{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,26]],"date-time":"2026-08-26T14:51:10Z","timestamp":1787755870471,"version":"build-2784847793"},"reference-count":105,"publisher":"American Society of Clinical Oncology (ASCO)","issue":"21","content-domain":{"domain":["ascopubs.org"],"crossmark-restriction":true},"short-container-title":["J Clin Oncol"],"published-print":{"date-parts":[[2026,7,20]]},"abstract":"<jats:sec>\n                    <jats:title>PURPOSE<\/jats:title>\n                    <jats:p>\n                      Mutations in\n                      <jats:italic toggle=\"yes\">TP53<\/jats:italic>\n                      , detected in over 20% of diffuse large B-cell lymphomas (DLBCLs), are associated with poor prognosis. However, clinical outcomes among patients with\n                      <jats:italic toggle=\"yes\">TP53<\/jats:italic>\n                      -mutant disease vary, with some patients showing treatment responses similar to those with wild-type\n                      <jats:italic toggle=\"yes\">TP53<\/jats:italic>\n                      . This study aims to understand the clinical and molecular determinants underlying poor outcomes in\n                      <jats:italic toggle=\"yes\">TP53<\/jats:italic>\n                      -mutant DLBCL.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS<\/jats:title>\n                    <jats:p>Clinical and molecular data for 3,091 patients were derived from 10 cohorts of patients with newly diagnosed DLBCL treated with frontline rituximab-based immunochemotherapy regimens. Targeted or whole-exome\/whole-genome sequencing was available for all patients. Bulk RNA-seq was analyzed for 591 patient samples. The primary outcome measures were progression-free survival (PFS) and overall survival (OS).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS<\/jats:title>\n                    <jats:p>\n                      <jats:italic toggle=\"yes\">TP53-<\/jats:italic>\n                      mutant DLBCL differed from wild-type disease in pattern and number of genetic lesions, malignant B-cell expression states, and tumor microenvironment composition.\n                      <jats:italic toggle=\"yes\">TP53<\/jats:italic>\n                      mutations were 6-fold more prevalent than\n                      <jats:italic toggle=\"yes\">MYC\/BCL2\/BCL6<\/jats:italic>\n                      double-\/triple-hit status, but conferred similar adverse prognostic risk. Among patients with\n                      <jats:italic toggle=\"yes\">TP53<\/jats:italic>\n                      -mutant disease, variant allele frequency (VAF) further stratified risk, with patients featuring VAF \u2265 75% (indicative of loss of heterozygosity) experiencing significantly inferior PFS\/OS. Downregulation of interferon signaling and lower macrophage content were identified in\n                      <jats:italic toggle=\"yes\">TP53<\/jats:italic>\n                      -mutant samples derived from patients with poor outcomes or VAF \u2265 75%.\n                      <jats:italic toggle=\"yes\">TP53<\/jats:italic>\n                      mutations were adversely prognostic among patients with DLBCL assigned to specific LymphGen subtypes (EZB, MCD), malignant B-cell states (S1), and ecotypes (LE4, LE7, LE8), whereas outcomes were similar to wild-type disease within other molecular subtypes. In re-examination of the Phoenix trial data, addition of ibrutinib to R-CHOP improved PFS in patients with\n                      <jats:italic toggle=\"yes\">TP53<\/jats:italic>\n                      -mutant DLBCL and abrogated the deleterious impact of high VAF, irrespective of patients' age.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSION<\/jats:title>\n                    <jats:p>\n                      The poor prognosis of\n                      <jats:italic toggle=\"yes\">TP53<\/jats:italic>\n                      -mutant DLBCL is dependent on intrinsic features, such as VAF, and modulated by co-occurring genomic lesions or lymphoma cell-intrinsic or microenvironmental expression patterns.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1200\/jco-25-01928","type":"journal-article","created":{"date-parts":[[2026,4,29]],"date-time":"2026-04-29T20:00:48Z","timestamp":1777492848000},"page":"2029-2047","update-policy":"https:\/\/doi.org\/10.1200\/crossmark","source":"Crossref","is-referenced-by-count":5,"title":["Integrative Molecular Analysis Reveals Determinants of Clinical Outcomes in\n                    <i>TP53<\/i>\n                    -Mutated Diffuse Large B-Cell Lymphoma"],"prefix":"10.1200","volume":"44","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3628-1716","authenticated-orcid":true,"given":"Manik","family":"Uppal","sequence":"first","affiliation":[{"name":"Division of Hematology\/Oncology, Icahn School of Medicine at Mount Sinai, New York, NY"},{"name":"Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, 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