Genetic mechanisms of chronic myeloid leukemia blastic transformation.

Current Hematologic Malignancy Reports
Tomasz Skorski

Abstract

The BCR-ABL1 oncogenic tyrosine kinase can transform pluripotent hematopoietic stem cells and initiate chronic myeloid leukemia in chronic phase (CML-CP), a myeloproliferative disorder characterized by excessive accumulation of mature myeloid cells. Patients in CML-CP usually respond to treatment with ABL1 tyrosine kinase inhibitors (TKIs) such as imatinib, though some patients who respond initially may become resistant later. CML-CP leukemia stem cells (LSCs) are intrinsically insensitive to TKIs and thus survive in the long term. These LSCs or their progeny may at some stage acquire additional genetic changes that cause the leukemia to transform further, from CML-CP to a more advanced phase, which has been subclassified as either accelerated phase (CML-AP) or blastic phase (CML-BP). CML-BP is characterized by a major clonal expansion of immature progenitors, which have either myeloid or lymphoid features. CML-BP responds poorly to treatment and is usually fatal. This review discusses the role of genomic instability leading to blastic transformation of CML and proposes some novel therapeutic approaches.

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Citations

Dec 25, 2012·Current Hematologic Malignancy Reports·Ross Kinstrie, Mhairi Copland
Jul 2, 2016·Iranian Journal of Cancer Prevention·Sanaz Tabarestani, Abolfazl Movafagh
Aug 25, 2015·Clinical Lymphoma, Myeloma & Leukemia·Simona SoveriniGiovanni Martinelli
Apr 30, 2015·Acta Biochimica Et Biophysica Sinica·Deepti PandeHari D Khanna
Mar 31, 2015·Annals of Hematology·Bradley Chereda, Junia V Melo
Dec 17, 2014·Critical Reviews in Oncology/hematology·Ke Yang, Li-wu Fu
May 29, 2016·Chinese Journal of Cancer·Zhi-Jie KangQuentin Liu
Nov 2, 2016·Integrative Biology : Quantitative Biosciences From Nano to Macro·Paola Lecca, Claudio Sorio
Apr 2, 2016·The Oncologist·Simona SoveriniGiovanni Martinelli

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