Chronic myelogenous leukemia: too much or too little growth, or both?
CML, characterized by the BCR/ABL gene rearrangement has been more extensively studied than any other malignancy. Over the last decade, significant progress has been made in our understanding of BCR-ABL-induced alterations in intracellular signaling. Unfortunately, we still only poorly understand the correlation between the clinical symptoms of chronic phase CML and the BCR-ABL oncoprotein. This is in part due to lack of a good in vivo animal model of chronic phase CML. In vivo and in vitro studies from the Clarkson group, recently reviewed in this journal (Leukemia 1997; 11: 1404-1428), have significantly enhanced our understanding of the pathophysiology of CML. However, further characterization of the effect of the BCR-ABL oncoprotein on signal molecules involved with cell differentiation, cell proliferation, cell survival and cell adhesion in primary Ph+ CML progenitors or in vivo models of CML will be needed to provide a full understanding of the pathophysiology of chronic phase CML.
Verfaillie
C M
CM
Division of Hematology, Oncology and Transplantation and Stem Cell Biology Program, University of Minnesota, Minneapolis, USA.
D000818:Animals; D016044:Fusion Proteins, bcr-abl / Q000235:genetics; D015321:Gene Rearrangement; D006801:Humans; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000235:genetics* / Q000473:pathology*
D016044:Fusion Proteins, bcr-abl