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Adult T‐cell leukemia/lymphoma ( ATL ) is an aggressive T‐cell malignancy caused by human T‐cell lymphotropic virus 1. Treatment options for acute  ATL  patients include chemotherapy, stem cell transplantation, and recently the anti‐chemokine (C‐C motif) receptor 4 antibody, although most patients still have a poor prognosis and there is a clear need for additional options.  HBI ‐8000 is a novel oral histone deacetylase inhibitor with proven efficacy for treatment of T‐cell lymphomas that recently received approval in China. In the present study, we evaluated the effects of  HBI ‐8000 on  ATL ‐derived cell lines and primary cells obtained from Japanese  ATL  patients. In most cases  HBI ‐8000 induced apoptosis in both primary  ATL  cells and cell lines. In addition, findings obtained with  DNA  microarray suggested Bim activation and, interestingly, the contribution of the  NLR  family, pyrin domain containing 3 ( NLRP 3) inflammasome pathway in  HBI ‐8000‐induced  ATL  cell death. Further investigations using si RNA s confirmed that Bim contributes to  HBI ‐8000‐induced apoptosis. Our results provide a rationale for a clinical investigation of the efficacy of  HBI ‐8000 in patients with  ATL . Although the role of  NLRP 3 inflammasome activation in  ATL  cell death remains to be verified,  HBI ‐8000 may be part of a novel therapeutic strategy for cancer based on the  NLRP 3 pathway.

Induction of apoptosis by HBI‐8000 in adult T‐cell leukemia/lymphoma is associated with activation of Bim and NLRP3