Abstract
Genetic elements responsible for key steps in the conversion of normal cells to malignancy, initially identified in oncogenic viruses, have normal cellular origins. These normal cell genes, protooncogenes, are highly conserved in an evolutionary context, and this fact, along with other data on expression and product localization, are hypothesized to play an important role in growth and differentiation. The number of such genes is limited to perhaps two dozen and they can be subdivided into families, thus implying fine-tuning functions. The conversion of protooncogenes to oncogenes can be based on mutation or selective stimulation based on chromosomal alterations, e.g., translocations, loss of control elements, or insertion of active promoters. A class of control elements, designated antioncogenes, has been tentatively identified in certain familial malignancies. Data are accumulating on the chromosomal localization of both onco- and antioncogenes, justifying prospects of defining cancer at the molecular level.
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