ABSTRACT
Human cancer is the phenotypic manifestation of an accumulation of mutations, most somatic but some hereditary, that lead to alterations in control of cell proliferation, differentiation, and survival. These alterations result from changes in complex patterns of gene expression. Over the past 15 years, a wide variety of oncogenes and tumor suppressor genes that are mutated in human cancer have been identified. The protein products of these genes can be grouped into a number of broad classes, the largest of which is transcription factors. For example, TP53, the most commonly mutated gene in human cancer, encodes a nuclear transcription factor believed to play a critical role in cell-cycle checkpoint control, and mutations observed in cancer cells alter its transcriptional regulatory properties (Kern et al., 1992).
