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The Molecular Genetics of Philadelphia Chromosome–Positive Leukemias

List of authors.
  • Razelle Kurzrock, M.D.,
  • Jordan U. Gutterman, M.D.,
  • and Moshe Talpaz, M.D.

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 . . .

Funding and Disclosures

Supported in part by the John D. and Catherine T. MacArthur Foundation. Research conducted in part by the Clayton Foundation for Research and the James E. Lyon Foundation for Research. Dr. Gutterman is a Senior Clayton Foundation Investigator.

Author Affiliations

From the Department of Clinical Immunology and Biological Therapy, the University of Texas M.D. Anderson Cancer Center, Houston, Tex. Address reprint requests to Dr. Kurzrock at M.D. Anderson Cancer Center, Dept. of Clinical Immunology and Biological Therapy, Box 41, 1515 Holcombe Blvd., Houston, TX 77030.

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