phidias51/semantic_markup.html

## semantic_markup.html
<!DOCTYPE html>
<html>
<head>

<style type="text/css">
assertion{
	background-color: #FAFAD2;
}
.assertion{
	background-color: #FAFAD2;
}

gene{
	background-color: #66CC99;
	padding-right: 3px;
	padding-left: 3px;
	border-radius: 5px;
	border: 1px solid black;
}

.gene{
	background-color: #66CC99;
	padding-right: 3px;
	padding-left: 3px;
	border-radius: 5px;
	border: 1px solid black;
}

mutant{
	background-color: #BFD4FF;
	padding-right: 3px;
	padding-left: 3px;
	border-radius: 5px;
}
.mutant{
	background-color: #BFD4FF;
	padding-right: 3px;
	padding-left: 3px;
	border-radius: 5px;
}

pathway{
	background-color: #E3BBED;
	padding-right: 3px;
	padding-left: 3px;
	border-radius: 5px;
}
.pathway{
	background-color: #E3BBED;
	padding-right: 3px;
	padding-left: 3px;
	border-radius: 5px;
}

disease{
	background-color: #FFB6C1;
	padding-right: 3px;
	padding-left: 3px;
	border-radius: 5px;
}

.disease{
	background-color: #FFB6C1;
	padding-right: 3px;
	padding-left: 3px;
	border-radius: 5px;
}
body {
	font-family: Verdana;
}
sidebar{
	float: right;
	border: 1px solid black;
	border-radius: 3px;
	background-color: #FFCC99;
	padding: 5px;
}
article{
	float: left;
	width: 700px;
}
</style>

<script type="text/javascript">


function init(){
	var disElements = document.getElementsByTagName("disease");
	for(var i=0; i < disElements.length; i++){

		disElements[i].addEventListener('click',function(event){
			window.open("http://omim.org/entry/" + event.srcElement.id);
		},true);
	}

	var geneElements = document.getElementsByTagName("gene");
	for(var i=0; i < geneElements.length; i++){

		geneElements[i].addEventListener('click',function(event){
			window.open("http://www.ncbi.nlm.nih.gov/gene/" + event.srcElement.id);
		},true);
	}

	var mutElements = document.getElementsByTagName("mutant");
	for(var i=0; i < mutElements.length; i++){
		mutElements[i].addEventListener('click', function(event){
			var url = "http://web.expasy.org/variant_pages/" + event.srcElement.id + ".html";
			window.open(url);
		}, false);
	}

	var pathElements = document.getElementsByTagName("pathway");
	for(var i=0; i < pathElements.length; i++){
		pathElements[i].addEventListener('click', function(event){
			window.open("http://www.genome.jp/dbget-bin/www_bget?pathway:" + event.srcElement.id);
		}, false);
	}


	var predElements = document.getElementsByTagName("predicate");
	for(var i=0; i < predElements.length; i++){
		predElements[i].addEventListener('click', function(event){
			console.log("predicate: " + event.srcElement.textContent);
		}, false);
	}

}

</script>
</head>
<body onload="init()">

<sidebar>
Legend
<ul>
<li><a class="gene">Gene</a></li>
<li><a class="mutant">Mutation</a></li>
<li><a class="pathway">Pathway</a></li>
<li><a class="assertion">Assertion</a></li>
</ul>
</sidebar>
<article>
<disease id="260350">Pancreatic ductal adenocarcinoma</disease> (PDAC) is an aggressive cancer with poor survival rates and frequently carries oncogenic KRAS mutation. However, <gene id="3845">KRAS</gene> has thus far not been a viable therapeutic target. We found that the abundance of <gene id="10413">YAP</gene> mRNA, which encodes Yes-associated protein (YAP), a protein regulated by the <pathway id="map04390">Hippo</pathway> pathway during tissue development and homeostasis, was increased in human PDAC tissue compared with that in normal pancreatic epithelia. In genetically engineered Kras(G12D) and <mutant id="VAR_016026">Kras(G12D)</mutant>:<mutant id="Trp53(R172H)">Trp53(R172H)</mutant> mouse models, <assertion>pancreas-specific deletion of <subject id="10413" class="gene">Yap</subject> halted the progression of early neoplastic lesions to PDAC without affecting normal pancreatic development and endocrine function</assertion>. Although Yap was dispensable for acinar to ductal metaplasia (ADM), an initial step in the progression to PDAC, Yap was critically required for the proliferation of mutant Kras or Kras:Trp53 neoplastic pancreatic ductal cells in culture and for their growth and progression to invasive PDAC in mice. <assertion><gene id="10413">Yap</gene> functioned as a critical transcriptional switch downstream of the oncogenic KRAS-mitogen-activated protein kinase (MAPK) pathway, promoting the expression of genes encoding secretory factors that cumulatively sustained neoplastic proliferation, a tumorigenic stromal response in the tumor microenvironment, and PDAC progression in Kras and Kras:Trp53 mutant pancreas tissue</assertion>. Together, our findings identified <assertion><subject class="gene">Yap</subject> as a <predicate>critical oncogenic <object class="gene">KRAS</object> effector</predicate></assertion> and a promising therapeutic target for PDAC and possibly other types of KRAS-mutant cancers.
</article>


</body>
</html>
	<!DOCTYPE html>
	<html>
	<head>

	<style type="text/css">
	assertion{
	background-color: #FAFAD2;
	}
	.assertion{
	background-color: #FAFAD2;
	}

	gene{
	background-color: #66CC99;
	padding-right: 3px;
	padding-left: 3px;
	border-radius: 5px;
	border: 1px solid black;
	}

	.gene{
	background-color: #66CC99;
	padding-right: 3px;
	padding-left: 3px;
	border-radius: 5px;
	border: 1px solid black;
	}

	mutant{
	background-color: #BFD4FF;
	padding-right: 3px;
	padding-left: 3px;
	border-radius: 5px;
	}
	.mutant{
	background-color: #BFD4FF;
	padding-right: 3px;
	padding-left: 3px;
	border-radius: 5px;
	}

	pathway{
	background-color: #E3BBED;
	padding-right: 3px;
	padding-left: 3px;
	border-radius: 5px;
	}
	.pathway{
	background-color: #E3BBED;
	padding-right: 3px;
	padding-left: 3px;
	border-radius: 5px;
	}

	disease{
	background-color: #FFB6C1;
	padding-right: 3px;
	padding-left: 3px;
	border-radius: 5px;
	}

	.disease{
	background-color: #FFB6C1;
	padding-right: 3px;
	padding-left: 3px;
	border-radius: 5px;
	}
	body {
	font-family: Verdana;
	}
	sidebar{
	float: right;
	border: 1px solid black;
	border-radius: 3px;
	background-color: #FFCC99;
	padding: 5px;
	}
	article{
	float: left;
	width: 700px;
	}
	</style>

	<script type="text/javascript">


	function init(){
	var disElements = document.getElementsByTagName("disease");
	for(var i=0; i < disElements.length; i++){

	disElements[i].addEventListener('click',function(event){
	window.open("http://omim.org/entry/" + event.srcElement.id);
	},true);
	}

	var geneElements = document.getElementsByTagName("gene");
	for(var i=0; i < geneElements.length; i++){

	geneElements[i].addEventListener('click',function(event){
	window.open("http://www.ncbi.nlm.nih.gov/gene/" + event.srcElement.id);
	},true);
	}

	var mutElements = document.getElementsByTagName("mutant");
	for(var i=0; i < mutElements.length; i++){
	mutElements[i].addEventListener('click', function(event){
	var url = "http://web.expasy.org/variant_pages/" + event.srcElement.id + ".html";
	window.open(url);
	}, false);
	}

	var pathElements = document.getElementsByTagName("pathway");
	for(var i=0; i < pathElements.length; i++){
	pathElements[i].addEventListener('click', function(event){
	window.open("http://www.genome.jp/dbget-bin/www_bget?pathway:" + event.srcElement.id);
	}, false);
	}



	var predElements = document.getElementsByTagName("predicate");
	for(var i=0; i < predElements.length; i++){
	predElements[i].addEventListener('click', function(event){
	console.log("predicate: " + event.srcElement.textContent);
	}, false);
	}

	}

	</script>
	</head>
	<body onload="init()">

	<sidebar>
	Legend
	<ul>
	<li><a class="gene">Gene</a></li>
	<li><a class="mutant">Mutation</a></li>
	<li><a class="pathway">Pathway</a></li>
	<li><a class="assertion">Assertion</a></li>
	</ul>
	</sidebar>
	<article>
	<disease id="260350">Pancreatic ductal adenocarcinoma</disease> (PDAC) is an aggressive cancer with poor survival rates and frequently carries oncogenic KRAS mutation. However, <gene id="3845">KRAS</gene> has thus far not been a viable therapeutic target. We found that the abundance of <gene id="10413">YAP</gene> mRNA, which encodes Yes-associated protein (YAP), a protein regulated by the <pathway id="map04390">Hippo</pathway> pathway during tissue development and homeostasis, was increased in human PDAC tissue compared with that in normal pancreatic epithelia. In genetically engineered Kras(G12D) and <mutant id="VAR_016026">Kras(G12D)</mutant>:<mutant id="Trp53(R172H)">Trp53(R172H)</mutant> mouse models, <assertion>pancreas-specific deletion of <subject id="10413" class="gene">Yap</subject> halted the progression of early neoplastic lesions to PDAC without affecting normal pancreatic development and endocrine function</assertion>. Although Yap was dispensable for acinar to ductal metaplasia (ADM), an initial step in the progression to PDAC, Yap was critically required for the proliferation of mutant Kras or Kras:Trp53 neoplastic pancreatic ductal cells in culture and for their growth and progression to invasive PDAC in mice. <assertion><gene id="10413">Yap</gene> functioned as a critical transcriptional switch downstream of the oncogenic KRAS-mitogen-activated protein kinase (MAPK) pathway, promoting the expression of genes encoding secretory factors that cumulatively sustained neoplastic proliferation, a tumorigenic stromal response in the tumor microenvironment, and PDAC progression in Kras and Kras:Trp53 mutant pancreas tissue</assertion>. Together, our findings identified <assertion><subject class="gene">Yap</subject> as a <predicate>critical oncogenic <object class="gene">KRAS</object> effector</predicate></assertion> and a promising therapeutic target for PDAC and possibly other types of KRAS-mutant cancers.
	</article>



	</body>
	</html>