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STAT3 Expression and Activity are Up-Regulated in Diffuse Large B Cell Lymphoma of Dogs
A L F V Assumpção1, P C Jark1,2, C C Hong1
1Department of Medical Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, Madison, WI, USA.
Journal of Veterinary Internal Medicine
|November 10, 2017
Summary
The Signal Transducer and Activator of Transcription 3 (STAT3) pathway is upregulated in canine diffuse large B cell lymphoma (DLBCL). This suggests that Janus Kinase (JAK) inhibitors could be a potential treatment for dogs with DLBCL.
Area of Science:
- Veterinary Oncology
- Molecular Biology
- Cancer Research
Background:
- The Janus Kinase (JAK) and Signal Transducer and Activator of Transcription (STAT) pathways are implicated in human diffuse large B cell lymphoma (DLBCL).
- Upregulated STAT3 is linked to poorer clinical outcomes in human DLBCL.
- The JAK-STAT pathway in canine DLBCL has not been previously investigated.
Purpose of the Study:
- To investigate the STAT3 pathway's deregulation in canine DLBCL.
- To evaluate STAT3 and mitogen-activated protein kinase ERK1/2 expression, activation, and cellular localization in canine DLBCL.
Main Methods:
- Retrospective analysis of 43 client-owned dogs with histopathologically diagnosed DLBCL.
- Immunohistochemistry and Western blot analysis to assess protein expression and activation.
- Comparison with normal canine lymph nodes.
Main Results:
- Canine DLBCL samples showed increased STAT3 and phosphorylated STAT3 (p-STAT3) immunolabeling compared to normal lymph nodes.
- STAT3 exhibited higher nuclear expression in lymphoma cells.
- Activation of mitogen-activated kinase ERK1/2 was also found to be upregulated in canine DLBCL.
Conclusions:
- Diffuse large B cell lymphoma in dogs exhibits an upregulated STAT3 pathway compared to normal canine lymph nodes.
- These findings support further research into JAK inhibitors for treating canine DLBCL.
- The study highlights the potential of targeting the JAK-STAT pathway in canine lymphoma.
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