Molecular mechanisms of Bcr-Abl-induced oncogenesis.
The chimeric Bcr-Abl oncogene has been implicated in the pathogenesis of chronic myelogenous leukemia (CML) and Philadelphia chromosome (Ph1)-positive acute lymphocytic leukemia (ALL). The Bcr-Abl protein is a complex structure comprising discrete domains associated with specific biochemical and biological functions. These domains function through their ability to activate distinct signal transduction pathways responsible for Bcr-Abl's oncogenic behavior. This review will present our current understanding of signal transduction pathways involved in Bcr-Abl-induced pathophysiology, with particular emphasis on potential targets for therapeutic intervention.
Gishizky
M L
ML
SUGEN, Inc, Redwood City, CA, USA. Mikhail@SUGEN.sf.ca.us
D000818:Animals; D016044:Fusion Proteins, bcr-abl / Q000096:biosynthesis / Q000502:physiology*; D006801:Humans; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000235:genetics* / Q000503:physiopathology; D009857:Oncogenes; D054198:Precursor Cell Lymphoblastic Leukemia-Lymphoma / Q000235:genetics* / Q000503:physiopathology; D015398:Signal Transduction
D016044:Fusion Proteins, bcr-abl