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OVER the past 15 years an examination of cancerous tissues has led to the identification of alterations in a number of genes that regulate cell growth and proliferation.1 These mutations have been identified in two distinct categories of genes, oncogenes and tumor-suppressor genes. Typically, mutations in oncogenes occur in one of the two alleles of the gene, and they act in a fashion dominant to the wild-type allele. Consequently, they are "gain of function" mutations that constitutively or permanently signal the cell to divide. Mutations in oncogenes appear to arise spontaneously in somatic tissues over the lifetime of the organism, . . .
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Arnold J. Levine (1992) studied this question.
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