Chronic myelogenous leukemia as gene activation model in oncology - Minireview

Authors
Citation
A. Zamecnikova, Chronic myelogenous leukemia as gene activation model in oncology - Minireview, NEOPLASMA, 47(5), 2000, pp. 269-273
Citations number
30
Categorie Soggetti
Onconogenesis & Cancer Research
Journal title
NEOPLASMA
ISSN journal
00282685 → ACNP
Volume
47
Issue
5
Year of publication
2000
Pages
269 - 273
Database
ISI
SICI code
0028-2685(2000)47:5<269:CMLAGA>2.0.ZU;2-R
Abstract
Many unique features of chronic myelogenous leukemia (CML) make it as a mod el for studying the development of leukemia in humans. Chronic myeloid leuk emia is a disease of the hematopoietic stein cell that progress in a multis tep fashion. The biphasic or triphasic clinical course of the disease exemp lies the multistep process of tumor. progression from the indolent chronic phase to a more aggressive and terminal blast crisis. CML was the first neo plastic disease shown to be associated with consistent karyotypic abnormali ty now known as the Philadelphia (Ph) chromosome. The result of the Philade lphia chromosome translocation t(9;22)(q34;q11) is the transposition of the c-nbi oncogene from chromosome 9 to chromosome 22, where it is fused with part of the bo gene. The translocation generates a new hybrid bcr-abl gene which plays a crucial role in the pathogenesis of CML. Presently, CML is pe rhaps the best understood cancer in humans and the model of oncogenesis med iated by the Ph chromosome translocation is one of the best-characterized e xample of gene activation in leukemia.