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A comparison of normal and leukemic stem cell biology in Chronic Myeloid Leukemia
Author(s) -
JØrgensen Heather G.,
Holyoake Tessa L.
Publication year - 2001
Publication title -
hematological oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 44
eISSN - 1099-1069
pISSN - 0278-0232
DOI - 10.1002/hon.667
Subject(s) - myeloid leukemia , progenitor cell , cancer research , philadelphia chromosome , stem cell , breakpoint cluster region , myeloid , biology , haematopoiesis , chronic myelogenous leukemia , abl , tyrosine kinase , tyrosine kinase inhibitor , disease , immunology , leukemia , medicine , signal transduction , chromosomal translocation , microbiology and biotechnology , cancer , genetics , gene
Chronic Myeloid Leukemia (CML), a myeloproliferative disease of stem cell origin, is characterized by the presence of the Philadelphia (Ph) chromosome and the bcr‐abl oncogene. The BCR‐ABL fusion gene product, thought to be causative in CML, has multiple effects on diverse cell functions such as growth, differentiation and turnover as well as adhesion and apoptosis. Persistent Ph‐negative progenitors co‐exist with leukemic cells, both in the marrow and blood of patients, in the early chronic phase of the disease. Despite accumulating knowledge of hemopoiesis and the disease process, CML remains incurable with conventional chemotherapy. Nonetheless, with the efficacy of the ABL tyrosine kinase inhibitor STI‐571 (signal transduction inhibitor 571) as a novel therapy in CML recently being realized in clinical trials, it is therefore timely to review our current understanding of the cell biology of this fascinating disease. Copyright © 2001 John Wiley & Sons, Ltd.