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Cell cycle control in acute myeloid leukemia.

ABSTRACT: Acute myeloid leukemia (AML) is the result of a multistep transforming process of hematopoietic precursor cells (HPCs) which enables them to proceed through limitless numbers of cell cycles and to become resistant to cell death. Increased proliferation renders these cells vulnerable to acquiring mutations and may favor leukemic transformation. Here, we review how deregulated cell cycle control contributes to increased proliferation in AML and favors genomic instability, a prerequisite to confer selective advantages to particular clones in order to adapt and independently proliferate in the presence of a changing microenvironment. We discuss the connection between differentiation and proliferation with regard to leukemogenesis and outline the impact of specific alterations on response to therapy. Finally, we present examples, how a better understanding of cell cycle regulation and deregulation has already led to new promising therapeutic strategies.

SUBMITTER: Schnerch D

PROVIDER: S-EPMC3433102 | biostudies-literature | 2012

REPOSITORIES: biostudies-literature

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Cell cycle control in acute myeloid leukemia.

Schnerch Dominik D Yalcintepe Jasmin J Schmidts Andrea A Becker Heiko H Follo Marie M Engelhardt Monika M Wäsch Ralph R

American journal of cancer research 20120820 5

Acute myeloid leukemia (AML) is the result of a multistep transforming process of hematopoietic precursor cells (HPCs) which enables them to proceed through limitless numbers of cell cycles and to become resistant to cell death. Increased proliferation renders these cells vulnerable to acquiring mutations and may favor leukemic transformation. Here, we review how deregulated cell cycle control contributes to increased proliferation in AML and favors genomic instability, a prerequisite to confer ...[more]

PMID: 22957304

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