag
---
[Jekyll](http://jekyllrb.com) is a static site generator, an open-source tool for creating simple yet powerful websites of all shapes and sizes. From [the project's readme](https://github.com/mojombo/jekyll/blob/master/README.markdown):
<!--more-->
> Jekyll is a simple, blog aware, static site generator. It takes a template directory [...] and spits out a complete, static website suitable for serving with Apache or your favorite web server. This is also the engine behind GitHub Pages, which you can use to host your projects page or blog right here from GitHub.
It's an immensely useful tool and one we encourage you to use here with Lanyon.
Find out more by [visiting the project on GitHub](https://github.com/mojombo/jekyll).

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---
layout: post
title: "Welcome to Jekyll!"
date: 2017-08-03 16:54:51 +0200
categories: jekyll update
---
Youll find this post in your `_posts` directory. Go ahead and edit it and re-build the site to see your changes. You can rebuild the site in many different ways, but the most common way is to run `jekyll serve`, which launches a web server and auto-regenerates your site when a file is updated.
To add new posts, simply add a file in the `_posts` directory that follows the convention `YYYY-MM-DD-name-of-post.ext` and includes the necessary front matter. Take a look at the source for this post to get an idea about how it works.
Jekyll also offers powerful support for code snippets:
{% highlight ruby %}
def print_hi(name)
puts "Hi, #{name}"
end
print_hi('Tom')
#=> prints 'Hi, Tom' to STDOUT.
{% endhighlight %}
Check out the [Jekyll docs][jekyll-docs] for more info on how to get the most out of Jekyll. File all bugs/feature requests at [Jekylls GitHub repo][jekyll-gh]. If you have questions, you can ask them on [Jekyll Talk][jekyll-talk].
[jekyll-docs]: https://jekyllrb.com/docs/home
[jekyll-gh]: https://github.com/jekyll/jekyll
[jekyll-talk]: https://talk.jekyllrb.com/

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prose:
rooturl: ''
siteurl: 'http://example.com/'
relativeLinks: 'http://example.com/links.jsonp'
media: 'images/media'
ignore:
- /_data
- /_includes
- /_layouts
- /blog
- .htaccess
- _config.yml
- Gemfile
- Gemfile.lock
- .gitignore
- .editorconfig
- .gitattributes
- favicon.ico
- favicon.png
metadata:
_posts:
- name: "published"
field:
label: "Published"
element: "checkbox"
value: "true"
- name: "layout"
field:
element: "hidden"
label: "Layout"
value: "post"
- name: "title"
field:
label: "Title"
element: "text"
value: "An Awesome Headline!"
- name: "description"
field:
element: "text"
label: "Description"
placeholder: "Enter Post Description"
- name: "date"
field:
element: "text"
label: "Post date - this will override date given in file name and permalink will change accordingly"
placeholder: "YYYY-MM-DD"
value: CURRENT_DATETIME
- name: "modified"
field:
element: "text"
label: "Last modified in quotes"
placeholder: "YYYY-MM-DD"
value: CURRENT_DATETIME
- name: "category"
field:
element: "select"
label: "Add categories"
placeholder: "Choose category"
value: base
options:
- name: "info"
value: info
- name: "news"
value: news
- name: "base"
value: base
alterable: true
- name: "tags"
field:
element: "multiselect"
label: "Add tags"
placeholder: "Choose tags"
value: default
options:
- name: "default"
value: default
alterable: true
- name: "imagefeature"
field:
element: "text"
label: "Featured Image or Video frame jpg for twitter card"
placeholder: "http url or path relative to images dir"
value: "sitelogo.png"
- name: "show_meta"
field:
element: "checkbox"
label: "Show tags and share buttons"
value: true
- name: "comments"
field:
element: "checkbox"
label: "Comments"
value: true
- name: "mathjax"
field:
element: "checkbox"
label: "MathJax"
value: false
- name: "gistembed"
field:
element: "checkbox"
label: "embed gist?"
value: false
- name: "noindex"
field:
element: "checkbox"
label: "noindex in robots.txt?"
value: false
- name: "hide_printmsg"
field:
element: "checkbox"
label: "hide info box while printing?"
value: false
- name: "sitemap"
field:
element: "checkbox"
label: "Keep in sitemap?"
value: true
- name: "summaryfeed"
field:
element: "checkbox"
label: "Show summary and not full post in rss feed?"
value: false
pages:
- name: "published"
field:
label: "Published"
element: "checkbox"
value: true
- name: "layout"
field:
element: "hidden"
label: "Layout"
value: "page"
- name: "title"
field:
label: "Title"
element: "text"
value: "An Awesome Headline!"
- name: "description"
field:
element: "text"
label: "Description"
placeholder: "Enter Page Description"
- name: "permalink"
field:
element: "text"
label: "Permalink - relative to root directory"
- name: "modified"
field:
element: "text"
label: "Last modified in quotes"
placeholder: "YYYY-MM-DD"
value: CURRENT_DATETIME
- name: "category"
field:
element: "select"
label: "Add categories"
placeholder: "Choose category"
value: info
options:
- name: "info"
value: info
- name: "news"
value: news
alterable: true
- name: "author"
field:
element: "select"
label: "Add author"
placeholder: "Choose author"
value: author1
options:
- name: "author1"
value: author1
- name: "author2"
value: author2
alterable: true
- name: "show_meta"
field:
element: "checkbox"
label: "Show tags and share buttons"
value: false
- name: "comments"
field:
element: "checkbox"
label: "Comments"
value: false
- name: "mathjax"
field:
element: "checkbox"
label: "MathJax"
value: false
- name: "gistembed"
field:
element: "checkbox"
label: "embed gist?"
value: false
- name: "noindex"
field:
element: "checkbox"
label: "noindex in robots.txt?"
value: false
- name: "hide_printmsg"
field:
element: "checkbox"
label: "hide info box while printing?"
value: false
- name: "sitemap"
field:
element: "checkbox"
label: "Keep in sitemap?"
value: true

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---
layout: default
title: Blog @ example.com
description: "Blogging on ...."
---
<div class="posts">
{% for post in paginator.posts %}
<div class="post">
<h1 class="post-title">
<a href="{{ site.url }}{{ post.url }}">
{{ post.title }}
</a>
</h1>
{% if post.modified.size > 2 %}<span class="post-date indexpg" itemprop="dateModified" content="{{ post.modified | date: "%Y-%m-%d" }}"><i class="fa fa-edit" title="Last updated"> {{ post.modified | date_to_string }}</i> {% if post.category contains "featured" %}<a href="{{ site.url }}/featured" title="Featured posts"><i class="fa fa-paperclip" title="Featured" class="social-icons"></i></a>{% endif %}</span>{% else %}<span class="post-date indexpg" itemprop="datePublished" content="{{ post.date | date: "%Y-%m-%d" }}"><i class="fa fa-calendar" title="Date published"> {{ post.date | date_to_string }}</i> {% if post.category contains "featured" %}<a href="{{ site.url }}/featured" title="Featured posts"><i class="fa fa-paperclip" title="Featured" class="social-icons"></i></a>{% endif %}</span>{% endif %}
{% if post.description.size > 140 %}{{ post.description | markdownify | remove: '<p>' | remove: '</p>' }}{% else %}{{ post.excerpt | markdownify | remove: '<p>' | remove: '</p>' }}{% endif %} <a href="{{ site.url }}{{ post.url }}" title="Read more"><strong>Read more...</strong></a>
</div>
{% unless forloop.last %}<hr class="transp">{% endunless %}
{% endfor %}
</div>
<div class="pagination">
{% if paginator.next_page %}
<a class="pagination-item older" href="{{ site.url }}/blog/page{{paginator.next_page}}">Older</a>
{% else %}
<span class="pagination-item older">Older</span>
{% endif %}
{% if paginator.previous_page %}
{% if paginator.page == 2 %}
<a class="pagination-item newer" href="{{ site.url }}/blog/">Newer</a>
{% else %}
<a class="pagination-item newer" href="{{ site.url }}/blog/page{{paginator.previous_page}}">Newer</a>
{% endif %}
{% else %}
<span class="pagination-item newer">Newer</span>
{% endif %}
</div>

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---
layout: null
---
<?xml version="1.0" encoding="UTF-8"?>
<rss version="2.0" xmlns:atom="http://www.w3.org/2005/Atom">
<channel>
<title>{{ site.title | xml_escape }}</title>
<description>{{ site.description | xml_escape }}</description>
<link>{{ site.url }}{{ site.baseurl }}/</link>
<atom:link href="{{ "/feed.xml" | prepend: site.baseurl | prepend: site.url }}" rel="self" type="application/rss+xml" />
<updated>{{ site.time | date_to_xmlschema }}</updated>
<id>{{ site.url }}</id>
<author>
<name>{{ site.owner.name }}</name>
</author>
{% for post in site.posts limit:10 %}
<item>
<title>{{ post.title | xml_escape }}</title>
{% if post.summaryfeed and post.excerpt %}
<description>{{ post.excerpt | xml_escape }}</description>
{% else %}
<description>{{ post.content | xml_escape }}</description>
{% endif %}
<pubDate>{{ post.date | date: "%a, %d %b %Y %H:%M:%S %z" }}</pubDate>
<link>{{ post.url | prepend: site.baseurl | prepend: site.url }}</link>
<guid isPermaLink="true">{{ post.url | prepend: site.baseurl | prepend: site.url }}</guid>
</item>
{% endfor %}
</channel>
</rss>

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@ -0,0 +1,103 @@
@article{jacobs_evolutionary_2014,
title = {An evolutionary arms race between {KRAB} zinc-finger genes {ZNF}91/93 and {SVA}/{L}1 retrotransposons},
volume = {516},
copyright = {© 2014 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.},
issn = {0028-0836},
url = {http://www.nature.com/nature/journal/v516/n7530/full/nature13760.html},
doi = {10.1038/nature13760},
abstract = {Throughout evolution primate genomes have been modified by waves of retrotransposon insertions. For each wave, the host eventually finds a way to repress retrotransposon transcription and prevent further insertions. In mouse embryonic stem cells, transcriptional silencing of retrotransposons requires KAP1 (also known as TRIM28) and its repressive complex, which can be recruited to target sites by KRAB zinc-finger (KZNF) proteins such as murine-specific ZFP809 which binds to integrated murine leukaemia virus DNA elements and recruits KAP1 to repress them. KZNF genes are one of the fastest growing gene families in primates and this expansion is hypothesized to enable primates to respond to newly emerged retrotransposons. However, the identity of KZNF genes battling retrotransposons currently active in the human genome, such as SINE-VNTR-Alu (SVA) and long interspersed nuclear element 1 (L1), is unknown. Here we show that two primate-specific KZNF genes rapidly evolved to repress these two distinct retrotransposon families shortly after they began to spread in our ancestral genome. ZNF91 underwent a series of structural changes 8-12 million years ago that enabled it to repress SVA elements. ZNF93 evolved earlier to repress the primate L1 lineage until [sim]12.5 million years ago when the L1PA3-subfamily of retrotransposons escaped ZNF93/'s restriction through the removal of the ZNF93-binding site. Our data support a model where KZNF gene expansion limits the activity of newly emerged retrotransposon classes, and this is followed by mutations in these retrotransposons to evade repression, a cycle of events that could explain the rapid expansion of lineage-specific KZNF genes.},
language = {en},
number = {7530},
urldate = {2015-10-12},
journal = {Nature},
author = {Jacobs, Frank M. J. and Greenberg, David and Nguyen, Ngan and Haeussler, Maximilian and Ewing, Adam D. and Katzman, Sol and Paten, Benedict and Salama, Sofie R. and Haussler, David},
month = dec,
year = {2014},
pmid = {25274305},
keywords = {evolution, interactions, transposon},
pages = {242--245}
}
@article{trapnell_defining_2015,
title = {Defining cell types and states with single-cell genomics},
volume = {25},
issn = {1088-9051, 1549-5469},
url = {http://genome.cshlp.org/content/25/10/1491},
doi = {10.1101/gr.190595.115},
abstract = {A revolution in cellular measurement technology is under way: For the first time, we have the ability to monitor global gene regulation in thousands of individual cells in a single experiment. Such experiments will allow us to discover new cell types and states and trace their developmental origins. They overcome fundamental limitations inherent in measurements of bulk cell population that have frustrated efforts to resolve cellular states. Single-cell genomics and proteomics enable not only precise characterization of cell state, but also provide a stunningly high-resolution view of transitions between states. These measurements may finally make explicit the metaphor that C.H. Waddington posed nearly 60 years ago to explain cellular plasticity: Cells are residents of a vast “landscape” of possible states, over which they travel during development and in disease. Single-cell technology helps not only locate cells on this landscape, but illuminates the molecular mechanisms that shape the landscape itself. However, single-cell genomics is a field in its infancy, with many experimental and computational advances needed to fully realize its full potential.},
language = {en},
number = {10},
urldate = {2015-10-14},
journal = {Genome Research},
author = {Trapnell, Cole},
month = oct,
year = {2015},
pmid = {26430159},
keywords = {chromatin, evolution, review, single-cell, Waddington},
pages = {1491--1498}
}
@article{kaufman_zebrafish_2016,
title = {A zebrafish melanoma model reveals emergence of neural crest identity during melanoma initiation},
volume = {351},
copyright = {Copyright © 2016, American Association for the Advancement of Science},
issn = {0036-8075, 1095-9203},
url = {http://science.sciencemag.org/content/351/6272/aad2197},
doi = {10.1126/science.aad2197},
abstract = {Visualizing the beginnings of melanoma
In cancer biology, a tumor begins from a single cell within a group of precancerous cells that share genetic mutations. Kaufman et al. used a zebrafish melanoma model to visualize cancer initiation (see the Perspective by Boumahdi and Blanpain). They used a fluorescent reporter that specifically lit up neural crest progenitors that are only present during embryogenesis or during adult melanoma tumor formation. The appearance of this tumor correlated with a set of gene regulatory elements, called super-enhancers, whose identification and manipulation may prove beneficial in detecting and preventing melanoma initiation.
Science, this issue p. 10.1126/science.aad3867; see also p. 453
Structured Abstract
INTRODUCTIONThe “cancerized field” concept posits that cells in a given tissue sharing an oncogenic mutation are cancer-prone, yet only discreet clones within the field initiate tumors. Studying the process of cancer initiation has remained challenging because of (i) the rarity of these events, (ii) the difficulty of visiualizing initiating clones in living organisms, and (iii) the transient nature of a newly transformed clone emerging before it expands to form an early tumor. A more complete understanding of the molecular processes that regulate cancer initiation could provide important prognostic information about which precancerous lesions are most prone to becoming cancer and also implicate druggable molecular pathways that, when inhibited, may prevent the cancer from ever starting.
RATIONALEThe majority of benign nevi carry oncogenic BRAFV600E mutations and can be considered a cancerized field of melanocytes, but they only rarely convert to melanoma. In an effort to define events that initiate cancer, we used a melanoma model in the zebrafish in which the human BRAFV600E oncogene is driven by the melanocyte-specific mitfa promoter. When bred into a p53 mutant background, these fish develop melanoma tumors over the course of many months. The zebrafish crestin gene is expressed embryonically in neural crest progenitors (NCPs) and is specifically reexpressed only in melanoma tumors, making it an ideal candidate for tracking melanoma from initiation onward.
RESULTSWe developed a crestin:EGFP reporter that recapitulates the embryonic neural crest expression pattern of crestin and its expression in melanoma tumors. We show through live imaging of transgenic zebrafish crestin reporters that within a cancerized field (BRAFV600E-mutant; p53-deficient), a single melanocyte reactivates the NCP state, and this establishes that a fate change occurs at melanoma initiation in this model. Early crestin+ patches of cells expand and are transplantable in a manner consistent with their possessing tumorigenic activity, and they exhibit a gene expression pattern consistent with the NCP identity readout by the crestin reporter. The crestin element is regulated by NCP transcription factors, including sox10. Forced sox10 overexpression in melanocytes accelerated melanoma formation, whereas CRISPR/Cas9 targeting of sox10 delayed melanoma onset. We show activation of super-enhancers at NCP genes in both zebrafish and human melanomas, identifying an epigenetic mechanism for control of this NCP signature leading to melanoma.
CONCLUSIONThis work using our zebrafish melanoma model and in vivo reporter of NCP identity allows us to see cancer from its birth as a single cell and shows the importance of NCP-state reemergence as a key event in melanoma initiation from a field of cancer-prone melanocytes. Thus, in addition to the typical fixed genetic alterations in oncogenes and tumor supressors that are required for cancer development, the reemergence of progenitor identity may be an additional rate-limiting step in the formation of melanoma. Preventing NCP reemergence in a field of cancer-prone melanocytes may thus prove therapeutically useful, and the association of NCP genes with super-enhancer regulatory elements implicates the associated druggable epigenetic machinery in this process. Download high-res image Open in new tab Download Powerpoint Neural crest reporter expression in melanoma.The crestin:EGFP transgene is specifically expressed in melanoma in BRAFV600E/p53 mutant melanoma-prone zebrafish. (Top) A single cell expressing crestin:EGFP expands into a small patch of cells over the course of 2 weeks, capturing the initiation of melanoma formation (bracket). (Bottom) A fully formed melanoma specifically expresses crestin:EGFP, whereas the rest of the fish remains EGFP-negative.
The “cancerized field” concept posits that cancer-prone cells in a given tissue share an oncogenic mutation, but only discreet clones within the field initiate tumors. Most benign nevi carry oncogenic BRAFV600E mutations but rarely become melanoma. The zebrafish crestin gene is expressed embryonically in neural crest progenitors (NCPs) and specifically reexpressed in melanoma. Live imaging of transgenic zebrafish crestin reporters shows that within a cancerized field (BRAFV600E-mutant; p53-deficient), a single melanocyte reactivates the NCP state, revealing a fate change at melanoma initiation in this model. NCP transcription factors, including sox10, regulate crestin expression. Forced sox10 overexpression in melanocytes accelerated melanoma formation, which is consistent with activation of NCP genes and super-enhancers leading to melanoma. Our work highlights NCP state reemergence as a key event in melanoma initiation.
Melanocytes with oncogenic or tumor suppressor mutations revert to expressing the crestin gene early in melanoma formation. [Also see Perspective by Boumahdi and Blanpain]
Melanocytes with oncogenic or tumor suppressor mutations revert to expressing the crestin gene early in melanoma formation. [Also see Perspective by Boumahdi and Blanpain]},
language = {en},
number = {6272},
urldate = {2016-01-29},
journal = {Science},
author = {Kaufman, Charles K. and Mosimann, Christian and Fan, Zi Peng and Yang, Song and Thomas, Andrew J. and Ablain, Julien and Tan, Justin L. and Fogley, Rachel D. and Rooijen, Ellen van and Hagedorn, Elliott J. and Ciarlo, Christie and White, Richard M. and Matos, Dominick A. and Puller, Ann-Christin and Santoriello, Cristina and Liao, Eric C. and Young, Richard A. and Zon, Leonard I.},
month = jan,
year = {2016},
pmid = {26823433},
keywords = {Development, epigenetics, evolution, melanoma, super\_enhancer, zebrafish},
pages = {aad2197}
}
@article{lipinski_cancer_2016,
title = {Cancer {Evolution} and the {Limits} of {Predictability} in {Precision} {Cancer} {Medicine}},
volume = {2},
issn = {2405-8033},
url = {http://www.sciencedirect.com/science/article/pii/S2405803315000692},
doi = {10.1016/j.trecan.2015.11.003},
abstract = {The ability to predict the future behavior of an individual cancer is crucial for precision cancer medicine. The discovery of extensive intratumor heterogeneity and ongoing clonal adaptation in human tumors substantiated the notion of cancer as an evolutionary process. Random events are inherent in evolution and tumor spatial structures hinder the efficacy of selection, which is the only deterministic evolutionary force. This review outlines how the interaction of these stochastic and deterministic processes, which have been extensively studied in evolutionary biology, limits cancer predictability and develops evolutionary strategies to improve predictions. Understanding and advancing the cancer predictability horizon is crucial to improve precision medicine outcomes.},
number = {1},
urldate = {2016-01-30},
journal = {Trends in Cancer},
author = {Lipinski, Kamil A. and Barber, Louise J. and Davies, Matthew N. and Ashenden, Matthew and Sottoriva, Andrea and Gerlinger, Marco},
month = jan,
year = {2016},
keywords = {evolution, heterogeneity, resistance, review},
pages = {49--63}
}
@article{beerenwinkel_computational_2016,
title = {Computational {Cancer} {Biology}: {An} {Evolutionary} {Perspective}},
volume = {12},
shorttitle = {Computational {Cancer} {Biology}},
url = {http://dx.doi.org/10.1371/journal.pcbi.1004717},
doi = {10.1371/journal.pcbi.1004717},
number = {2},
urldate = {2016-02-05},
journal = {PLoS Comput Biol},
author = {Beerenwinkel, Niko and Greenman, Chris D. and Lagergren, Jens},
month = feb,
year = {2016},
keywords = {cancer, concepts, darwinian, epigenetics, evolution, mathematical modeling, review, statistics, variant},
pages = {e1004717},
pmid = {26845763}
}

103
files/mypubs.bib Normal file
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@ -0,0 +1,103 @@
@article{jacobs_evolutionary_2014,
title = {An evolutionary arms race between {KRAB} zinc-finger genes {ZNF}91/93 and {SVA}/{L}1 retrotransposons},
volume = {516},
copyright = {© 2014 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.},
issn = {0028-0836},
url = {http://www.nature.com/nature/journal/v516/n7530/full/nature13760.html},
doi = {10.1038/nature13760},
abstract = {Throughout evolution primate genomes have been modified by waves of retrotransposon insertions. For each wave, the host eventually finds a way to repress retrotransposon transcription and prevent further insertions. In mouse embryonic stem cells, transcriptional silencing of retrotransposons requires KAP1 (also known as TRIM28) and its repressive complex, which can be recruited to target sites by KRAB zinc-finger (KZNF) proteins such as murine-specific ZFP809 which binds to integrated murine leukaemia virus DNA elements and recruits KAP1 to repress them. KZNF genes are one of the fastest growing gene families in primates and this expansion is hypothesized to enable primates to respond to newly emerged retrotransposons. However, the identity of KZNF genes battling retrotransposons currently active in the human genome, such as SINE-VNTR-Alu (SVA) and long interspersed nuclear element 1 (L1), is unknown. Here we show that two primate-specific KZNF genes rapidly evolved to repress these two distinct retrotransposon families shortly after they began to spread in our ancestral genome. ZNF91 underwent a series of structural changes 8-12 million years ago that enabled it to repress SVA elements. ZNF93 evolved earlier to repress the primate L1 lineage until [sim]12.5 million years ago when the L1PA3-subfamily of retrotransposons escaped ZNF93/'s restriction through the removal of the ZNF93-binding site. Our data support a model where KZNF gene expansion limits the activity of newly emerged retrotransposon classes, and this is followed by mutations in these retrotransposons to evade repression, a cycle of events that could explain the rapid expansion of lineage-specific KZNF genes.},
language = {en},
number = {7530},
urldate = {2015-10-12},
journal = {Nature},
author = {Jacobs, Frank M. J. and Greenberg, David and Nguyen, Ngan and Haeussler, Maximilian and Ewing, Adam D. and Katzman, Sol and Paten, Benedict and Salama, Sofie R. and Haussler, David},
month = dec,
year = {2014},
pmid = {25274305},
keywords = {evolution, interactions, transposon},
pages = {242--245}
}
@article{trapnell_defining_2015,
title = {Defining cell types and states with single-cell genomics},
volume = {25},
issn = {1088-9051, 1549-5469},
url = {http://genome.cshlp.org/content/25/10/1491},
doi = {10.1101/gr.190595.115},
abstract = {A revolution in cellular measurement technology is under way: For the first time, we have the ability to monitor global gene regulation in thousands of individual cells in a single experiment. Such experiments will allow us to discover new cell types and states and trace their developmental origins. They overcome fundamental limitations inherent in measurements of bulk cell population that have frustrated efforts to resolve cellular states. Single-cell genomics and proteomics enable not only precise characterization of cell state, but also provide a stunningly high-resolution view of transitions between states. These measurements may finally make explicit the metaphor that C.H. Waddington posed nearly 60 years ago to explain cellular plasticity: Cells are residents of a vast “landscape” of possible states, over which they travel during development and in disease. Single-cell technology helps not only locate cells on this landscape, but illuminates the molecular mechanisms that shape the landscape itself. However, single-cell genomics is a field in its infancy, with many experimental and computational advances needed to fully realize its full potential.},
language = {en},
number = {10},
urldate = {2015-10-14},
journal = {Genome Research},
author = {Trapnell, Cole},
month = oct,
year = {2015},
pmid = {26430159},
keywords = {chromatin, evolution, review, single-cell, Waddington},
pages = {1491--1498}
}
@article{kaufman_zebrafish_2016,
title = {A zebrafish melanoma model reveals emergence of neural crest identity during melanoma initiation},
volume = {351},
copyright = {Copyright © 2016, American Association for the Advancement of Science},
issn = {0036-8075, 1095-9203},
url = {http://science.sciencemag.org/content/351/6272/aad2197},
doi = {10.1126/science.aad2197},
abstract = {Visualizing the beginnings of melanoma
In cancer biology, a tumor begins from a single cell within a group of precancerous cells that share genetic mutations. Kaufman et al. used a zebrafish melanoma model to visualize cancer initiation (see the Perspective by Boumahdi and Blanpain). They used a fluorescent reporter that specifically lit up neural crest progenitors that are only present during embryogenesis or during adult melanoma tumor formation. The appearance of this tumor correlated with a set of gene regulatory elements, called super-enhancers, whose identification and manipulation may prove beneficial in detecting and preventing melanoma initiation.
Science, this issue p. 10.1126/science.aad3867; see also p. 453
Structured Abstract
INTRODUCTIONThe “cancerized field” concept posits that cells in a given tissue sharing an oncogenic mutation are cancer-prone, yet only discreet clones within the field initiate tumors. Studying the process of cancer initiation has remained challenging because of (i) the rarity of these events, (ii) the difficulty of visiualizing initiating clones in living organisms, and (iii) the transient nature of a newly transformed clone emerging before it expands to form an early tumor. A more complete understanding of the molecular processes that regulate cancer initiation could provide important prognostic information about which precancerous lesions are most prone to becoming cancer and also implicate druggable molecular pathways that, when inhibited, may prevent the cancer from ever starting.
RATIONALEThe majority of benign nevi carry oncogenic BRAFV600E mutations and can be considered a cancerized field of melanocytes, but they only rarely convert to melanoma. In an effort to define events that initiate cancer, we used a melanoma model in the zebrafish in which the human BRAFV600E oncogene is driven by the melanocyte-specific mitfa promoter. When bred into a p53 mutant background, these fish develop melanoma tumors over the course of many months. The zebrafish crestin gene is expressed embryonically in neural crest progenitors (NCPs) and is specifically reexpressed only in melanoma tumors, making it an ideal candidate for tracking melanoma from initiation onward.
RESULTSWe developed a crestin:EGFP reporter that recapitulates the embryonic neural crest expression pattern of crestin and its expression in melanoma tumors. We show through live imaging of transgenic zebrafish crestin reporters that within a cancerized field (BRAFV600E-mutant; p53-deficient), a single melanocyte reactivates the NCP state, and this establishes that a fate change occurs at melanoma initiation in this model. Early crestin+ patches of cells expand and are transplantable in a manner consistent with their possessing tumorigenic activity, and they exhibit a gene expression pattern consistent with the NCP identity readout by the crestin reporter. The crestin element is regulated by NCP transcription factors, including sox10. Forced sox10 overexpression in melanocytes accelerated melanoma formation, whereas CRISPR/Cas9 targeting of sox10 delayed melanoma onset. We show activation of super-enhancers at NCP genes in both zebrafish and human melanomas, identifying an epigenetic mechanism for control of this NCP signature leading to melanoma.
CONCLUSIONThis work using our zebrafish melanoma model and in vivo reporter of NCP identity allows us to see cancer from its birth as a single cell and shows the importance of NCP-state reemergence as a key event in melanoma initiation from a field of cancer-prone melanocytes. Thus, in addition to the typical fixed genetic alterations in oncogenes and tumor supressors that are required for cancer development, the reemergence of progenitor identity may be an additional rate-limiting step in the formation of melanoma. Preventing NCP reemergence in a field of cancer-prone melanocytes may thus prove therapeutically useful, and the association of NCP genes with super-enhancer regulatory elements implicates the associated druggable epigenetic machinery in this process. Download high-res image Open in new tab Download Powerpoint Neural crest reporter expression in melanoma.The crestin:EGFP transgene is specifically expressed in melanoma in BRAFV600E/p53 mutant melanoma-prone zebrafish. (Top) A single cell expressing crestin:EGFP expands into a small patch of cells over the course of 2 weeks, capturing the initiation of melanoma formation (bracket). (Bottom) A fully formed melanoma specifically expresses crestin:EGFP, whereas the rest of the fish remains EGFP-negative.
The “cancerized field” concept posits that cancer-prone cells in a given tissue share an oncogenic mutation, but only discreet clones within the field initiate tumors. Most benign nevi carry oncogenic BRAFV600E mutations but rarely become melanoma. The zebrafish crestin gene is expressed embryonically in neural crest progenitors (NCPs) and specifically reexpressed in melanoma. Live imaging of transgenic zebrafish crestin reporters shows that within a cancerized field (BRAFV600E-mutant; p53-deficient), a single melanocyte reactivates the NCP state, revealing a fate change at melanoma initiation in this model. NCP transcription factors, including sox10, regulate crestin expression. Forced sox10 overexpression in melanocytes accelerated melanoma formation, which is consistent with activation of NCP genes and super-enhancers leading to melanoma. Our work highlights NCP state reemergence as a key event in melanoma initiation.
Melanocytes with oncogenic or tumor suppressor mutations revert to expressing the crestin gene early in melanoma formation. [Also see Perspective by Boumahdi and Blanpain]
Melanocytes with oncogenic or tumor suppressor mutations revert to expressing the crestin gene early in melanoma formation. [Also see Perspective by Boumahdi and Blanpain]},
language = {en},
number = {6272},
urldate = {2016-01-29},
journal = {Science},
author = {Kaufman, Charles K. and Mosimann, Christian and Fan, Zi Peng and Yang, Song and Thomas, Andrew J. and Ablain, Julien and Tan, Justin L. and Fogley, Rachel D. and Rooijen, Ellen van and Hagedorn, Elliott J. and Ciarlo, Christie and White, Richard M. and Matos, Dominick A. and Puller, Ann-Christin and Santoriello, Cristina and Liao, Eric C. and Young, Richard A. and Zon, Leonard I.},
month = jan,
year = {2016},
pmid = {26823433},
keywords = {Development, epigenetics, evolution, melanoma, super\_enhancer, zebrafish},
pages = {aad2197}
}
@article{lipinski_cancer_2016,
title = {Cancer {Evolution} and the {Limits} of {Predictability} in {Precision} {Cancer} {Medicine}},
volume = {2},
issn = {2405-8033},
url = {http://www.sciencedirect.com/science/article/pii/S2405803315000692},
doi = {10.1016/j.trecan.2015.11.003},
abstract = {The ability to predict the future behavior of an individual cancer is crucial for precision cancer medicine. The discovery of extensive intratumor heterogeneity and ongoing clonal adaptation in human tumors substantiated the notion of cancer as an evolutionary process. Random events are inherent in evolution and tumor spatial structures hinder the efficacy of selection, which is the only deterministic evolutionary force. This review outlines how the interaction of these stochastic and deterministic processes, which have been extensively studied in evolutionary biology, limits cancer predictability and develops evolutionary strategies to improve predictions. Understanding and advancing the cancer predictability horizon is crucial to improve precision medicine outcomes.},
number = {1},
urldate = {2016-01-30},
journal = {Trends in Cancer},
author = {Lipinski, Kamil A. and Barber, Louise J. and Davies, Matthew N. and Ashenden, Matthew and Sottoriva, Andrea and Gerlinger, Marco},
month = jan,
year = {2016},
keywords = {evolution, heterogeneity, resistance, review},
pages = {49--63}
}
@article{beerenwinkel_computational_2016,
title = {Computational {Cancer} {Biology}: {An} {Evolutionary} {Perspective}},
volume = {12},
shorttitle = {Computational {Cancer} {Biology}},
url = {http://dx.doi.org/10.1371/journal.pcbi.1004717},
doi = {10.1371/journal.pcbi.1004717},
number = {2},
urldate = {2016-02-05},
journal = {PLoS Comput Biol},
author = {Beerenwinkel, Niko and Greenman, Chris D. and Lagergren, Jens},
month = feb,
year = {2016},
keywords = {cancer, concepts, darwinian, epigenetics, evolution, mathematical modeling, review, statistics, variant},
pages = {e1004717},
pmid = {26845763}
}

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---
---
/* TEAM */
Primary Contact: foo
Site: {{ site.url }}/about/
Twitter: https://twitter.com/{{ site.owner.twitter }}
/* THANKS */
Design Contributors: {{ site.url }}/disclosure/
/* SITE */
Last Updated: {{ site.time | date:"%Y/%m/%d" }}
Standards: HTML5, CSS3
Software: Sublime Text, Chrome, Jekyll, Git, Sass

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---
# You don't need to edit this file, it's empty on purpose.
# Edit theme's home layout instead if you wanna make some changes
# See: https://jekyllrb.com/docs/themes/#overriding-theme-defaults
layout: home
layout: default
permalink: index.html
title: Personal Homepage of foo boo
description: "Blogging on ...."
---
## [lanyon-plus](https://github.com/dyndna/lanyon-plus)
Based on Jekyll theme: [Lanyon](http://lanyon.getpoole.com) by [**Mark Otto**](https://github.com/mdo)
* add-ons by [Samir Amin](http://sbamin.com)
* [Site features]({{ site.url}}/disclosure#i-classfa-fa-thumbs-o-up-credits-for-site-featuresi)
* License: Open sourced under the [MIT license](http://sbamin.com/disclosure/#theme-major-credit--license).
Maximum four posts on front page where first two posts are featured, and remaining are date sorted.
{% if site.twitter_widget_id %}
<div class="text-tweets">
<div class="tweets">
<a class="twitter-timeline"
data-dnt="true"
width="600"
height="250"
href="https://twitter.com/{{ site.owner.twitter }}"
data-widget-id="{{ site.twitter_widget_id }}"
data-tweet-limit="2"
data-chrome="noheader nofooter noborders noscrollbar transparent">
Recent Tweets</a>
</div>
<script>
!function(d,s,id){var js,fjs=d.getElementsByTagName(s)[0],p=/^http:/.test(d.location)?'http':'https';if(!d.getElementById(id)){js=d.createElement(s);js.id=id;js.src=p+"://platform.twitter.com/widgets.js";fjs.parentNode.insertBefore(js,fjs);}}(document,"script","twitter-wjs");
</script>
</div>
{% else %}
Twitter stream will show up here if `twitter_widget_id` is present is `_config.yml`. [Demo](http://sbamin.com)
{% endif %}
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{% for post in site.categories.featured limit:2 %}
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<h1 class="post-title">
<a href="{{ site.url }}{{ post.url }}">
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{% if post.description.size > 140 %}{{ post.description | markdownify | remove: '<p>' | remove: '</p>' }}{% else %}{{ post.excerpt | markdownify | remove: '<p>' | remove: '</p>' }}{% endif %} <a href="{{ site.url }}{{ post.url }}" title="Read more"><strong>Read more...</strong></a>
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{% for post in site.posts limit:2 %}
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{{ post.title }}
</a>
</h1>
{% if post.modified.size > 2 %}<span class="post-date indexpg" itemprop="dateModified" content="{{ post.modified | date: "%Y-%m-%d" }}"><i class="fa fa-edit" title="Last updated"> {{ post.modified | date_to_string }}</i></span>{% else %}<span class="post-date indexpg" itemprop="datePublished" content="{{ post.date | date: "%Y-%m-%d" }}"><i class="fa fa-calendar" title="Date published"> {{ post.date | date_to_string }}</i></span>{% endif %}
{% if post.description.size > 140 %}{{ post.description | markdownify | remove: '<p>' | remove: '</p>' }}{% else %}{{ post.excerpt | markdownify | remove: '<p>' | remove: '</p>' }}{% endif %} <a href="{{ site.url }}{{ post.url }}" title="Read more"><strong>Read more...</strong></a>
</div>
{% unless forloop.last %}<hr class="transp">{% endunless %}
{% endunless %}
{% endfor %}
</div>
<h3 class="post-title">
<div class="pagination" style="margin: 0.5rem;">
<a class="pagination-item older" href="{{ site.url }}/blog"><i class="fa fa-edit"> Blog</i></a>
<a class="pagination-item newer" href="{{ site.url }}/tags"><i class="fa fa-tags"> Tags</i></a>
</div>
</h3>

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---
---
callback([
{% for post in site.posts reversed | sort: title %}
{
"text": "{{post.title | replace:'"','\"'}}",
"href": "{{site.url}}{{post.url}}"
} {% unless forloop.last %},{% endunless%}
{% endfor %}
])

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---
layout: page
title: About
permalink: /about/
show_meta: true
# imagefeature path is relative to images/ directory.
imagefeature: foo.png
published: true
description: "About example.com...."
category: views
comments: false
mathjax: false
noindex: false
sitemap:
priority: 0.7
changefreq: 'monthly'
lastmod: 2016-02-13
# tags will be used as html meta keywords.
tags:
- "foo boo"
- "city tx"
---
<div class="post-author text-center">
<img src="{{ site.urlimg }}{{ site.owner.avatar }}" alt="{{ site.owner.name }}'s photo" itemprop="image" class="post-avatar img-circle img-responsive"/>
<span class="social-icons" style="padding-top: 10px; padding-bottom: 1px;">
<a href="{{ site.url }}/cv" title="Curriculum Vitae" class="social-icons"><i class="iconm iconm-profile" style="vertical-align: top;"></i></a>
<a href="{{ site.url }}/about/publications/" class="social-icons" title="Publications"><i class="iconm iconm-file-pdf"></i></a>
<a href="{{ site.owner.linkedin }}" class="social-icons" title="LinkedIn profile"><i class="iconm iconm-linkedin2"></i></a>
</span>
</div>
Lorem ipsum dolor sit amet, consectetur adipiscing elit. In ornare lectus a purus rutrum, a hendrerit quam condimentum. Donec vel ante maximus, vulputate libero ac, rhoncus justo. Phasellus purus nisl, auctor id tristique eu, maximus quis leo. Mauris ultricies ante quis vehicula accumsan. Nulla facilisi. Lorem ipsum dolor sit amet, consectetur adipiscing elit. Ut mi elit, feugiat non scelerisque eget, ultrices nec est. Morbi a est iaculis, commodo quam congue, posuere quam. Phasellus venenatis finibus eros, vitae malesuada nisl gravida vitae.
Praesent ac sem quis diam fermentum fermentum. Nullam turpis metus, elementum sit amet venenatis sed, placerat eget erat. Ut convallis ipsum vitae volutpat tristique. Cras a tempor lorem, quis aliquet dui. Nunc vel leo erat. Donec posuere massa sed justo luctus, accumsan porttitor ligula laoreet. Suspendisse sit amet nisi ultrices, venenatis lorem vel, posuere turpis. Fusce eget dictum nisi. Proin eu diam nisi. Quisque ut quam quis sem tincidunt efficitur vitae nec ex. Pellentesque ut dolor eros. Ut faucibus semper ultricies. Vestibulum nec nisl in magna porttitor dictum.
Donec egestas eros arcu, id fermentum orci faucibus ac. Pellentesque facilisis elit eu tellus ultrices pulvinar. Cum sociis natoque penatibus et magnis dis parturient montes, nascetur ridiculus mus. In ut eros et mi dapibus condimentum. Sed ante metus, porttitor ut aliquet vitae, ullamcorper quis ex. Donec ac efficitur arcu, a malesuada dolor. Nulla magna arcu, semper quis augue sed, rhoncus porta urna. Duis dictum dapibus diam, ac sodales ipsum lobortis vel. Nulla ac dictum metus. Morbi sollicitudin tortor eu diam tristique, ut tincidunt tortor euismod. Integer non tincidunt metus. In tempus sem dapibus, venenatis mi placerat, condimentum orci. Nunc et tellus diam.
Nam imperdiet consequat lorem. Donec sagittis tortor eu dolor efficitur ullamcorper. Pellentesque dolor arcu, vestibulum quis laoreet at, tincidunt nec mauris. Praesent id laoreet arcu. Quisque blandit nunc at elit auctor, eget tempor nunc sodales. Cras venenatis lacinia tempus. Proin erat nisl, pharetra a massa volutpat, rhoncus pellentesque nisi. Mauris in elit dictum, egestas tellus et, laoreet velit. Nam auctor tempus augue sit amet fermentum. Nulla accumsan arcu quis efficitur aliquam. Nulla dapibus in neque eget facilisis. Nullam nisi augue, maximus at lectus sit amet, ornare malesuada ante. Morbi volutpat justo a urna pharetra elementum. Proin tempor ac felis ac consequat. Proin feugiat, nulla ac sagittis consequat, ante diam auctor tortor, in suscipit leo ante id dolor. Vivamus posuere pellentesque magna, sagittis blandit neque convallis sed.
*[volutpat]: Tooltip for abbreviation.

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---
layout: publ
category: myaoi
permalink: /about/aoi/
title: "Articles of interest"
published: true
description: "Sample page showing bookmarked papers"
tags:
- papers
- articles
- research
- starred
comments: true
modified: "2016-02-13"
bibtex: "/files/myaoi.bib"
#bibtex: "http://foo-alternate.com/files/myaoi.bib"
show_meta: true
noindex: false
nofollow: true
sitemap:
priority: 0.5
changefreq: 'monthly'
lastmod: 2016-02-13
style: |
.container {
max-width: 48rem;
}
---
{% comment %}
<!-- bibbase.org should work with following code unless you are hosting domain over https. -->
{% if page.bibtex %}
{% if page.bibtex contains 'http' %}
{% assign domain = '' %}
{% else %}
{% assign domain = site.url %}
{% endif %}
{% capture biburl %}{{ domain }}{{ page.bibtex }}{% endcapture %}
<script src="http://bibbase.org/show?bib={{ biburl | cgi_escape }}&amp;jsonp=1&amp;authorFirst=1"></script>
{% endif %}
{% endcomment %}
If category is *myaoi*, then html content from bibtex file at `_includes/myaoi.html` will be shown below.

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---
layout: page
permalink: /contact/
title: Contact
show_meta: false
published: true
description: "Contact example.com"
comments: false
mathjax: false
noindex: false
sitemap:
priority: 0.5
changefreq: 'monthly'
lastmod: 2016-02-13
tags:
- "foo boo"
- "driving directions"
- address
---
| <i class="fa fa-twitter"></i> | [@{{ site.owner.twitter }}](https://twitter.com/{{ site.owner.twitter }}) |
| - | :- |
| <i class="fa fa-envelope"></i> | foo<br>XYZ<br>1234 ABC ST<br>Washington, DC 11111 |
| - | :- |
| <i class="fa fa-car"></i> | [Driving directions]({{ site.url }}/directions) |
| - | :- |
| <i class="fa fa-paper-plane"> | foo@xyz |
| - | :- |
<a href="https://twitter.com/share" class="twitter-share-button" data-via="{{ site.owner.twitter }}" data-size="small" data-dnt="true">Tweet</a> <a href="javascript:window.print()" class="social-icons" title="Printer friendly format"><i class="fa fa-print"></i></a>
<script>!function(d,s,id){var js,fjs=d.getElementsByTagName(s)[0],p=/^http:/.test(d.location)?'http':'https';if(!d.getElementById(id)){js=d.createElement(s);js.id=id;js.src=p+'://platform.twitter.com/widgets.js';fjs.parentNode.insertBefore(js,fjs);}}(document, 'script', 'twitter-wjs');</script>
{% if site.twitter_widget_id %}
<div class="text-tweets">
<div class="tweets">
<a class="twitter-timeline"
data-dnt="true"
width="600"
height="250"
href="https://twitter.com/{{ site.owner.twitter }}"
data-widget-id="{{ site.twitter_widget_id }}"
data-tweet-limit="2"
data-chrome="noheader nofooter noborders noscrollbar transparent">
Recent Tweets</a>
</div>
<script>
!function(d,s,id){var js,fjs=d.getElementsByTagName(s)[0],p=/^http:/.test(d.location)?'http':'https';if(!d.getElementById(id)){js=d.createElement(s);js.id=id;js.src=p+"://platform.twitter.com/widgets.js";fjs.parentNode.insertBefore(js,fjs);}}(document,"script","twitter-wjs");
</script>
</div>
{% else %}
Twitter stream will show up here if `twitter_widget_id` is present is `_config.yml`
{% endif %}

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---
layout: page
permalink: /cv/
title: Curriculum Vitae
category: base
published: true
description: "Curriculum Vitae / Resume"
tags:
- cv
- resume
- "foo boo"
comments: false
imagesummary: foo.png
modified: "2016-02-13"
sitemap:
priority: 0.7
changefreq: 'monthly'
lastmod: 2016-02-13
style: |
.container {
max-width: 48rem;
}
---
<span class="social-icons">
<a href="https://twitter.com/share?text=Curriculum Vitae - {{ site.owner.name }}&amp;url={{ site.url }}/cv&amp;via={{ site.owner.twitter }}" class="social-icons" target="_blank" title="Share on twitter"> <i class="fa fa-twitter meta"></i></a>
<a href="https://plus.google.com/share?url={{ site.url }}/cv" class="social-icons" target="_blank" title="Share on Google+"> <i class="fa fa-google-plus"></i></a>
<a href="{{ site.owner.linkedin }}" class="social-icons" title="LinkedIn profile"><i class="fa fa-linkedin"></i></a>
<a href="{{ site.url }}/files/cv.pdf" class="social-icons" title="Printer friendly format"><i class="fa fa-print"></i></a>
</span>
{:.text-center}
[Publications]({{ site.url }}/about/publications/) \| [ORCID profile](https://orcid.org/{{ site.owner.orcid }}) \| [Google Scholar profile](https://scholar.google.com/citations?user={{ site.owner.gscholar }}&hl=en)
<!-- Alternaetly, user html5 embed tag -->
<iframe src="{{ site.url }}/files/cv.pdf" width="100%" style="height: 100vh;"></iframe>

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---
layout: page
permalink: /disclosure/
title: "Disclosure"
description: "This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License"
nofollow: false
published: true
modified: "2016-01-13"
---
This work is licensed under a <a rel="license" href="http://creativecommons.org/licenses/by-nc-sa/4.0/">Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License</a>.
### Theme Credit:
* Base: [*lanyon*](https://github.com/poole/lanyon) by [Mark Otto](https://github.com/mdo)
* Add-ons: [Samir B. Amin](https://twitter.com/sbamin) at [SBAmin.com](http://www.sbamin.com)
{% highlight c %}
Released under MIT License
Copyright (c) 2014 Mark Otto.
Permission is hereby granted, free of charge, to any person obtaining a copy of this software and associated documentation files (the "Software"), to deal in the Software without restriction, including without limitation the rights to use, copy, modify, merge, publish, distribute, sublicense, and/or sell copies of the Software, and to permit persons to whom the Software is furnished to do so, subject to the following conditions:
The above copyright notice and this permission notice shall be included in all copies or substantial portions of the Software.
THE SOFTWARE IS PROVIDED "AS IS", WITHOUT WARRANTY OF ANY KIND, EXPRESS OR IMPLIED, INCLUDING BUT NOT LIMITED TO THE WARRANTIES OF MERCHANTABILITY, FITNESS FOR A PARTICULAR PURPOSE AND NONINFRINGEMENT. IN NO EVENT SHALL THE AUTHORS OR COPYRIGHT HOLDERS BE LIABLE FOR ANY CLAIM, DAMAGES OR OTHER LIABILITY, WHETHER IN AN ACTION OF CONTRACT, TORT OR OTHERWISE, ARISING FROM, OUT OF OR IN CONNECTION WITH THE SOFTWARE OR THE USE OR OTHER DEALINGS IN THE SOFTWARE.
{% endhighlight %}
***
### <i class="fa fa-thumbs-o-up"> Credits for site features</i>:
* [Jekyll](https://jekyllrb.com){:target="_blank"}
* [Footer social icons by Lauren Clark](http://codepen.io/Deadlymuffin/pen/hGiqo/){:target="_blank"}
* [CSS and jekyll tips from HMFAYSAL OMEGA by HMFAYSAL](https://github.com/hmfaysal/hmfaysal-omega-theme){:target="_blank"}
* Icons by [Font Awesome Icons](http://fortawesome.github.io/Font-Awesome/icons/){:target="_blank"} and [IcoMoon](https://icomoon.io){:target="_blank"}
* [Responsive YouTube Playlist Embedding by John](http://avexdesigns.com/responsive-youtube-embed/){:target="_blank"}
* [Related posts without plugin by Ross Gardler](http://rgardler.github.io/2015/07/28/adding-related-posts-to-jekyll-blog/){:target="_blank"}
* [Archive page by Reyhan Dhuny and Michael Rowe](http://reyhan.org/2013/03/jekyll-archive-without-plugins.html){:target="_blank"}
* [Print css by Pieter Beulque and David Walsh](http://www.webdesignerdepot.com/2010/01/10-tips-for-better-print-style-sheets/){:target="_blank"}
* [Embed gists by Blair Vanderhoof](https://github.com/blairvanderhoof/gist-embed){:target="_blank"}
* [code highlighting css from *jekyll-now* by Barry Clark](https://github.com/barryclark/jekyll-now){:target="_blank"}
* CSS minify via [refresh-sf](http://refresh-sf.com){:target="_blank"}
* Search box:
* By [Justin James](https://github.com/digitaldrummerj){:target="_blank"}
* By [Paula Borowska](https://twitter.com/paulaborowska){:target="_blank"} at [envato tuts+](http://webdesign.tutsplus.com/tutorials/css-experiments-with-a-search-form-input-and-button--cms-22069){:target="_blank"}
* By [Amit Agrawal](http://www.labnol.org/about/){:target="_blank"} at [Digital Inspiration](http://www.labnol.org/internet/google-custom-search-css/28360/){:target="_blank"}
* Tag cloud:
* By [Tobias Sjosten](https://github.com/tobiassjosten/tobiassjosten.github.io){:target="_blank"}
* By [Thibaut Courouble](https://github.com/Thibaut){:target="_blank"} at [cssflow.com](http://www.cssflow.com/snippets/sliding-tags){:target="_blank"}
* By [Michael Lanyon](https://github.com/lanyonm){:target="_blank"} at [lanyonm.github.io](https://github.com/lanyonm/lanyonm.github.io){:target="_blank"}
* Bibliography:
* [Zot/Bib/Web](https://github.com/davidswelt/zot_bib_web){:target="_blank"} by [David Reitter](https://github.com/davidswelt){:target="_blank"} for *jekyll* page layout and css
* [Zotero Reference Manager API](https://www.zotero.org){:target="_blank"} for bibliography management
* [BibBase.org](http://bibbase.org){:target="_blank"} for external linking over `http`

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---
layout: publ
category: mypubs
permalink: /about/publications/
title: "Sample Publications"
published: true
description: "Sample publication page"
tags:
- papers
- articles
- research
comments: true
modified: "2016-02-13"
bibtex: "/files/mypubs.bib"
#bibtex: "http://foo-alternate.com/files/mypubs.bib"
show_meta: true
noindex: false
nofollow: true
sitemap:
priority: 0.5
changefreq: 'monthly'
lastmod: 2016-02-13
style: |
.container {
max-width: 48rem;
}
---
{% comment %}
<!-- bibbase.org should work with following code unless you are hosting domain over https. -->
{% if page.bibtex %}
{% if page.bibtex contains 'http' %}
{% assign domain = '' %}
{% else %}
{% assign domain = site.url %}
{% endif %}
{% capture biburl %}{{ domain }}{{ page.bibtex }}{% endcapture %}
<script src="http://bibbase.org/show?bib={{ biburl | cgi_escape }}&amp;jsonp=1&amp;authorFirst=1"></script>
{% endif %}
{% endcomment %}
If category is *mypubs*, then html content from bibtex file at `_includes/mypubs.html` will be shown below.

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---
layout: page
permalink: /readme/
title: "README - How to set up lanyon-plus jekyll theme"
description: "README for setting up lanyon-plus jekyll theme on github pages or custom domain having static website"
---
{% raw %}
## lanyon-plus
### Based on Jekyll theme: [Lanyon](http://lanyon.getpoole.com) by [Mark Otto](https://github.com/mdo)
* add-ons by [Samir B. Amin](https://sbamin.com)
* License: Open sourced under the [MIT license](LICENSE.md).
### Required edits:
#### _config.yml
* Edit lines where text string `foo` is present with relevant information.
* Add relevant author and owner information
* For proper sidebar, meta info below post title, and footer bar, add at least twitter, google plus info under `owner` and `sidebar` section.
* Uncomment and add relevant user names/keys to enable features, e.g., google analytics, disqus comments, twitter widget, google custom search.
#### CNAME
* Read [Using a custom domain with GitHub Pages](https://help.github.com/articles/using-a-custom-domain-with-github-pages/) for set-up details.
* If you are hosting website on domain other than `github.io`, rename `CNAME.sample` file to `CNAME`, and add your custom domain name, e.g., `example.com` (only one domain is allowed), otherwise remove `CNAME` file if you want to host at default `github.io`.
* If you are hosting website on `github.io`, replace `example.com` with `https://<github-username>.github.io/<repository_name>` (for project site) or `https://<github-username>.github.io` (for user site) under `site.url` and `site.urlimg` in `_config.yml` and `_prose.yml` file.
#### .travis.yml
* See more at [https://travis-ci.org/getting_started](https://travis-ci.org/getting_started)
#### _prose.yml
* [https://github.com/prose/prose/wiki/Getting-Started](https://github.com/prose/prose/wiki/Getting-Started)
* Edit `example.com` with your domain name.
* You may edit names for custom categories.
#### robots.txt
* replace `example.com` with your valid url.
* Edit search engine inclusion/exclusion if desired.
#### page specific edits
* `_data/socialmedia.html`
* Replace user `foo` with appropriate username
* `_includes/`
* Check if file paths for appropriate urls have valid css files, scripts, icons, and images in `head.html` and `head_minimal.html`, else comment html tags which are not being used.
* Also, check if variables (twitter, google plus, linkedin, google analytics key and disqus username, etc.) are specified in `_config.yml` located under root path.
* You may edit `meta_info.html`, `footer.html` and similar include files to add/remove elements in page meta bar, footer, etc.
* For publications page, `mypubs.html` and `myaoi.html` are trimmed outputs from [zot_bib_web](https://github.com/davidswelt/zot_bib_web). Github pages can not dynamically build these pages. Alternately, you may export `bib` format for publications under `/files/` directory which can be parsed dynamically using [bibbase.org](http://bibbase.org)
* `_includes/footer.html`: Edit copyright information as needed.
* `_layouts`
* To add/remove/reorder page/post contents, edit `default.html` plus `page.html` or `post.html`.
* `_posts`
* Live blog posts goes here with markdown formatted post. File name format must have following date-title format `yyyy-mm-dd-title.md` for jekyll to render blog post correctly.
* YAML sample header shows all available options. Minimal required elements are: layout, title and date. Date tag overrides date given in post file name.
* `blog/index.html`
* Edit blog title and description.
* `images/`
* Under `icons` directory, keep appropriate sized favicons and thumbnails as specified in `_includes/head.html` and `_includes/head_minimal.html`
* Also, keep `favicon.png` and `favicon.ico` in root directory.
* Final, `images/icons/` should have following images with exact filenames and image size as specified in respective filenames. These images can be generated using online *favicon generator*. Replace `foo` with your site title or other name if desired.
~~~
example.com/images/icons/apple-touch-icon-precomposed.png
example.com/images/icons/apple-touch-icon-72x72-precomposed.png
example.com/images/icons/apple-touch-icon-114x114-precomposed.png
example.com/images/icons/apple-touch-icon-144x144-precomposed.png
example.com/images/icons/apple-touch-icon-180x180.png
example.com/images/icons/android-icon-192x192.png
~~~
* `pages/about.md`
* YAML variable `imagefeature` shoud have image path relative to `images/` directory, i.e., `foo.png` will link to `example.com/images/foo.png`
* Specify `site.owner.avatar` and `site.owner.twitter` along with other variables in `_config.yml`
* `syspages/`:
* Edit page title and description in YAML front matter.
* For web search to work, specify [Google Custom Search Engine](https://cse.google.com) API key for `google_search` variable.
* Tag generation is experimental and dynamic size for tag box may need to be adjusted if you have more than 100 posts with one or two frequently occurring tags.
* All `{% for ... %}...{% endfor %}` loop operations will increase site build time, and remove such features (tags, meta info, related posts, etc.) under `_includes`, `_layouts` and `syspages` if required.
* `pages/contact.md`
* Edit page title and description.
* Edit address, driving direction url, etc.
* `pages/cv.md`
* Edit `_config.yml` to add twitter, google plus, linkedin, google scholar, ORCID profile info under owner heading.
* Add pdf at `{{ site.url }}/cv/cv.pdf`
* `pages/publications.md`
* Add your publications at `/files/mypubs.bib` and `_includes/mypubs.html`. See above under `_includes` for more.
* `pages/disclosure.md`
* Appreciated if you keep relevant credits in disclosure page.
* `humans.txt`
* Replace `foo` with your name.
* `rfeed.xml`
* Not required unless you are cross-posting about R language on blog aggregation site(s).
END
{% endraw %}

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/*CSS pending minification*/

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@font-face {
font-family: 'icomoon';
src: url('../fonts/icomoon.eot?o6nkuq');
src: url('../fonts/icomoon.eot?o6nkuq#iefix') format('embedded-opentype'),
url('../fonts/icomoon.ttf?o6nkuq') format('truetype'),
url('../fonts/icomoon.woff?o6nkuq') format('woff'),
url('../fonts/icomoon.svg?o6nkuq#icomoon') format('svg');
font-weight: normal;
font-style: normal;
}
.headicons {
display: inline-block;
margin-left: 20px;
}
.masthead-title .headicons a {
color: #505050;
text-decoration: none;
}
i.iconm {
/* use !important to prevent issues with browser extensions that change fonts */
font-family: 'icomoon' !important;
speak: none;
font-style: normal;
font-weight: normal;
font-variant: normal;
text-transform: none;
line-height: 1;
padding: 0px 4px 0px 4px;
/* Better Font Rendering =========== */
-webkit-font-smoothing: antialiased;
-moz-osx-font-smoothing: grayscale;
}
i.iconside {
/* use !important to prevent issues with browser extensions that change fonts */
font-family: 'icomoon' !important;
speak: none;
font-style: normal;
font-weight: normal;
font-size: 1.0rem;
font-variant: normal;
text-transform: none;
line-height: 1;
/* Better Font Rendering =========== */
-webkit-font-smoothing: antialiased;
-moz-osx-font-smoothing: grayscale;
}
.iconm {
-o-transition:.5s;
-ms-transition:.5s;
-moz-transition:.5s;
-webkit-transition:.5s;
transition: .5s;
background-color: #ffffff;
}
.iconm:hover {
background-color: #999999;
border-radius: 30px;
color: white;
}
.iconm-home:before {
content: "\e900";
}
.iconm-pencil2:before {
content: "\e906";
}
.iconm-quill:before {
content: "\e907";
}
.iconm-blog:before {
content: "\e909";
}
.iconm-profile:before {
content: "\e923";
}
.iconm-envelop:before {
content: "\e945";
}
.iconm-location:before {
content: "\e947";
}
.iconm-compass2:before {
content: "\e94a";
}
.iconm-user:before {
content: "\e971";
}
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---
layout: null
---
<?xml version="1.0" encoding="UTF-8"?>
<rss version="2.0" xmlns:atom="http://www.w3.org/2005/Atom">
<channel>
<title>{{ site.title | xml_escape }}</title>
<description>{{ site.description | xml_escape }}</description>
<link>{{ site.url }}{{ site.baseurl }}/</link>
<atom:link href="{{ "/rfeed.xml" | prepend: site.baseurl | prepend: site.url }}" rel="self" type="application/rss+xml" />
<updated>{{ site.time | date_to_xmlschema }}</updated>
<id>{{ site.url }}</id>
<author>
<name>{{ site.owner.name }}</name>
</author>
{% for post in site.tags.R limit:10 %}
<item>
<title>{{ post.title | xml_escape }}</title>
{% if post.summaryfeed and post.excerpt %}
<description>{{ post.excerpt | xml_escape }}</description>
{% else %}
<description>{{ post.content | xml_escape }}</description>
{% endif %}
<pubDate>{{ post.date | date: "%a, %d %b %Y %H:%M:%S %z" }}</pubDate>
<link>{{ post.url | prepend: site.baseurl | prepend: site.url }}</link>
<guid isPermaLink="true">{{ post.url | prepend: site.baseurl | prepend: site.url }}</guid>
</item>
{% endfor %}
</channel>
</rss>

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User-agent: Googlebot
Disallow: /assets/
Disallow: /CNAME
Disallow: /*.md$
Disallow: /files/
User-agent: Googlebot-Image
Disallow: /assets/
Disallow: /CNAME
Disallow: /*.md$
Disallow: /files/
User-agent: Twitterbot
Disallow: /assets/
Disallow: /CNAME
Disallow: /*.md$
Disallow: /files/
User-agent: Bingbot
Disallow: /assets/
Disallow: /CNAME
Disallow: /*.md$
Disallow: /files/
User-agent: DuckDuckBot
Disallow: /assets/
Disallow: /CNAME
Disallow: /*.md$
Disallow: /files/
User-agent: ia_archiver
Disallow: /assets/
Disallow: /CNAME
Disallow: /*.md$
Disallow: /files/
User-agent: Applebot
Disallow: /assets/
Disallow: /CNAME
Disallow: /*.md$
Disallow: /files/
User-agent: facebookexternalhit
Disallow: /assets/
Disallow: /CNAME
Disallow: /*.md$
Disallow: /files/
User-agent: Facebot
Disallow: /assets/
Disallow: /CNAME
Disallow: /*.md$
Disallow: /files/
User-agent: *
Disallow: /
Sitemap: https://example.com/sitemap.xml

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---
layout: null
---
<?xml version="1.0" encoding="UTF-8"?>
<urlset xmlns="http://www.sitemaps.org/schemas/sitemap/0.9">
{% for post in site.posts %}
{% unless post.published == false %}
<url>
<loc>{{ site.url }}{{ post.url }}</loc>
{% if post.sitemap.lastmod %}
<lastmod>{{ post.sitemap.lastmod | date: "%Y-%m-%d" }}</lastmod>
{% elsif post.date %}
<lastmod>{{ post.date | date_to_xmlschema }}</lastmod>
{% else %}
<lastmod>{{ site.time | date_to_xmlschema }}</lastmod>
{% endif %}
{% if post.sitemap.changefreq %}
<changefreq>{{ post.sitemap.changefreq }}</changefreq>
{% else %}
<changefreq>monthly</changefreq>
{% endif %}
{% if post.sitemap.priority %}
<priority>{{ post.sitemap.priority }}</priority>
{% else %}
<priority>0.5</priority>
{% endif %}
</url>
{% endunless %}
{% endfor %}
{% for page in site.pages %}
{% unless page.sitemap == false %}
<url>
<loc>{{ site.url }}{{ page.url | remove: "index.html" }}</loc>
{% if page.sitemap.lastmod %}
<lastmod>{{ page.sitemap.lastmod | date: "%Y-%m-%d" }}</lastmod>
{% elsif page.date %}
<lastmod>{{ page.date | date_to_xmlschema }}</lastmod>
{% else %}
<lastmod>{{ site.time | date_to_xmlschema }}</lastmod>
{% endif %}
{% if page.sitemap.changefreq %}
<changefreq>{{ page.sitemap.changefreq }}</changefreq>
{% else %}
<changefreq>monthly</changefreq>
{% endif %}
{% if page.sitemap.priority %}
<priority>{{ page.sitemap.priority }}</priority>
{% else %}
<priority>0.3</priority>
{% endif %}
</url>
{% endunless %}
{% endfor %}
</urlset>

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---
layout: default_minimal
title: "404: Page not found"
description: "Error 404: Requested page not found"
permalink: /404.html
sitemap: false
noindex: true
nofollow: true
category: base
---
<p>Sorry! The page you were trying to view does not exist.</p>
<p>Perhaps you may have error while typing web address. If not, you may tweet me to fix missing link. Thanks!</p>
<div class="text-center">
<a href="https://twitter.com/share" class="twitter-share-button" data-via="{{ site.owner.twitter }}" data-size="large" data-dnt="true">Tweet</a>
<script>!function(d,s,id){var js,fjs=d.getElementsByTagName(s)[0],p=/^http:/.test(d.location)?'http':'https';if(!d.getElementById(id)){js=d.createElement(s);js.id=id;js.src=p+'://platform.twitter.com/widgets.js';fjs.parentNode.insertBefore(js,fjs);}}(document, 'script', 'twitter-wjs');</script>
</div>
{:.text-center}
You may also visit [tags]({{ site.url }}/tags) or [archive]({{ site.url }}/archive) page to browse website contents.
<hr class="gh">
{% if site.google_search %}
<div id="searchbox2" style="margin:0 auto; display: table;">
<div class="searchcont2">
<!-- span class="searchicon2"><i class="fa fa-search fa-2x"></i></span -->
<form role="search" method="get" action="{{ site.url }}/cse/">
<input id="searchString2" name="searchString2"
placeholder=" Search" type="text">
</form>
</div>
</div>
{% endif %}

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---
layout: page
title: Archive
description: "Archive"
permalink: /archive/
category: base
---
<section id="archive">
<h3>This year's posts</h3>
{%for post in site.posts %}
{% unless post.next %}
<ul class="post-list">
{% else %}
{% capture year %}{{ post.date | date: '%Y' }}{% endcapture %}
{% capture nyear %}{{ post.next.date | date: '%Y' }}{% endcapture %}
{% if year != nyear %}
</ul>
<h3>{{ post.date | date: '%Y' }}</h3>
<ul class="post-list">
{% endif %}
{% endunless %}
<li><a href="{{ site.url }}{{ post.url }}">{{ post.title }}<span class="entry-date"><time datetime="{{ post.date | date_to_xmlschema }}">{{ post.date | date: "%b %d, %Y" }}</time></span></a></li>
{% endfor %}
</ul>
</section>

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---
layout: default_minimal
title: "Search"
description: "Search"
permalink: /cse/
sitemap: false
noindex: true
nofollow: true
category: base
---
{:.text-center}
You may also visit [tags]({{ site.url }}/tags) or [archive]({{ site.url }}/archive) page to browse website contents.
{:.text-center}
<a href="javascript:goBack()" class="social-icons" title="Return to previous page"><i class="fa fa-arrow-circle-left fa-2x"></i></a>
<script>
function goBack() {
window.history.back();
}
</script>
{% if site.google_search %}
<hr class="gh">
<div id="searchbox2" align="center">
<div class="searchcont2">
<!-- span class="searchicon2"><i class="fa fa-search fa-2x"></i></span -->
<form role="search" method="get" action="{{ site.url }}/cse/">
<input id="searchString2" name="searchString2"
placeholder=" Search" type="text">
</form>
</div>
</div>
<script>
(function() {
var cx = '{{ site.google_search }}';
var gcse = document.createElement('script');
gcse.type = 'text/javascript';
gcse.async = true;
gcse.src = (document.location.protocol == 'https:' ? 'https:' : 'http:') +
'//cse.google.com/cse.js?cx=' + cx;
var s = document.getElementsByTagName('script')[0];
s.parentNode.insertBefore(gcse, s);
})();
</script>
<gcse:searchresults-only queryParameterName="searchString2" enableAutoComplete="true" autoCompleteMatchType='any' autoCompleteMaxCompletions="5" autoCompleteMaxPromotions="1"></gcse:searchresults-only>
<!-- <gcse:searchbox-only resultsUrl="{{ site.url }}/cse/" queryParameterName="searchString"></gcse:searchbox-only> -->
{% else %}
This page will serve search results if Google Custom Search key is set in `_config.yml`
{% endif %}

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---
layout: page
title: Featured Posts
description: "Featured posts"
permalink: /featured/
sitemap: false
noindex: true
category: base
---
<hr class="gh">
<div class="posts">
{% for post in site.categories.featured %}
<div class="post">
<h1 class="post-title">
<a href="{{ site.url }}{{ post.url }}">
{{ post.title }}
</a>
</h1>
{% if post.modified.size > 2 %}<span class="post-date indexpg" itemprop="dateModified" content="{{ post.modified | date: "%Y-%m-%d" }}"><i class="fa fa-edit" title="Last updated"> {{ post.modified | date_to_string }}</i></span>{% else %}<span class="post-date indexpg" itemprop="datePublished" content="{{ post.date | date: "%Y-%m-%d" }}"><i class="fa fa-calendar" title="Date published"> {{ post.date | date_to_string }}</i></span>{% endif %}
{% if post.description.size > 140 %}{{ post.description | markdownify | remove: '<p>' | remove: '</p>' }}{% else %}{{ post.excerpt | markdownify | remove: '<p>' | remove: '</p>' }}{% endif %} <a href="{{ site.url }}{{ post.url }}" title="Read more"><strong>Read more...</strong></a>
</div>
{% unless forloop.last %}<hr class="transp">{% endunless %}
{% endfor %}
</div>

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---
title: "Redirecting to Blog"
layout: redirect
sitemap: false
permalink: /news/
redirect_to: /blog/
#teaser: SYSTEM GENERATED PAGE FOR PAGE REDIRECT FUNCTION. DO NOT EDIT/RENAME/REMOVE THIS PAGE.
---

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---
title: "Redirecting to About/Publications"
layout: redirect
sitemap: false
permalink: /publications/
redirect_to: /about/publications/
#teaser: SYSTEM GENERATED PAGE FOR PAGE REDIRECT FUNCTION. DO NOT EDIT/RENAME/REMOVE THIS PAGE.
---

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---
title: "Redirecting to Curriculum Vitae page"
layout: redirect
sitemap: true
permalink: /resume/
redirect_to: /cv/
#teaser: SYSTEM GENERATED PAGE FOR PAGE REDIRECT FUNCTION. DO NOT EDIT/RENAME/REMOVE THIS PAGE.
---

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---
layout: default_minimal
title: "Search"
description: "Search"
permalink: /search/
sitemap: false
noindex: true
nofollow: true
category: base
---
{% if site.google_search %}
<div id="searchbox2" style="margin:0 auto; display: table;">
<div class="searchcont2">
<!-- span class="searchicon2"><i class="fa fa-search fa-2x"></i></span -->
<form role="search" method="get" action="{{ site.url }}/cse/">
<input id="searchString2" name="searchString2"
placeholder=" Search" type="text">
</form>
</div>
</div>
{% else %}
Google Custom Search key is not set in `_config.yml`
{% endif %}

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---
layout: page
title: "Tag Cloud"
permalink: "/tags/"
description: "Browse website by tag based index"
comments: false
sitemap: false
category: base
---
{:.text-center}
## <i class="fa fa-paperclip" title="Featured"></i> <a href="{{ site.url }}/featured">Featured Posts</a>
<hr class="style17" style="margin:1.0rem 0;">
{% comment %}
Tag generation is experimental and dynamic size for tag box may need to be adjusted if you have more than 100 posts with one or two frequently occurring tags. Also,all for loop operations will increase site build time.
{% endcomment %}
{% capture site_tags %}{% for tag in site.tags %}{{ tag | first }}{% unless forloop.last %},{% endunless %}{% endfor %}{% endcapture %}
{% assign tags_list = site_tags | split:',' | sort %}
<ul class="slidetags">
{% for item in (0..site.tags.size) %}{% unless forloop.last %}
{% capture this_word %}{{ tags_list[item] | strip_newlines }}{% endcapture %}
<li style="font-size:{{ site.tags[this_word].size | times: 100 | divided_by: site.tags.size | plus: 70 }}%"><a href="#{{ this_word }}">{{ this_word }} <span>{{ site.tags[this_word].size }}</span></a></li>
{% endunless %}{% endfor %}
</ul>
{% for item in (0..site.tags.size) %}{% unless forloop.last %}
{% capture this_word %}{{ tags_list[item] | strip_newlines }}{% endcapture %}
<h2 id="{{ this_word }}">{{ this_word }}</h2>
<ul class="post-list">
{% for post in site.tags[this_word] %}{% if post.title != null %}
<li><a href="{{ site.url }}{{ post.url }}">{{ post.title }}<span class="entry-date"><time datetime="{{ post.date | date_to_xmlschema }}">{{ post.date | date: "%b %d, %Y" }}</time></span></a></li>
{% endif %}{% endfor %}
</ul>
{% endunless %}{% endfor %}