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Tumor suppressor genes and oncogenes are important regulatory genes which encode proteins regulating transitions in and out of the cell cycle and which also have a role in the gateway to terminal differentiation (Tripathy & Benz, 1992). Defects in tumor suppressor genes and oncogenes result in uncontrolled cell division, which leads to cancer (Tripathy & Benz, 1992). Oncogenes are mutated proto-oncogenes that have a role in malignancy of tumors and most frequently regulate cell cycle re-entry. Gain-of-function mutations result in transformation of proto-oncogenes into dominant oncogenes. Tumor suppressor genes encode proteins that suppress cell growth and most frequently result in exit from the cell cycle. Lossof-function mutations in tumor suppressor genes result in tumor malignancy and can account for hereditary cancers. Every gene has two alleles present in the genome (with a few exceptions in the hemizygous regions of the sex chromosomes). For tumor suppressor genes to be inactivated either deletion of one allele and somatic mutation of the other allele is required resulting in a loss of heterozygosity (Swellam et al., 2004), or somatic deletion of both of the alleles is required resulting in a complete loss of homozygosity (Quelle et al., 1997). Tumor suppressor genes can also be inactivated by hypermethylation of the gene resulting in promoter suppression so that genes can not be transcribed further (Herman et al., 1997). Telomere shortening and tumor suppressor gene promoter hyper-methylation can be used as potential breast cancer biomarkers (Radpour et al., 2010). Regulation of cell proliferation and differentiation is important in due course of growth and development of an organism. Cell proliferation is not an infinitely continuous process as cells undergo a finite number of cumulative population doublings (CPDs) in culture before entering replicative senescence (RS) (Hayflick, 1965). Cell replication or growth is controlled by a complex network of signals that control the cell cycle, the orderly sequence of events that all cells pass through as they grow to approximately twice their size, copy their chromosomes, and divide into two new cells. The cell cycle consists of 4 phases; G1, S, G2, and M phase (Enoch & Nurse, 1991). DNA duplication takes place in S phase and cytokinesis in M phase. G1 and G2 are gap phases, which provide the time for cells to

Tumor Suppressor Gene p16/INK4A/CDKN2A and Its Role in Cell Cycle Exit, Differentiation, and Determination of Cell Fate