Tumor suppressor genes encode proteins that arrest progression of the cell cycle, promote apoptosis, or both, functioning as safety checkpoints that prevent errors in cell division from producing uncontrolled growth; they fall into functional categories including DNA-damage-recognition and repair proteins that trigger programmed cell death when repair fails, and repressors of genes required for cell-cycle continuation. The Two-Hit Hypothesis states that because a diploid organism carries two alleles of each gene, both alleles of a tumor suppressor must be inactivated before the loss of function is manifested — one intact copy still produces protective protein — making tumor suppressor mutations recessive at the cellular level, in contrast to activating oncogene mutations, which are dominant and require only a single hit. The concept belongs to cancer biology and molecular genetics, connecting Mendelian allele theory and cell-cycle checkpoint regulation to carcinogenesis; a recognized exception is the dominant negative, in which a mutant protein product interferes with the product of the remaining normal allele.
Tumor suppressor genes encode proteins that arrest progression of the cell cycle, promote apoptosis, or both, functioning as safety checkpoints that prevent errors in cell division from producing unc…