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Leuk Lymphoma. 2011 Feb;52 Suppl 1:45-53. doi: 10.3109/10428194.2010.546919.

Regulation of mammalian target of rapamycin and mitogen activated protein kinase pathways by BCR-ABL.

Author information

1
Robert H. Lurie Comprehensive Cancer Center and Division of Hematology/Oncology, Northwestern University Medical School and Jesse Brown VA Medical Center, Chicago, IL, USA.

Abstract

A large body of evidence has established that BCR-ABL regulates engagement and activation of mammalian target of rapamycin (mTOR) and mitogen activated protein kinase (MAPK) signaling cascades. mTOR-mediated signals, as well as signals transduced by ERK, JNK, and p38 MAPK, are important components of the aberrant signaling induced by BCR-ABL. Such deregulation of mTOR or MAPK pathways contributes to BCR-ABL leukemogenesis, and their targeting with selective inhibitors provides an approach to enhance antileukemic responses and/or overcome leukemic cell resistance in chronic myeloid leukemia (CML) and Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia (ALL). This review explores recent advances in our understanding of mTOR and MAPK signaling in BCR-ABL-expressing leukemias and discusses the potential therapeutic targeting of these pathways in CML and Ph+ ALL.

PMID:
21299459
DOI:
10.3109/10428194.2010.546919
[Indexed for MEDLINE]

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