Human Gene Set: KEGG_NON_SMALL_CELL_LUNG_CANCER


Standard name KEGG_NON_SMALL_CELL_LUNG_CANCER
Systematic name M19818
Brief description Non-small cell lung cancer
Full description or abstract Non-small-cell lung cancer (NSCLC) accounts for approximately 80% 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 and c-erbB-2, 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. Overexpression of c-erbB-2 or EGFR leads to a proliferative advantage. 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.
Collection C2: Curated
      CP: Canonical Pathways
            CP:KEGG_LEGACY: KEGG Legacy Pathways
Source publication  
Exact source hsa05223
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External links http://www.genome.jp/kegg/pathway/hsa/hsa05223.html
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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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GTEx compendium
Human tissue compendium (Novartis)
Global Cancer Map (Broad Institute)
NCI-60 cell lines (National Cancer Institute)
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