help  | about  | cite  | software

Pathway : Non-small cell lung cancer

Identifier  05223 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 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 effectorTherefore loss of RASSF1A might shift the balance of RAS activity towards a growth-promoting effect

1 Data Sets

108 Genes

0 Proteins