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Expression of MALT1 oncogene in hematopoietic stem/progenitor cells recapitulates the pathogenesis of human lymphoma in mice. | LitMetric

AI Article Synopsis

  • Chromosomal translocations involving the MALT1 gene are key features of MALT lymphoma, but previous attempts to replicate this in mouse models using B cells have been unsuccessful.
  • Researchers induced MALT1 expression in mouse hematopoietic stem/progenitor cells, leading to the development of tumors with characteristics similar to human MALT lymphoma, including specific genetic and clinical traits.
  • The study also found that deleting the p53 gene sped up tumor development and transformed MALT lymphoma into a more aggressive form (ABC-DLBCL), while inhibiting MALT1 activity reduced survival rates of tumor cells, highlighting MALT1's crucial role in B-cell lymphoma progression.

Article Abstract

Chromosomal translocations involving the MALT1 gene are hallmarks of mucosa-associated lymphoid tissue (MALT) lymphoma. To date, targeting these translocations to mouse B cells has failed to reproduce human disease. Here, we induced MALT1 expression in mouse Sca1(+)Lin(-) hematopoietic stem/progenitor cells, which showed NF-κB activation and early lymphoid priming, being selectively skewed toward B-cell differentiation. These cells accumulated in extranodal tissues and gave rise to clonal tumors recapitulating the principal clinical, biological, and molecular genetic features of MALT lymphoma. Deletion of p53 gene accelerated tumor onset and induced transformation of MALT lymphoma to activated B-cell diffuse large-cell lymphoma (ABC-DLBCL). Treatment of MALT1-induced lymphomas with a specific inhibitor of MALT1 proteolytic activity decreased cell viability, indicating that endogenous Malt1 signaling was required for tumor cell survival. Our study shows that human-like lymphomas can be modeled in mice by targeting MALT1 expression to hematopoietic stem/progenitor cells, demonstrating the oncogenic role of MALT1 in lymphomagenesis. Furthermore, this work establishes a molecular link between MALT lymphoma and ABC-DLBCL, and provides mouse models to test MALT1 inhibitors. Finally, our results suggest that hematopoietic stem/progenitor cells may be involved in the pathogenesis of human mature B-cell lymphomas.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3387079PMC
http://dx.doi.org/10.1073/pnas.1204127109DOI Listing

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