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Curr Hematol Malig Rep. 2012 Jun;7(2):125-32. doi: 10.1007/s11899-012-0121-6.

Chronic myeloid leukemia stem cell biology.

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1
Department of Medicine, Stem Cell Program and Moores Cancer Center, University of California, San Diego, La Jolla, CA 92093-0820, USA.

Abstract

Leukemia progression and relapse is fueled by leukemia stem cells (LSC) that are resistant to current treatments. In the progression of chronic myeloid leukemia (CML), blast crisis progenitors are capable of adopting more primitive but deregulated stem cell features with acquired resistance to targeted therapies. This in turn promotes LSC behavior characterized by aberrant self-renewal, differentiation, and survival capacity. Multiple reports suggest that cell cycle alterations, activation of critical signaling pathways, aberrant microenvironmental cues from the hematopoietic niche, and aberrant epigenetic events and deregulation of RNA processing may facilitate the enhanced survival and malignant transformation of CML progenitors. Here we review the molecular evolution of CML LSC that promotes CML progression and relapse. Recent advances in these areas have identified novel targets that represent important avenues for future therapeutic approaches aimed at selectively eradicating the LSC population while sparing normal hematopoietic progenitors in patients suffering from chronic myeloid malignancies.

PMID:
22467334
PMCID:
PMC3342507
DOI:
10.1007/s11899-012-0121-6
[Indexed for MEDLINE]
Free PMC Article
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