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Jak3 activation is significantly associated with ALK expression in anaplastic large cell lymphoma

Raymond Lai1, George Z Rassidakis, Quan Lin

  • 1Department of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.

Human Pathology
|September 13, 2005
PubMed

Insights

Janus kinase 3 (Jak3) activation is primarily found in ALK-positive anaplastic large cell lymphoma (ALCL). This suggests Jak3 collaborates with anaplastic lymphoma kinase (ALK) to activate signal transducer and activator of transcription 3 (Stat3), promoting tumor growth.

Area of Science:

  • Oncology
  • Molecular Biology
  • Immunology

Background:

  • Janus kinase 3 (Jak3) activates signal transducer and activator of transcription 3 (Stat3), an oncogene.
  • Previous studies implicated Jak3 in ALK-positive anaplastic large cell lymphoma (ALCL) pathogenesis via Stat3 and anaplastic lymphoma kinase (ALK) activation.

Purpose of the Study:

  • To evaluate the expression frequency of Jak3 and its activated form (pJak3) in ALCL tumors.
  • To determine the role of Jak3 activation in ALK-positive versus ALK-negative ALCL.

Main Methods:

  • Immunohistochemical staining was used to assess Jak3 and pJak3 expression.
  • 48 systemic ALCL tumors from a tissue microarray were analyzed.
  • Expression levels were compared between ALK-positive and ALK-negative ALCL subtypes.

Main Results:

  • Activated Jak3 (pJak3) was detected in 81% of ALK-positive ALCL tumors versus 11% of ALK-negative tumors (P < .0001).
  • Phosphorylated Stat3 (pStat3) was present in 86% of ALK-positive and 40% of ALK-negative ALCL tumors.
  • pJak3 expression was significantly associated with pStat3 in ALK-positive ALCL but not in ALK-negative ALCL.

Conclusions:

  • Jak3 activation is predominantly restricted to ALK-positive ALCL.
  • Jak3 likely collaborates with ALK to activate Stat3, promoting tumor cell survival and proliferation in ALK-positive ALCL.
  • Stat3 activation in ALK-negative ALCL appears to be independent of Jak3.

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