Leukemia Research
Volume 26, Issue 8 , Pages 713-720, August 2002

Bcr–Abl variants: biological and clinical aspects

  • Anjali S. Advani

      Affiliations

    • Departments of Hematology and Oncology, Duke University Medical Center, Durham, NC 27710, USA
  • ,
  • Ann Marie Pendergast

      Affiliations

    • Department of Pharmacology and Cancer Biology, LSRC Room C233A, La Salle St. Extension, Duke University Medical Center, Durham, NC 27710, USA
    • Corresponding Author InformationCorresponding author. Fax: +1-919-681-7148

Received 8 November 2001; accepted 25 November 2001.

Abstract 

Bcr–Abl is an oncogene that arises from fusion of the Bcr gene with the c-Abl proto-oncogene. Three different Bcr–Abl variants can be formed, depending on the amount of Bcr gene included: p185, p210, and p230. The three variants are associated with distinct types of human leukemias. Examination of the signaling pathways differentially regulated by the Bcr–Abl proteins will help us gain better insight into Bcr–Abl mediated leukemogenesis.

Abbreviations:  Ph, Philadelphia chromosome, Bcr, breakpoint cluster region, ALL, acute lymphocytic leukemia, CML, chronic myelogenous leukemia, CNL, chronic neutrophilic leukemia, AUL, acute undifferentiated leukemia, AML, acute myelogenous leukemia, Ph+, Philadelphia chromosome positive, CALGB, cancer and leukemia group B, BMT, bone marrow transplant, CML-N, cases of chronic neutrophilic leukemia that are Ph+, CMML, chronic myelomonocytic leukemia, RT-PCR, reverse transcriptase polymerase chain reaction, CFU-erythroid, colony forming unit-erythroid, CFU-GM, colony forming unit-granulocyte macrophage, PCR, polymerase chain reaction, STI-571, signal transduction inhibitor 571, ATP, adenosine triphosphate, mRNA, messenger RNA

Keywords:  Philadelphia chromosome, Bcr–Abl, Acute lymphocytic leukemia, Chronic myelogenous leukemia, Chronic neutrophilic leukemia

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PII: S0145-2126(01)00197-7

Leukemia Research
Volume 26, Issue 8 , Pages 713-720, August 2002