{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T19:26:18Z","timestamp":1791919578274,"version":"4.3.4"},"reference-count":230,"publisher":"MDPI AG","issue":"9","license":[{"start":{"date-parts":[[2024,4,29]],"date-time":"2024-04-29T00:00:00Z","timestamp":1714348800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Head and Neck Cancer SPORE and Skin Cancer SPORE Career Enhancement Program (CEP)"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>Discovered as inflammatory cytokines, MIF and DDT exhibit widespread expression and have emerged as critical mediators in the response to infection, inflammation, and more recently, in cancer. In this comprehensive review, we provide details on their structures, binding partners, regulatory mechanisms, and roles in cancer. We also elaborate on their significant impact in driving tumorigenesis across various cancer types, supported by extensive in vitro, in vivo, bioinformatic, and clinical studies. To date, only a limited number of clinical trials have explored MIF as a therapeutic target in cancer patients, and DDT has not been evaluated. The ongoing pursuit of optimal strategies for targeting MIF and DDT highlights their potential as promising antitumor candidates. Dual inhibition of MIF and DDT may allow for the most effective suppression of canonical and non-canonical signaling pathways, warranting further investigations and clinical exploration.<\/jats:p>","DOI":"10.3390\/ijms25094849","type":"journal-article","created":{"date-parts":[[2024,5,1]],"date-time":"2024-05-01T03:30:49Z","timestamp":1714534249000},"page":"4849","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":20,"title":["Macrophage Migration Inhibitory Factor (MIF) and D-Dopachrome Tautomerase (DDT): Pathways to Tumorigenesis and Therapeutic Opportunities"],"prefix":"10.3390","volume":"25","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7078-8134","authenticated-orcid":false,"given":"Caroline Naomi","family":"Valdez","sequence":"first","affiliation":[{"name":"School of Medicine, Yale University, 333 Cedar St., New Haven, CT 06510, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gabriela Athziri","family":"S\u00e1nchez-Zuno","sequence":"additional","affiliation":[{"name":"Section of Rheumatology, Allergy and Immunology, Department of Internal Medicine, Yale University, 333 Cedar St., New Haven, CT 06510, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Richard","family":"Bucala","sequence":"additional","affiliation":[{"name":"School of Medicine, Yale University, 333 Cedar St., New Haven, CT 06510, USA"},{"name":"Section of Rheumatology, Allergy and Immunology, Department of Internal Medicine, Yale University, 333 Cedar St., New Haven, CT 06510, USA"},{"name":"Yale Cancer Center, Yale University, 333 Cedar St., New Haven, CT 06510, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6244-7575","authenticated-orcid":false,"given":"Thuy T.","family":"Tran","sequence":"additional","affiliation":[{"name":"School of Medicine, Yale University, 333 Cedar St., New Haven, CT 06510, USA"},{"name":"Yale Cancer Center, Yale University, 333 Cedar St., New Haven, CT 06510, USA"},{"name":"Section of Medical Oncology, Department of Internal Medicine, Yale University, 333 Cedar St., New Haven, CT 06510, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2024,4,29]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"72","DOI":"10.1073\/pnas.56.1.72","article-title":"Delayed hypersensitivity in vitro: Its mediation by cell-free substances formed by lymphoid cell-antigen interaction","volume":"56","author":"David","year":"1966","journal-title":"Proc. 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