1)Tumor suppressor genes generally function in inhibiting uncontrolled cell proliferation and maintaining DNA integrity through the

repair of DNA damage, both of which when go wrong become hallmark features of cancer. Some tumor suppressor genes work at the cell surface and code for cell adhesion and the at cytoskeleton to maintain its stability. Examples of these are the E-cadherin and NF2 genes respectively. Others work at the nuclear level controlling the cell cycle progression, initiating cell death or cell cycle arrest as well as promoting DNA repair. These are RB1, p53 as well as BRACA1 and BRACA2 genes. 2)Cancer cells sustain itself by adopting mechanisms to evade apoptosis through the mutation of the p53 gene. In most cases this mutation does not follows the two hit hypothesis where both copies of the allele are mutated before the cancerous effects are manifested. It is commonly a single point mutation. p53 induces specific cell responses including cell cycle arrest, senescence, cell differentiation and apoptosis. When cells with damaged DNA escape apoptosis and there is no halt to the cell cycle at the check points to repair it, the cells may survive and proliferate with a mutated genome. This results in chromosomes becoming fragmented, and incorrectly rejoined creating through successive rounds of cell division an increasingly mutated genome leading to carcinogenesis. 3)Retinoblastoma is a neoplasm that arises from a defective RB gene. In most cases, the defective gene is acquired sporadically. The remaining cases are acquired familially. 4)Another major group of genes that are primary sites for cancer causing mutations are proto-oncogenes. These groups of genes promote cell growth and cell division, development and differentiation. It also regulates the intracellular communication network in controlling cell growth, gene expression, DNA replication, cytoskeletal architecture, cell to cell contact and cellular metabolism. Oncogenes are altered forms of proto-oncogenes that lead to increased activity of these gene products and thus cause cancer. For example, some oncogenes cause overproduction of growth factors leading to uncontrolled cell proliferation. The oncogenes also bind to target gene promoters causing up-regulation of genes involved in cell proliferation. Furthermore, because of mutation of protooncogenes that code for proteins that participate in the transduction of signals in cell division, the mutant proteins in cancer no longer need the external stimulus to initiate transduction signals and thus cells constantly divide. Other groups of genes include the mismatch repair genes (MMR) which are often lost or defective

in cancers. These genes function to fix DNA with bases that were incorrectly inserted or deleted when there is no real damage to the nucleotide itself. These errors typically occur during DNA recombination and DNA replication. This mechanism is vital in preventing DNA damage and thus mutation of the genes would easily give rise to carcinogenesis.