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Additional immunohistochemical studies were conducted on 98 cases. Differential expression, pathway enrichment, and survival analyses were used to characterise proteomic alterations and identify prognostic features.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>SMARCA-deficient tumours showed frequent expression of complement-inactivating proteins CD55 and CD59 with distinctive apical and membranous localisation. SMARCA4-deficient patients had significantly poorer survival than both SMARCA2-deficient and SMARCA-proficient patients. Among neoadjuvantly treated SMARCA-deficient tumours, coordinated upregulation of DNA repair proteins separated patients into two prognostic subgroups. The DNA repair\u2013low subgroup had markedly worse survival than both the DNA repair\u2013high subgroup and SMARCA-proficient controls, whereas the DNA repair\u2013high subgroup showed a trend toward improved outcomes. This DNA repair\u2013associated pattern was not observed in neoadjuvantly treated SMARCA-proficient tumours.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>SMARCA-deficient EAC comprises biologically distinct subgroups with prognostic proteomic signatures. CD55 and CD59 expression may contribute to resistance to antibody-based immunotherapies by complement evasion, while DNA repair profiles could guide post-surgical treatment in neoadjuvantly treated patients.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1038\/s41416-026-03534-7","type":"journal-article","created":{"date-parts":[[2026,7,8]],"date-time":"2026-07-08T13:28:05Z","timestamp":1783517285000},"page":"1119-1130","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Proteomic characterization of SMARCA-deficient esophageal adenocarcinoma reveals complement evasion and DNA repair-associated prognostic subgroups"],"prefix":"10.1038","volume":"135","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0883-6481","authenticated-orcid":false,"given":"Bastian","family":"Grothey","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Max","family":"Kr\u00e4mer","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matteo","family":"Montalbano","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Su Ir","family":"Lyu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6590-8181","authenticated-orcid":false,"given":"Christiane J.","family":"Bruns","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas","family":"Zander","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8806-4786","authenticated-orcid":false,"given":"Reinhard","family":"B\u00fcttner","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3537-6011","authenticated-orcid":false,"given":"Alexander","family":"Quaas","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,7,8]]},"reference":[{"key":"3534_CR1","doi-asserted-by":"publisher","first-page":"209","DOI":"10.3322\/caac.21660","volume":"71","author":"H Sung","year":"2021","unstructured":"Sung H, Ferlay J, Siegel RL, Laversanne M, Soerjomataram I, Jemal A, et al. 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