{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T15:02:46Z","timestamp":1790694166135,"version":"4.1.0"},"reference-count":40,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T00:00:00Z","timestamp":1790294400000},"content-version":"vor","delay-in-days":24,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,9,1]],"date-time":"2026-09-01T00:00:00Z","timestamp":1788220800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Pathology International"],"published-print":{"date-parts":[[2026,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Germline\n                    <jats:italic>TP53<\/jats:italic>\n                    p.R72P polymorphism has been associated with lung cancer susceptibility, somatic\n                    <jats:italic>TP53<\/jats:italic>\n                    mutation acquisition, and differential apoptotic signaling. Its influence on pathologic response to neoadjuvant immune checkpoint inhibition (ICI) has not been previously evaluated. This study investigates the impact of germline\n                    <jats:italic>TP53<\/jats:italic>\n                    p.R72P genotype on response to neoadjuvant ICI therapy in nonsmall cell lung cancer (NSCLC). NSCLC patients treated with neoadjuvant anti\u2013PD\u20101 therapy followed by resection were stratified by germline p.R72P status and the presence of concomitant somatic\n                    <jats:italic>TP53<\/jats:italic>\n                    mutations. Histopathologic review assessed immunotherapy\u2010associated histopathologic features of tumor regression, and the findings were correlated with PD\u2010L1 tumor proportion scores (TPS) and next\u2010generation sequencing data. The subgroup harboring both germline p.R72P and somatic\n                    <jats:italic>TP53<\/jats:italic>\n                    mutations achieved a complete pathologic response (cPR) rate of 75% (3 of 4 cases), numerically higher than that observed in p.R72P\u2010positive\/\n                    <jats:italic>TP53<\/jats:italic>\n                    \u2010wild\u2010type tumors (25%, 2 of 8 cases), p.R72P\u2010negative\/\n                    <jats:italic>TP53<\/jats:italic>\n                    \u2010mutant tumors (50%, 4 of 8 cases), and p.R72P\u2010negative\/\n                    <jats:italic>TP53<\/jats:italic>\n                    \u2010wild\u2010type controls (0%, 0 of 6 cases) (\n                    <jats:italic>p<\/jats:italic>\n                    \u2009&lt;\u20090.05). In this single\u2010center, exploratory cohort, germline\n                    <jats:italic>TP53<\/jats:italic>\n                    p.R72P status was associated with differences in pathologic response to neoadjuvant therapy. Tumors with combined germline p.R72P polymorphism and somatic\n                    <jats:italic>TP53<\/jats:italic>\n                    mutation might represent a genomic subgroup with a higher cPR rate.\n                  <\/jats:p>","DOI":"10.1111\/pin.70183","type":"journal-article","created":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T07:38:22Z","timestamp":1790321902000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Germline TP53 Polymorphism and Its Interaction With Somatic TP53 Mutations Shapes Response to Immune Checkpoint Inhibitors in Nonsmall Cell Lung Cancer: The Role of TP53 p.R72P as a Germline Biomarker"],"prefix":"10.1111","volume":"76","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8413-4668","authenticated-orcid":false,"given":"Selin","family":"Kurt","sequence":"first","affiliation":[{"name":"Department of Pathology Albert Einstein College of Medicine\/Montefiore Medical Center Bronx New York USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0772-0150","authenticated-orcid":false,"given":"Kritika","family":"Krishnamurthy","sequence":"additional","affiliation":[{"name":"Department of Pathology Albert Einstein College of Medicine\/Montefiore Medical Center Bronx New York USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,9,25]]},"reference":[{"key":"e_1_2_10_2_1","doi-asserted-by":"publisher","DOI":"10.1093\/annonc\/mdy218"},{"key":"e_1_2_10_3_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMc1808251"},{"key":"e_1_2_10_4_1","doi-asserted-by":"publisher","DOI":"10.1016\/S1470-2045(20)30453-8"},{"key":"e_1_2_10_5_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.ccell.2018.03.018"},{"key":"e_1_2_10_6_1","doi-asserted-by":"publisher","DOI":"10.1126\/science.aaa1348"},{"key":"e_1_2_10_7_1","doi-asserted-by":"publisher","DOI":"10.3389\/fmolb.2020.602328"},{"key":"e_1_2_10_8_1","doi-asserted-by":"publisher","DOI":"10.1158\/1078-0432.CCR-16-2554"},{"key":"e_1_2_10_9_1","doi-asserted-by":"publisher","DOI":"10.1186\/s12920-019-0592-6"},{"key":"e_1_2_10_10_1","doi-asserted-by":"publisher","DOI":"10.1158\/1078-0432.CCR-18-0163"},{"key":"e_1_2_10_11_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.cancergencyto.2003.07.010"},{"key":"e_1_2_10_12_1","doi-asserted-by":"publisher","DOI":"10.1038\/ng1093"},{"key":"e_1_2_10_13_1","doi-asserted-by":"publisher","DOI":"10.1038\/ng1879"},{"issue":"5","key":"e_1_2_10_14_1","first-page":"731","article-title":"Is the p53 Codon 72 Polymorphism a Key Biomarker for Cervical Cancer Development? 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