Non-small cell lung cancer (Homo sapiens)

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(update FHIT section)
Current revision (23:21, 12 July 2019) (view source)
(added details for retinoic acid signaling and added new interaction type)
 
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<Pathway xmlns="http://pathvisio.org/GPML/2013a" Name="Non-small cell lung cancer" Version="20180412" Organism="Homo sapiens">
<Pathway xmlns="http://pathvisio.org/GPML/2013a" Name="Non-small cell lung cancer" Version="20180412" Organism="Homo sapiens">
   <Comment Source="WikiPathways-description">Lung cancer is a leading cause of cancer death among men and women in industrialized countries. Non-small-cell lung cancer (NSCLC) accounts for approximately 85% of lung cancer and represents a heterogeneous group of cancers, consisting mainly of squamous cell (SCC), adeno (AC) and large-cell carcinoma. Molecular mechanisms altered in NSCLC include activation of oncogenes, such as K-RAS, EGFR and EML4-ALK, and inactivation of tumorsuppressor genes, such as p53, p16INK4a, RAR-beta, and RASSF1. Point mutations within the K-RAS gene inactivate GTPase activity and the p21-RAS protein continuously transmits growth signals to the nucleus. Mutations or overexpression of EGFR leads to a proliferative advantage. EML4-ALK fusion leads to constitutive ALK activation, which causes cell proliferation, invasion, and inhibition of apoptosis. Inactivating mutation of p53 can lead to more rapid proliferation and reduced apoptosis. The protein encoded by the p16INK4a inhibits formation of CDK-cyclin-D complexes by competitive binding of CDK4 and CDK6. Loss of p16INK4a expression is a common feature of NSCLC. RAR-beta is a nuclear receptor that bears vitamin-A-dependent transcriptional activity. RASSF1A is able to form heterodimers with Nore-1, an RAS effector.Therefore loss of RASSF1A might shift the balance of RAS activity towards a growth-promoting effect.</Comment>
   <Comment Source="WikiPathways-description">Lung cancer is a leading cause of cancer death among men and women in industrialized countries. Non-small-cell lung cancer (NSCLC) accounts for approximately 85% of lung cancer and represents a heterogeneous group of cancers, consisting mainly of squamous cell (SCC), adeno (AC) and large-cell carcinoma. Molecular mechanisms altered in NSCLC include activation of oncogenes, such as K-RAS, EGFR and EML4-ALK, and inactivation of tumorsuppressor genes, such as p53, p16INK4a, RAR-beta, and RASSF1. Point mutations within the K-RAS gene inactivate GTPase activity and the p21-RAS protein continuously transmits growth signals to the nucleus. Mutations or overexpression of EGFR leads to a proliferative advantage. EML4-ALK fusion leads to constitutive ALK activation, which causes cell proliferation, invasion, and inhibition of apoptosis. Inactivating mutation of p53 can lead to more rapid proliferation and reduced apoptosis. The protein encoded by the p16INK4a inhibits formation of CDK-cyclin-D complexes by competitive binding of CDK4 and CDK6. Loss of p16INK4a expression is a common feature of NSCLC. RAR-beta is a nuclear receptor that bears vitamin-A-dependent transcriptional activity. RASSF1A is able to form heterodimers with Nore-1, an RAS effector.Therefore loss of RASSF1A might shift the balance of RAS activity towards a growth-promoting effect.</Comment>
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Line 879: Line 886:
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Line 969: Line 1,003:
       <bp:ID xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" rdf:datatype="http://www.w3.org/2001/XMLSchema#string">CL:0002328</bp:ID>
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       <bp:Ontology xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" rdf:datatype="http://www.w3.org/2001/XMLSchema#string">Cell Type</bp:Ontology>
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-
    </bp:openControlledVocabulary>
 
-
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-
      <bp:TERM xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" rdf:datatype="http://www.w3.org/2001/XMLSchema#string">lung cancer pathway</bp:TERM>
 
-
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-
      <bp:Ontology xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" rdf:datatype="http://www.w3.org/2001/XMLSchema#string">Pathway Ontology</bp:Ontology>
 
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     <bp:openControlledVocabulary xmlns:bp="http://www.biopax.org/release/biopax-level3.owl#">
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Line 1,003: Line 1,032:
       <bp:AUTHORS rdf:datatype="http://www.w3.org/2001/XMLSchema#string">Roth JA</bp:AUTHORS>
       <bp:AUTHORS rdf:datatype="http://www.w3.org/2001/XMLSchema#string">Roth JA</bp:AUTHORS>
       <bp:AUTHORS rdf:datatype="http://www.w3.org/2001/XMLSchema#string">Ji L</bp:AUTHORS>
       <bp:AUTHORS rdf:datatype="http://www.w3.org/2001/XMLSchema#string">Ji L</bp:AUTHORS>
 +
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 +
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      <bp:TERM xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" rdf:datatype="http://www.w3.org/2001/XMLSchema#string">lung cancer pathway</bp:TERM>
 +
      <bp:ID xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" rdf:datatype="http://www.w3.org/2001/XMLSchema#string">PW:0000703</bp:ID>
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      <bp:Ontology xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" rdf:datatype="http://www.w3.org/2001/XMLSchema#string">Pathway Ontology</bp:Ontology>
 +
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 +
    <bp:PublicationXref xmlns:bp="http://www.biopax.org/release/biopax-level3.owl#" xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" rdf:id="b72">
 +
      <bp:ID rdf:datatype="http://www.w3.org/2001/XMLSchema#string">23322901</bp:ID>
 +
      <bp:DB rdf:datatype="http://www.w3.org/2001/XMLSchema#string">PubMed</bp:DB>
 +
      <bp:TITLE rdf:datatype="http://www.w3.org/2001/XMLSchema#string">Molecular pathways: current role and future directions of the retinoic acid pathway in cancer prevention and treatment.</bp:TITLE>
 +
      <bp:SOURCE rdf:datatype="http://www.w3.org/2001/XMLSchema#string">Clin Cancer Res</bp:SOURCE>
 +
      <bp:YEAR rdf:datatype="http://www.w3.org/2001/XMLSchema#string">2013</bp:YEAR>
 +
      <bp:AUTHORS rdf:datatype="http://www.w3.org/2001/XMLSchema#string">Connolly RM</bp:AUTHORS>
 +
      <bp:AUTHORS rdf:datatype="http://www.w3.org/2001/XMLSchema#string">Nguyen NK</bp:AUTHORS>
 +
      <bp:AUTHORS rdf:datatype="http://www.w3.org/2001/XMLSchema#string">Sukumar S</bp:AUTHORS>
     </bp:PublicationXref>
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   </Biopax>
   </Biopax>
</Pathway>
</Pathway>

Current revision

Error rendering pathway page

This revision of the pathway probably contains invalid GPML code. If this happens to the most recent revision, try reverting the pathway using the pathway history displayed below or contact the site administrators (see WikiPathways:About) to resolve this problem.

Pathway history

View all...
CompareRevisionActionTimeUserComment
105155view23:21, 12 July 2019Khanspersadded details for retinoic acid signaling and added new interaction type
105154view22:21, 12 July 2019Khanspersupdate FHIT section
105004view04:55, 28 June 2019KhanspersModified description
96916view14:37, 19 April 2018EgonwReplaced secondary ChEBI identifiers with primary identifiers.
96911view04:38, 19 April 2018Khanspersupdated kras
96909view19:34, 18 April 2018Khanspersadded pathway node xrefs
96857view23:28, 14 April 2018AlexanderPicoOntology Term : 'disease pathway' added !
96856view00:06, 14 April 2018KhanspersOntology Term : 'bronchial epithelial cell' added !
96855view00:05, 14 April 2018KhanspersOntology Term : 'lung cancer pathway' added !
96854view00:05, 14 April 2018KhanspersModified description
96853view00:03, 14 April 2018KhanspersModified description
96852view23:58, 13 April 2018KhanspersNew pathway

Error details

exception 'Exception' with message 'Unable to convert to /var/www/wikipathways/images/5/54/WP4255_prev.svg:
<BR>Status:1
<BR>Message:Exception in thread "main" java.lang.NullPointerException
	at org.pathvisio.core.Engine.getPathwayImporters(Unknown Source)
	at org.pathvisio.core.Engine.importPathway(Unknown Source)
	at org.pathvisio.core.util.Converter.main(Unknown Source)

<BR>Command:java -Xmx1024M -jar /var/www/wikipathways/wpi/bin/pathvisio_core.jar "/var/www/wikipathways" "/var/www/wikipathways/images/5/54/WP4255_prev.svg" 2>&1<BR>' in /var/www/wikipathways/wpi/extensions/Pathways/Pathway.php:1255
Stack trace:
#0 /var/www/wikipathways/wpi/extensions/Pathways/Pathway.php(1227): Pathway::convertWithPathVisio(false, '/var/www/wikipa...')
#1 /var/www/wikipathways/wpi/extensions/Pathways/Pathway.php(1137): Pathway->saveConvertedByPathVisioCache('svg')
#2 /var/www/wikipathways/wpi/extensions/Pathways/PathwayPage.php(21): Pathway->updateCache('svg')
#3 [internal function]: renderPathwayPage(Object(Parser), '<?xml version="...', Object(StripState))
#4 /var/www/wikipathways/includes/Hooks.php(125): call_user_func_array('renderPathwayPa...', Array)
#5 /var/www/wikipathways/includes/parser/Parser.php(318): wfRunHooks('ParserBeforeStr...', Array)
#6 /var/www/wikipathways/includes/OutputPage.php(405): Parser->parse('<?xml version="...', Object(Title), Object(ParserOptions), true, true, 105155)
#7 /var/www/wikipathways/includes/OutputPage.php(391): OutputPage->addWikiTextTitle('<?xml version="...', Object(Title), true, true)
#8 /var/www/wikipathways/includes/OutputPage.php(500): OutputPage->addWikiTextTitleTidy('<?xml version="...', Object(Title), true)
#9 /var/www/wikipathways/includes/DifferenceEngine.php(313): OutputPage->addWikiTextTidy('<?xml version="...')
#10 /var/www/wikipathways/includes/DifferenceEngine.php(271): DifferenceEngine->renderNewRevision()
#11 /var/www/wikipathways/includes/Article.php(729): DifferenceEngine->showDiffPage(false)
#12 /var/www/wikipathways/includes/Wiki.php(437): Article->view()
#13 /var/www/wikipathways/includes/Wiki.php(59): MediaWiki->performAction(Object(OutputPage), Object(Article), Object(Title), Object(User), Object(WebRequest))
#14 /var/www/wikipathways/index.php(93): MediaWiki->initialize(Object(Title), Object(Article), Object(OutputPage), Object(User), Object(WebRequest))
#15 {main}
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