{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"medRxiv"}],"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T11:00:56Z","timestamp":1790420456776,"version":"4.1.0"},"posted":{"date-parts":[[2026,9,23]]},"group-title":"Oncology","reference-count":51,"publisher":"openRxiv","license":[{"start":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T00:00:00Z","timestamp":1790121600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.medrxiv.org\/about\/FAQ#license"}],"funder":[{"name":"National Cancer Institute","award":["P50 CA261605"],"award-info":[{"award-number":["P50 CA261605"]}]},{"name":"National Institutes of Health","award":["F30 CA281125"],"award-info":[{"award-number":["F30 CA281125"]}]},{"name":"National Institutes of Health","award":["T32 GM007347"],"award-info":[{"award-number":["T32 GM007347"]}]},{"name":"National Institutes of Health","award":["K12CA090625"],"award-info":[{"award-number":["K12CA090625"]}]},{"name":"National Institutes of Health","award":["K08CA240901"],"award-info":[{"award-number":["K08CA240901"]}]},{"name":"National Institutes of Health","award":["R01CA272875"],"award-info":[{"award-number":["R01CA272875"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2026,9,21]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                <jats:sec>\n                  <jats:title>Background<\/jats:title>\n                  <jats:p>Cancer-associated fibroblasts (CAF) are major regulators of the tumor microenvironment (TME), yet the pathways governing CAF function remain incompletely understood. Type 2 deiodinase (DIO2, D2), which converts thyroxine (T4) to the active thyroid hormone triiodothyronine (T3), has not been systematically investigated in CAF across different solid tumors.<\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Methods<\/jats:title>\n                  <jats:p>\n                    We analyzed\n                    <jats:italic>DIO2<\/jats:italic>\n                    expression using single-cell RNA sequencing (scRNA-seq) from primary thyroid tumors, a large integrated scRNASeq thyroid cancer atlas, and publicly available scRNA-seq datasets representing six additional solid tumor types. Bulk RNA sequencing data from the Oncology Research Information Exchange Network (ORIEN) database were used to examine correlations among\n                    <jats:italic>DIO2<\/jats:italic>\n                    , CAF subtype markers, and overall survival (OS). A genetically engineered TPO-CreERT2\/BrafV600E\/Trp53-deficient (TBP) mouse model was evaluated for CAF-specific\n                    <jats:italic>Dio2<\/jats:italic>\n                    expression and pharmacologic inhibition of D2 activity. TBP mice were crossed with\n                    <jats:italic>Dio2<\/jats:italic>\n                    <jats:sup>-\/-<\/jats:sup>\n                    (Dio2 KO) mice to investigate the role of Dio2 in cancer development and progression.\n                  <\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>\n                    <jats:italic>DIO2<\/jats:italic>\n                    expression was highly restricted to CAF and was largely absent from epithelial-derived cancer, immune, and endothelial cells. Across thyroid cancer and six additional malignancies,\n                    <jats:italic>DIO2<\/jats:italic>\n                    was consistently detected in CAF, demonstrating that CAF-specific DIO2 expression is a conserved feature of multiple tumor types. Within thyroid cancer,\n                    <jats:italic>DIO2<\/jats:italic>\n                    was enriched in myofibroblastic CAF (myCAF) compared with inflammatory CAF (iCAF), and bulk transcriptomic analyses demonstrated stronger correlations between DIO2 expression and canonical myCAF markers than iCAF markers across numerous cancers. Elevated\n                    <jats:italic>DIO2<\/jats:italic>\n                    expression was associated with worse OS in pancreatic and bladder cancers, paralleling the adverse prognostic impact of increased myCAF abundance. In contrast, thyroid cancer demonstrated an inverse association attributable to loss of epithelial DIO2 expression during tumor dedifferentiation. The TBP mouse model recapitulated human disease, with\n                    <jats:italic>Dio2<\/jats:italic>\n                    expression restricted to CAF, robust stromal fibrosis, and measurable D2 enzymatic activity that was suppressed by cefuroxime and lenvatinib. Genetic loss of\n                    <jats:italic>Dio2<\/jats:italic>\n                    in the TME resulted in significantly reduced tumor growth.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Conclusions<\/jats:bold>\n                  <\/jats:p>\n                  <jats:p>DIO2 is a conserved marker of CAF, and myCAF, across multiple solid tumors and is associated with adverse clinical outcomes in some cancers. The TBP mouse provides a robust preclinical model to define the mechanistic role of DIO2 in CAF biology and to evaluate DIO2-directed therapeutic strategies targeting the tumor microenvironment.<\/jats:p>\n                <\/jats:sec>","DOI":"10.64898\/2026.09.14.26362848","type":"posted-content","created":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T20:45:13Z","timestamp":1790196313000},"source":"Crossref","is-referenced-by-count":0,"title":["Type 2 Deiodinase in Cancer-Associated Fibroblasts: A Potential Therapeutic Target in Many Types of Cancer"],"prefix":"10.64898","author":[{"given":"Mary Grace","family":"Carroll","sequence":"first","affiliation":[{"name":"Division of Endocrinology, Department of Medicine, University of Colorado Anschutz, Aurora, CO"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Noha","family":"Mukhtar","sequence":"additional","affiliation":[{"name":"King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jacob","family":"Calhoun","sequence":"additional","affiliation":[{"name":"Division of Endocrinology, Department of Medicine, University of Colorado Anschutz, Aurora, CO"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Breaunna","family":"Garza","sequence":"additional","affiliation":[{"name":"Division of Endocrinology, Department of Medicine, University of Colorado Anschutz, Aurora, CO"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthew A.","family":"Loberg","sequence":"additional","affiliation":[{"name":"Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hua-Chang","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Quanhu","family":"Sheng","sequence":"additional","affiliation":[{"name":"Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alyse","family":"Staley","sequence":"additional","affiliation":[{"name":"University of Colorado Cancer Center Biostatistics Core, Department of Pediatrics, University of Colorado Anschutz, Aurora, CO"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tatiana L.","family":"Fonseca","sequence":"additional","affiliation":[{"name":"Division of Endocrinology, Department of Internal Medicine, University of Texas Medical Branch, Galveston, TX"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Antonio C.","family":"Bianco","sequence":"additional","affiliation":[{"name":"Division of Endocrinology, Department of Internal Medicine, University of Texas Medical Branch, Galveston, TX"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthew D.","family":"Ringel","sequence":"additional","affiliation":[{"name":"Department of Molecular Medicine and Therapeutics, The Ohio State University Wexner Medical Center, Columbus, OH"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pamela","family":"Brock","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, The Ohio State University Wexner Medical Center, Columbus, OH"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrew J.","family":"Gunderson","sequence":"additional","affiliation":[{"name":"Department of Surgery, The Ohio State University Wexner Medical Center, Columbus, OH"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ahmad A.","family":"Tarhini","sequence":"additional","affiliation":[{"name":"Departments of Cutaneous Oncology and Immunology, Moffitt Cancer Center, Tampa, FL"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"W. Douglas","family":"Cress","sequence":"additional","affiliation":[{"name":"Department of Molecular Oncology, Moffitt Cancer Center, Tampa, FL"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael J.","family":"Cavnar","sequence":"additional","affiliation":[{"name":"Department of Surgery, University of Kentucky, Lexington, KY"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephen","family":"Edge","sequence":"additional","affiliation":[{"name":"Departments of Surgical Oncology and Cancer Prevention and Control, Roswell Park Comprehensive Cancer Center, Buffalo, NY"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Varinder","family":"Kaur","sequence":"additional","affiliation":[{"name":"Division of Hematology and Oncology, Department of Medicine, University of Virginia, Charlottsville, VA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3427-0562","authenticated-orcid":false,"given":"George 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