Abstract
Early models of cancer genetics categorized cancer genes into oncogenes, which are growth inducing, and tumor suppressor genes. Cells harboring mutant p53 genes lose the ability to arrest in G1after exposure to gamma radiation or other genotoxins. It was gathered that mice with p53 genes disruptions are completely viable, but they exhibit an enhanced rate of tumor formation and the abrogation of the G1 checkpoint after exposure to DNA-damaging agents. BRCA1 and BRCA2 are structurally unrelated genes with converging clinical effects. Disabling mutations in either gene render an individual more susceptible to breast and ovarian cancer. Although both genes carry the hallmarks of a tumor suppressor gene, their main function is not growth regulation. MLH1 and MSH2 genes are responsible for syndrome of hereditary nonpolyposis colorectal cancer. The cancer susceptibility gene, PTEN/MMAC is an example of a genetic guardian whose primary function is to regulate cell death and survival. This review has found that, PTEN, localized to 10q23, has been identified through position cloning as the gene responsible for Cowden’s syndrome.
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