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Here, we identify a subgroup, PTCL-NOS\n                    <jats:sup>\n                      <jats:italic>SMARCB1-<\/jats:italic>\n                    <\/jats:sup>\n                    , which is characterized by the lack of the SMARCB1 protein and occurs more frequently in young patients. Human and murine PTCL-NOS\n                    <jats:sup>\n                      <jats:italic>SMARCB1-<\/jats:italic>\n                    <\/jats:sup>\n                    show similar DNA methylation profiles, with hypermethylation of T-cell-related genes and hypomethylation of genes involved in myeloid development. Single-cell analyses of human and murine tumors revealed a rich and complex network of interactions between tumor cells and an immunosuppressive and exhausted tumor microenvironment (TME). In a drug screen, we identified histone deacetylase inhibitors (HDACi) as a class of drugs effective against PTCL-NOS\n                    <jats:sup>\n                      <jats:italic>Smarcb1-<\/jats:italic>\n                    <\/jats:sup>\n                    . In vivo treatment of mouse tumors with SAHA, a pan-HDACi, triggered remodeling of the TME, promoting replenishment of lymphoid compartments and reversal of the exhaustion phenotype. These results provide a rationale for further exploration of HDACi combination therapies targeting PTCL-NOS\n                    <jats:sup>\n                      <jats:italic>SMARCB1-<\/jats:italic>\n                    <\/jats:sup>\n                    within the TME.\n                  <\/jats:p>","DOI":"10.1038\/s41467-024-52826-0","type":"journal-article","created":{"date-parts":[[2024,10,3]],"date-time":"2024-10-03T10:02:11Z","timestamp":1727949731000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["Lack of SMARCB1 expression characterizes a subset of human and murine peripheral T-cell 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