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

Amanda J. Redig, Eliza Vakana, Leonidas C. Platanias

Research output: Contribution to journalReview articlepeer-review

26 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)45-53
Number of pages9
JournalLeukemia and Lymphoma
Volume52
Issue numberSUPPL. 1
DOIs
StatePublished - Feb 1 2011

Keywords

  • BCR-ABL
  • CML
  • mTOR

ASJC Scopus subject areas

  • Hematology
  • Oncology
  • Cancer Research

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