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Activation status of the JAK/STAT3 pathway in mantle cell lymphoma

Marwan A Yared1, Joseph D Khoury, L Jeffrey Medeiros

  • 1Department of Hematopathology, The University of Texas, M. D. Anderson Cancer Center, Houston, USA.

Archives of Pathology & Laboratory Medicine
|July 29, 2005
PubMed
Abstract

Insights

Constitutive activation of Signal Transducer and Activator of Transcription 3 (STAT3) occurs in 47% of mantle cell lymphoma (MCL) cases. Janus Kinase 3 (JAK3) likely mediates STAT3 activation in small cell MCL but not the blastoid variant.

Area of Science:

  • Oncology
  • Molecular Biology
  • Hematology

Background:

  • Signal transducer and activator of transcription 3 (STAT3) is oncogenic.
  • Previous studies indicated constitutive STAT3 activation in a subset of mantle cell lymphoma (MCL) tumors.

Purpose of the Study:

  • To comprehensively assess STAT3 activation and phosphorylation in MCL.
  • To determine if Janus Kinase (JAK) activation contributes to STAT3 signaling in MCL.

Main Methods:

  • Evaluated 43 MCL tumors using immunohistochemistry.
  • Utilized phospho-specific antibodies against STAT3 and JAK.
  • Analyzed 3 MCL cell lines with immunoprecipitation.

Main Results:

  • Heterogeneous expression of phospho-STAT3 (pSTAT3) observed in 47% of MCL cases.
  • Phospho-JAK3 (pJAK3) detected in 44% of tumors, correlating with pSTAT3.
  • Blastoid variant showed pSTAT3 positivity without pJAK3 in 67% of cases.

Conclusions:

  • STAT3 is constitutively activated in nearly half of MCL tumors.
  • JAK3 is implicated in STAT3 activation in the small cell variant of MCL.
  • STAT3 activation in blastoid MCL may involve JAK3-independent pathways.

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