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BCL-W makes only minor contributions to MYC-driven lymphoma development
Sarah T Diepstraten1,2, John E La Marca1,2, Catherine Chang1
1Blood Cells and Blood Cancer Division, The Walter and Eliza Hall Institute of Medical Research (WEHI), Parkville, VIC, Australia.
Oncogene
|August 11, 2023
Summary
BCL-W is not essential for the development of MYC-driven lymphoma. Tumors lacking BCL-W do not show altered sensitivity to BH3-mimetic drugs, indicating BCL-W
Area of Science:
- Oncology
- Molecular Biology
- Cancer Therapeutics
Background:
- Venetoclax, a BCL-2 inhibitor, shows success in treating certain leukemias.
- New BH3-mimetic drugs targeting MCL-1 or BCL-XL are in clinical trials but face toxicity challenges.
- BFL-1/A1 is implicated as a resistance factor in hematologic malignancies, but BCL-W's role is less understood.
Purpose of the Study:
- To investigate the role of BCL-W in the development of MYC-driven lymphoma.
- To determine if BCL-W influences the sensitivity of lymphoma cells to BH3-mimetic drugs.
Main Methods:
- Utilized genetically engineered mouse models to study lymphomagenesis in the absence of BCL-W.
- Analyzed BCL-2 family member expression in tumors developed with and without BCL-W.
- Assessed the sensitivity of these tumors to various BH3-mimetic drugs.
Main Results:
- BCL-W is dispensable for the development of MYC-driven lymphomas.
- Lymphomas arising without BCL-W did not exhibit compensatory changes in other BCL-2 family members.
- Tumors lacking BCL-W showed no altered sensitivity to BH3-mimetic drugs.
Conclusions:
- BCL-W does not play a significant role in the pathogenesis of MYC-driven lymphoma.
- Targeting BCL-W is unlikely to be a primary strategy for overcoming resistance to BH3-mimetic drugs in these lymphomas.
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