Eukaryotic cells contain a family of genes termed cellular oncogenes or proto-oncogenes thought to regulate normal cell growth and development. In some abnormal circumstances, such as following transduction by retroviruses, activation of these genes causes tumors and leukemias in animals. Possible mechanisms of activation of cellular oncogenes include: (1) point mutation, deletion, insertion; (2) amplification; (3) activation by internal rearrangement, chromosomal translocation or promoter insertion, and (4) recombinatorial events resulting in the formation of novel chimeric genes, and others. In this review, we consider data implicating activation of cellular oncogenes in the pathogenesis of leukemia in man. We discuss possible mechanisms whereby oncogene activation may induce leukemias as well as the potential diagnostic and therapeutic implication

Eukaryotic cells contain a family of genes termed cellular oncogenes or proto-oncogenes thought to regulate normal cell growth and development. In some abnormal circumstances, such as following transduction by retroviruses, activation of these genes causes leukemias in animals. Possible mechanisms of activation of cellular oncogenes include: point mutation, deletion, or insertion; amplification; activation by internal rearrangement, chromosomal translocation, or promoter insertion; recombinatorial events resulting in the formation of novel chimeric genes; among others. In this review, we consider data implicating activation of cellular oncogenes in the pathogenesis of leukemia in humans. We discuss possible mechanisms whereby oncogene activation may induce leukemias, as well as potential diagnostic and therapeutic implications.