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Age-associated clonal B cells drive B cell lymphoma in mice
José P Castro1,2,3, Anastasia V Shindyapina1, Alessandro Barbieri4
1Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Nature Aging
|August 8, 2024
Summary
Aging drives B cell lymphoma in mice through specific genetic and epigenetic changes. Interventions targeting mTOR or c-Myc may prevent pre-malignant B cell alterations during aging.
Area of Science:
- Immunology
- Oncology
- Aging Research
Background:
- Cancer is strongly linked to aging, yet the underlying mechanisms remain unclear.
- Understanding how aging influences cancer development is crucial for prevention and treatment.
Purpose of the Study:
- To investigate the development of B cell lymphoma in naturally aged mice.
- To identify the cellular and molecular drivers of age-related B cell malignancies.
Main Methods:
- Studied spontaneous B cell lymphoma in aged mouse models.
- Analyzed age-associated clonal B cells (ACBCs) for genetic and epigenetic alterations.
- Investigated the role of c-Myc activation and promoter hypermethylation.
- Assessed the impact of ACBC transfer into young recipients.
- Evaluated the effects of mTOR and c-Myc inhibition in aged mice.
Main Results:
- Identified an age-associated clonal B cell (ACBC) population driving lymphoma.
- ACBCs exhibit c-Myc activation, hypermethylation, somatic mutations, and increased biological age.
- ACBCs expand independently of germinal centers and support malignancy upon transfer.
- Inhibition of mTOR or c-Myc reduced pre-malignant B cell changes in aged mice.
- Epigenetic changes in mouse B cells resemble those in human B cell lymphomas.
Conclusions:
- Aging promotes B cell lymphoma through intrinsic cellular changes and microenvironmental factors.
- ACBCs are key drivers of spontaneous B cell cancer during aging.
- Targeting mTOR or c-Myc presents a potential strategy for preventing age-related B cell malignancies.
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