Abstract
ACTIVATION of cellular oncogenes by chromosomal translocation has been strongly implicated in the pathogenesis of several cancers. One of the most striking examples of this phenomenon occurs in leukemias involving the Philadelphia (Ph1) chromosome. The Ph1 chromosome is a shortened chromosome 22 that arises from a reciprocal translocation, t(9;22)(q34;q11).1 , 2 This cytogenetic aberration occurs in the majority of patients with chronic myelogenous leukemia (CML)3 and in a much smaller proportion of patients with acute lymphoblastic leukemia (ALL) or acute myelogenous leukemia (AML).4 , 5 The Ph1 translocation results in transposition of the cellular abl (c-abl) gene from its usual residence . . .
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