Bruton's tyrosine kinase is not essential for Bcr-Abl-mediated transformation of lymphoid or myeloid cells

M. MacPartlin, A. M. Smith, Brian Druker, L. A. Honigberg, M. W. Deininger

Research output: Contribution to journalArticle

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Abstract

Bcr-Abl, a constitutively active tyrosine kinase, is the cause of chronic myeloid leukemia (CML) and a subset of acute lymphoblastic leukemias (ALL). Bruton's tyrosine kinase (BTK), a member of the Tec family of tyrosine kinases with a crucial role in B-cell development, is consistently tyrosine phosphorylated in Bcr-Abl expressing murine pre B cells. BTK has been implicated in Bcr-Abl-mediated B-cell transformation and resistance to imatinib, implying that inhibiting BTK may be therapeutically beneficial. We decided to test whether BTK is a critical node in Bcr-Abl transformation and potential drug target in imatinib-resistant Bcr-Abl-positive cells. We depleted BTK in Ba/F3 and 32D cells expressing native and kinase domain (KD) mutant (E255K and T315I) Bcr-Abl, using shRNA. BTK levels were reduced to

Original languageEnglish (US)
Pages (from-to)1354-1360
Number of pages7
JournalLeukemia
Volume22
Issue number7
DOIs
StatePublished - Jul 2008

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Myeloid Cells
Lymphocytes
B-Lymphocytes
B-Lymphoid Precursor Cells
Leukemia, Myelogenous, Chronic, BCR-ABL Positive
Precursor Cell Lymphoblastic Leukemia-Lymphoma
Protein-Tyrosine Kinases
Small Interfering RNA
Tyrosine
Agammaglobulinaemia tyrosine kinase
Phosphotransferases
Pharmaceutical Preparations

ASJC Scopus subject areas

  • Hematology
  • Cancer Research

Cite this

Bruton's tyrosine kinase is not essential for Bcr-Abl-mediated transformation of lymphoid or myeloid cells. / MacPartlin, M.; Smith, A. M.; Druker, Brian; Honigberg, L. A.; Deininger, M. W.

In: Leukemia, Vol. 22, No. 7, 07.2008, p. 1354-1360.

Research output: Contribution to journalArticle

MacPartlin, M. ; Smith, A. M. ; Druker, Brian ; Honigberg, L. A. ; Deininger, M. W. / Bruton's tyrosine kinase is not essential for Bcr-Abl-mediated transformation of lymphoid or myeloid cells. In: Leukemia. 2008 ; Vol. 22, No. 7. pp. 1354-1360.
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