About: Non-Small Cell Lung Cancer Pathway

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Attributes	Values
rdf:type	Class
rdfs:label	Non-Small Cell Lung Cancer Pathway
rdfs:subClassOf	Cancer Pathway
Semantic_Type	Functional Concept
Preferred_Name	Non-Small Cell Lung Cancer Pathway
UMLS_CUI	C2984258
KEGG_ID	hsa05223
ALT_DEFINITION	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 tumor suppressor 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 gene 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.KEGG
FULL_SYN	Non-Small Cell Lung Cancer PathwayPTNCI NSCLC PathwaySYNCI Non-small cell lung cancerPTKEGG
code	C91445
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