{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,19]],"date-time":"2026-05-19T13:15:16Z","timestamp":1779196516090,"version":"3.51.4"},"reference-count":84,"publisher":"BMJ","issue":"5","license":[{"start":{"date-parts":[[2026,5,19]],"date-time":"2026-05-19T00:00:00Z","timestamp":1779148800000},"content-version":"unspecified","delay-in-days":18,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"funder":[{"DOI":"10.13039\/100004325","name":"AstraZeneca","doi-asserted-by":"publisher","award":["N\/A"],"award-info":[{"award-number":["N\/A"]}],"id":[{"id":"10.13039\/100004325","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["bmj.com"],"crossmark-restriction":true},"short-container-title":["J Immunother Cancer"],"accepted":{"date-parts":[[2026,4,15]]},"published-print":{"date-parts":[[2026,5]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Immune checkpoint blockade (ICB) has revolutionized cancer therapy, yet resistance\u2014both primary and acquired\u2014remains a significant obstacle, affecting the majority of patients.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Here, we leverage a large-scale, real-world clinicogenomic dataset to systematically explore the molecular underpinnings of ICB resistance in the post-progression setting. We analyze over 5,000 pan-cancer patients with clinical and pre-\/post-treatment genomic and transcriptomic data and systematically compare the clinical and molecular features of acquired versus primary ICB resistance.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Post-ICB progression, acquired resistance showed extended survival compared to primary resistance across all cancer types. This clinical phenotype was paralleled by a universally immune-inflamed, albeit dysfunctional, tumor microenvironment (TME) at the onset of acquired resistance, with sustained or ICB-induced inflammatory and interferon responses. We confirm previously described mechanisms of acquired resistance, including\n                      <jats:italic>B2M<\/jats:italic>\n                      loss-of-function (LoF) in non-small cell lung cancer (NSCLC), and identify novel potential mediators, including LoF of\n                      <jats:italic>TGFBR2<\/jats:italic>\n                      in NSCLC,\n                      <jats:italic>CYLD<\/jats:italic>\n                      in head and neck cancer, and\n                      <jats:italic>RUNX1<\/jats:italic>\n                      in triple-negative breast cancer. Further supporting their involvement in resistance, these acquired ICB alterations associated with immune-escaped TMEs, characterized by active immunomodulatory oncogenic signaling, hyperproliferation and invasiveness, or altered tumor metabolism.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>These findings emphasize the heterogeneity of molecular drivers of acquired resistance to ICB within and across cancers, and highlight the potential for personalized therapeutic interventions post-progression to improve patient outcomes.<\/jats:p>\n                  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