{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,26]],"date-time":"2026-08-26T07:21:40Z","timestamp":1787728900792,"version":"build-2784847793"},"reference-count":152,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2026,8,19]],"date-time":"2026-08-19T00:00:00Z","timestamp":1787097600000},"content-version":"vor","delay-in-days":18,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,8,1]],"date-time":"2026-08-01T00:00:00Z","timestamp":1785542400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clinical &amp;amp; Translational Med"],"published-print":{"date-parts":[[2026,8]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>The interferon\u2010induced transmembrane (IFITM) protein family, including IFITM1, IFITM2, IFITM3, and the less\u2010characterized IFITM5 and IFITM10, has emerged as a recurrent yet mechanistically complex group of players in cancer, reported as oncogenic in one setting and tumor\u2010restraining in another, immunosensitizing in one context and immunotherapy\u2010resistance\u2010promoting in the next. Rather than treating this literature as contradictory, we argue it is unresolved, and we organize it around a four\u2010axis framework defined by the interaction of member identity, interferon (IFN)\u2010input quality, cellular compartment, and tumor milieu.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Main body<\/jats:title>\n                    <jats:p>We first establish the foundational biology that compels this framework: family members are not interchangeable, occupying distinct subcellular compartments and partner networks; their abundance is set jointly by upstream IFN signaling and tumor\u2010cell\u2010intrinsic regulators; and post\u2010translational state gates their function independently of expression. We then refine the prevailing view of IFN signaling as monolithic, reformulating the direction of IFITM functional output around an acute\u2010versus\u2010chronic IFN distinction in which transient signaling drives major histocompatibility complex class I (MHC\u2010I) induction, antigen presentation, and immunogenicity, whereas sustained signaling promotes programmed death\u2010ligand 1 (PD\u2010L1)\u2010coupled adaptive immune resistance and engagement of the interferon\u2010stimulated gene resistance signature (ISG.RS). Surveying tumor\u2010cell\u2010intrinsic, immune\u2010cell\u2010intrinsic, stromal, and microbiota\u2010conditioned compartments across diverse malignancies, we show that the sign of any IFITM effect is set by where, when, and which member is expressed. The field's most prominent conflicts are reframed as falsifiable hypotheses with defined discriminating experiments.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>We conclude that translational maturity remains limited to biomarker discovery, and that compartment\u2010resolved, IFN\u2010quality\u2010stratified, immune\u2010competent studies, not further expression surveys, are the necessary next step.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key points<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"bullet\">\n                        <jats:list-item>\n                          <jats:p>Member, IFN quality, compartment, and milieu define IFITM cancer effects.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>IFITM paralogs engage distinct signaling networks across tumor and immune cells.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Acute IFN favors MHC\u2010I immunogenicity; chronic IFN drives PD\u2010L1 resistance.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Context resolves opposing IFITM effects into experimentally testable predictions.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Near\u2010term translation favors biomarker stratification over direct IFITM targeting.<\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/ctm2.70767","type":"journal-article","created":{"date-parts":[[2026,8,19]],"date-time":"2026-08-19T07:00:37Z","timestamp":1787122837000},"source":"Crossref","is-referenced-by-count":0,"title":["Interferon\u2010induced transmembrane (IFITM) proteins at the tumour\u2013immune interface: A four\u2010axis framework for their context\u2010dependent roles"],"prefix":"10.1002","volume":"16","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1634-6615","authenticated-orcid":false,"given":"Zhe","family":"Liu","sequence":"first","affiliation":[{"name":"Department of Dermatology The Second Hospital of Jilin University  Changchun China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jie","family":"Meng","sequence":"additional","affiliation":[{"name":"Department of Ultrasonic Medicine The Second Hospital of Jilin University  Changchun 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