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Genetic Events Other than BCR-ABL1

Genetic Events Other than BCR-ABL1 The BCR-ABL1 oncoprotein is the cause of chronic myeloid leukemia and occurs as a consequence of the translocation t(9;22), a well-defined genetic event that results in the formation of the Philadelphia chromosome. While this genomic aberration is recognized to be the main culprit of the chronic phase of chronic myeloid leukemia, the natural clonal evolution of this myeloproliferative neoplasm involves the accumulation of secondary alterations through genomic instability. Thus, efforts to dissect the frequency and nature of the genomic events at diagnosis and at later stages are producing valuable insights into understanding the mechanisms of blastic transformation and development of resistance in chronic myeloid leukemia. The identification of alternative BCR-ABL1-dependent and BCR-ABL1-independent targets that sustain the survival of leukemic blasts and/or leukemia-initiating cells will facilitate the development of novel viable therapeutic options for patients who become resistant or intolerant to the currently available therapeutic options based on tyrosine kinase inhibitors. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Current Hematologic Malignancy Reports Springer Journals

Genetic Events Other than BCR-ABL1

Current Hematologic Malignancy Reports , Volume 9 (1) – Jan 10, 2014

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References (114)

Publisher
Springer Journals
Copyright
Copyright © 2014 by Springer Science+Business Media New York
Subject
Medicine & Public Health; Hematology; Oncology; Geriatrics/Gerontology
ISSN
1558-8211
eISSN
1558-822X
DOI
10.1007/s11899-013-0194-x
pmid
24407376
Publisher site
See Article on Publisher Site

Abstract

The BCR-ABL1 oncoprotein is the cause of chronic myeloid leukemia and occurs as a consequence of the translocation t(9;22), a well-defined genetic event that results in the formation of the Philadelphia chromosome. While this genomic aberration is recognized to be the main culprit of the chronic phase of chronic myeloid leukemia, the natural clonal evolution of this myeloproliferative neoplasm involves the accumulation of secondary alterations through genomic instability. Thus, efforts to dissect the frequency and nature of the genomic events at diagnosis and at later stages are producing valuable insights into understanding the mechanisms of blastic transformation and development of resistance in chronic myeloid leukemia. The identification of alternative BCR-ABL1-dependent and BCR-ABL1-independent targets that sustain the survival of leukemic blasts and/or leukemia-initiating cells will facilitate the development of novel viable therapeutic options for patients who become resistant or intolerant to the currently available therapeutic options based on tyrosine kinase inhibitors.

Journal

Current Hematologic Malignancy ReportsSpringer Journals

Published: Jan 10, 2014

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