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Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells
Published on: February 21, 2018
c-Jun expression and activation are restricted to CD30+ lymphoproliferative disorders
Elias Drakos1, Vasiliki Leventaki, Ellen J Schlette
1Department of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
The American Journal of Surgical Pathology
|February 28, 2007
Summary
Cellular Jun (c-Jun) is activated in CD30 lymphomas, including Hodgkin lymphoma and ALCL. This activation, indicated by phosphorylated c-Jun, suggests a role in the development of these specific lymphomas.
Area of Science:
- Oncology
- Molecular Biology
- Immunology
Background:
- Cellular Jun (c-Jun) is a transcription factor regulating cell processes.
- c-Jun activation occurs via phosphorylation at specific serine residues.
- CD30 lymphomas are a group of lymphoid malignancies characterized by CD30 expression.
Purpose of the Study:
- To investigate the expression and activation of c-Jun in various CD30 lymphomas.
- To determine if c-Jun plays a role in the pathogenesis of CD30 lymphomas.
Main Methods:
- Tissue microarrays and immunohistochemistry were used.
- c-Jun expression and serine-73 phosphorylation were analyzed.
- The study included classical Hodgkin lymphoma, anaplastic large cell lymphoma (ALK+ and ALK-), primary cutaneous ALCL, CD30 DLBCL, and lymphomatoid papulosis.
Main Results:
- c-Jun was expressed in all investigated CD30 lymphoproliferative disorders, notably in classical Hodgkin lymphoma and ALCL.
- Phosphorylated c-Jun (p-c-Jun), the activated form, was more frequent in classical Hodgkin lymphoma and ALK+ ALCL.
- p-c-Jun levels correlated with total c-Jun levels, indicating a positive feedback loop.
Conclusions:
- CD30 lymphomas exhibit distinct patterns of c-Jun expression and activation.
- Activated c-Jun may be involved in the pathogenesis of CD30 lymphomas.
- Further research into c-Jun's role could offer therapeutic insights.
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