{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T20:28:16Z","timestamp":1792787296353,"version":"4.5.0"},"reference-count":55,"publisher":"BMJ","issue":"4","license":[{"start":{"date-parts":[[2025,4,8]],"date-time":"2025-04-08T00:00:00Z","timestamp":1744070400000},"content-version":"unspecified","delay-in-days":7,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"funder":[{"name":"National High Level Hospital","award":["CFH2022-2Z-4016"],"award-info":[{"award-number":["CFH2022-2Z-4016"]}]},{"name":"National High Level Hospital","award":["PUMCH-B-033"],"award-info":[{"award-number":["PUMCH-B-033"]}]}],"content-domain":{"domain":["bmj.com"],"crossmark-restriction":true},"short-container-title":["J Immunother Cancer"],"accepted":{"date-parts":[[2025,3,20]]},"published-print":{"date-parts":[[2025,4]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Clinical evidence has established anti-PD-1 antibody as a transformative treatment modality for relapsed\/refractory peripheral T-cell lymphoma (r\/r PTCL), yet reveals a therapeutic plateau with drug resistance observed in 60% of r\/r PTCL. The biological determinants underlying this resistance\u2014particularly the complex interplay between tumor-intrinsic characteristics (including tumor mutation burden and oncogenic mutations) and immune microenvironment features (notably PD-L1 expression)\u2014remain insufficiently illustrated. Therefore, we systematically depicted the comprehensive mutation profile of r\/r PTCL patients and correlated them with the efficacy and prognosis of anti-PD-1 therapy.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Here, we enrolled a cohort of 109 patients with r\/r PTCL and performed targeted next-generation sequencing of 440 cancer-associated genes. Clinical information was collected and correlated with genetic mutations. We constructed\n                      <jats:italic>JAK3<\/jats:italic>\n                      mutant models using Jurkat and BA\/F3 cell lines. We performed single-cell transcriptomics, western blotting, and flow cytometry to elucidate the molecular mechanism. Additionally, we built a\n                      <jats:italic>JAK3<\/jats:italic>\n                      -mutant syngeneic mouse model to demonstrate in vivo antitumor efficacy of Tofacitinib and anti-PD-1 therapy.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      We identified and validated that PD-L1 was a predictor for the efficacy of anti-PD-1 therapy in PTCL patients. The subset of PTCL patients (13.5%) characterized by enrichment of the APOBEC-related mutation signature had worse overall survival (p=0.031) compared with non-APOBEC-enriched samples.\n                      <jats:italic>JAK3<\/jats:italic>\n                      and\n                      <jats:italic>EZH2<\/jats:italic>\n                      mutations were associated with lower PD-L1 expression (p&lt;0.05), and\n                      <jats:italic>JAK3<\/jats:italic>\n                      mutations were independently correlated with shorter progression-free survival (HR=6.07, p=0.0144). Among all types of\n                      <jats:italic>JAK3<\/jats:italic>\n                      mutations, single-cell transcriptomics, western blotting, and flow cytometry revealed that\n                      <jats:italic>JAK3<\/jats:italic>\n                      p.A573V and p.M511I mutations led to decreased PD-L1 expression in Jurkat and BA\/F3 cell lines through inactivation of STAT3. Compared with\n                      <jats:italic>JAK3<\/jats:italic>\n                      wild-type syngeneic mouse models,\n                      <jats:italic>JAK3<\/jats:italic>\n                      p.A573V and p.M511I mutant mice were more sensitive to Tofacitinib but not anti-PD-1 antibody.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      In conclusion, we found that\n                      <jats:italic>JAK3<\/jats:italic>\n                      mutations, especially\n                      <jats:italic>JAK3<\/jats:italic>\n                      p.A573V and\n                      <jats:italic>JAK3<\/jats:italic>\n                      p.M511I mutations, lead to poor prognosis of anti-PD-1 therapy through the STAT3\/PD-L1 pathway. Tofacitinib is more suitable than anti-PD-1 antibody for\n                      <jats:italic>JAK3<\/jats:italic>\n                      mutant PTCL patients.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Trial registration number<\/jats:title>\n                    <jats:p>\n                      <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"clintrialgov\" xlink:href=\"NCT03502629\">NCT03502629<\/jats:ext-link>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1136\/jitc-2024-010783","type":"journal-article","created":{"date-parts":[[2025,4,8]],"date-time":"2025-04-08T21:00:18Z","timestamp":1744146018000},"page":"e010783","update-policy":"https:\/\/doi.org\/10.1136\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":17,"title":["<i>JAK3<\/i>\n                    <sup>A573V<\/sup>\n                    and\n                    <i>JAK3<\/i>\n                    <sup>M511I<\/sup>\n                    mutations in peripheral T-cell lymphoma mediating resistance to anti-PD-1 therapy through the STAT3\/PD-L1 pathway"],"prefix":"10.1136","volume":"13","clinical-trial-number":[{"clinical-trial-number":"nct03502629","registry":"10.18810\/clinical-trials-gov"},{"clinical-trial-number":"nct03502629","registry":"10.18810\/clinical-trials-gov"}],"author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0249-1192","authenticated-orcid":false,"given":"Ning","family":"Lou","sequence":"first","affiliation":[{"name":"Department of Medical Oncology, National Cancer Center\/National Clinical Research Center for Cancer\/Cancer Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing Key Laboratory of Clinical Study on Anticancer Molecular Targeted Drugs, Beijing, China"},{"name":"Clinical Pharmacology Research Center, Peking Union Medical College Hospital, State Key Laboratory of Complex Severe and Rare Diseases, NMPA Key Laboratory for Clinical Research and Evaluation of Drug, Beijing Key Laboratory of Clinical PK & PD Investigation for Innovative Drugs\uff0cChinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mengwei","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Medical Oncology, National Cancer Center\/National Clinical Research Center for Cancer\/Cancer Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing Key Laboratory of Clinical Study on Anticancer Molecular Targeted Drugs, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zucheng","family":"Xie","sequence":"additional","affiliation":[{"name":"Department of Medical Oncology, National Cancer Center\/National Clinical Research Center for Cancer\/Cancer Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, 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