Molecular Pathology of Chronic Myelogenous Leukemia
1990; SAGE Publishing; Volume: 11; Issue: 1 Linguagem: Inglês
10.1159/000217675
ISSN1423-0380
AutoresIza Gorska-Flipot, C. S. Norman, L. Addy, Mark Minden,
Tópico(s)Acute Lymphoblastic Leukemia research
ResumoThe presence of Philadelphia chromosome t(9:22) is a hallmark of 95% of clinical cases of chronic myelogenous leukemia (CML) as well as 20% of adult acute lympho-blastic leukemia (ALL) and 5 % of acute myeloid leukemia (AML). The product of t(9;22) is a fusion protein BCR-ABL. The fusion proteins of CML, ALL and AML have increased tyro-sine kinase activity and show a transforming potential in vitro and in animal models. The shorter p 190 protein is associated almost only with ALL and AML, while the protein p210 is present in both chronic phase and blast crisis of CML and also in 50% of Philadelphia-positive (Ph1+) ALL. In CML the transition from chronic phase to blast crisis is usually accompanied by additional genetic events, e.g. additional chromosomal abnormalities, and oncogene activation(s). The detailed understanding of molecular basis of CML, and Ph1+ ALL and AML provides highly sensitive molecular and serological methods to complement classical cytogenetics. The advantages and limitations of these techniques are described and discussed below.
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