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Recent advances in the molecular genetics of cancer have provided a molecular basis for the concept that cell division is essential in the genesis of human cancer. The activation of oncogenes and inactivation of tumorsuppressor genes allows cancer development. The activation of oncogenes, whether by mutation, translocation, or amplification, requires cell division. Genetic errors that precede the development of a fully malignant tumor also include the loss of inactivation during mitosis of several tumor-suppressor genes that function to control normal cellular behavior (1-3). Most of the models currently favored suggest that the first hit is the inactivation by a mutational event of one of the two alleles of a tumor-supressor gene present in diploid cells, followed by a reduction to homozygosity of the faulty chromosome (4). The initial mutagenic event and the loss of the wild-type allele of the tumorsuppressor gene both require cell division. Thus, for expression of the full malignant phenotype, cells are absolutely required to divide. Epidemiologic evidence indicates that increased cell proliferation induced by external or internal stimulation is indeed a common denominator in the pathogenesis of many human cancers. "Increased" may imply division of a subset of cells that would ordinarily not be dividing or increased mitotic activity above the baseline rate. The amount of irreparable DNA damage is a function of the level of cell division. Rapid cell division may "fix" DNA-damaging events by not allowing enough time for normal repair. Cells that would ordinarily not be replicating (e.g., the Schwann cells in the

Epidemiologic evidence for the increased cell proliferation model of carcinogenesis.