Human Gene Set: KEGG_PANCREATIC_CANCER


Standard name KEGG_PANCREATIC_CANCER
Systematic name M9726
Brief description Pancreatic cancer
Full description or abstract Normal duct epithelium progresses to infiltrating cancer through a series of histologically defined precursors (PanINs). The overexpression of HER-2/neu and activating point mutations in the K-ras gene occur early, inactivation of the p16 gene at an intermediate stage, and the inactivation of p53, SMAD4, and BRCA2 occur relatively late. Activated K-ras engages multiple effector pathways. Although EGF receptors are conventionally regarded as upstream activators of RAS proteins, they can also act as RAS signal transducers via RAS-induced autocrine activation of the EGFR family ligands. Pancreatic ductal adenocarcinoma (PDA) show elevated expression of EGF receptors (e.g. HER2/neu) and their ligands (e.g.TGF-alpha) consistent with the presence of this autocrine loop. Moreover, PDA shows extensive genomic instability and aneuploidy. Telomere attrition and mutations in p53 and BRCA2 are likely to contribute to these phenotypes. Inactivation of the SMAD4 tumour suppressor gene leads to loss of the inhibitory influence of the transforming growth factor-beta signalling pathway.
Collection C2: Curated
      CP: Canonical Pathways
            CP:KEGG_LEGACY: KEGG Legacy Pathways
Source publication  
Exact source hsa05212
Related gene sets  
External links http://www.genome.jp/pathway/hsa05212
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Source species Homo sapiens
Contributed by KEGG (Kyoto Encyclopedia of Genes and Genomes)
Source platform or
identifier namespace
Human_NCBI_Gene_ID
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Global Cancer Map (Broad Institute)
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GTEx compendium
Human tissue compendium (Novartis)
Global Cancer Map (Broad Institute)
NCI-60 cell lines (National Cancer Institute)
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Version history  

The content of the gene sets in the KEGG_LEGACY collection has not been updated since KEGG restricted their usage terms in 2011. More recent sets are available in the KEGG_MEDICUS collection, derived from KEGG's openly available MEDICUS subset.


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