ArticleThe American journal of pathology2010
Msh6 protects mature B cells from lymphoma by preserving genomic stability.
Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- DNA mismatch repair defect and intratumor heterogeneous deficiency differently impact immune responses in diffuse large B-cell lymphoma.Oncoimmunology · 2024Article
- Epigenetic disorders: Lessons from the animals-animal models in chromatinopathies.Frontiers in cell and developmental biology · 2022Review
- Article
- Extracolonic manifestations of lynch syndrome.Clinics in colon and rectal surgery · 2012Article
- KAP1 regulates gene networks controlling mouse B-lymphoid cell differentiation and function.Blood · 2012Article
- Article
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Authors and funding
10 authors.
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Abstract
Most human B-cell non-Hodgkin's lymphomas arise from germinal centers. Within these sites, the mismatch repair factor MSH6 participates in antibody diversification. Reminiscent of the neoplasms arising in patients with Lynch syndrome III, mice deficient in MSH6 die prematurely of lymphoma. In this study, we characterized the B-cell tumors in MSH6-deficient mice and describe their histological, immunohistochemical, and molecular features, which include moderate microsatellite instability. Based on histological markers and gene expression, the tumor cells seem to be at or beyond the germinal center stage. The simultaneous loss of MSH6 and of activation-induced cytidine deaminase did not appreciably affect the survival of these animals, suggesting that these germinal center-like tumors arose by an activation-induced cytidine deaminase-independent pathway. We conclude that MSH6 protects B cells from neoplastic transformation by preserving genomic stability.
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