{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,12]],"date-time":"2026-08-12T13:38:43Z","timestamp":1786541923122,"version":"build-2736575974"},"reference-count":265,"publisher":"MDPI AG","issue":"16","license":[{"start":{"date-parts":[[2026,8,12]],"date-time":"2026-08-12T00:00:00Z","timestamp":1786492800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100004281","name":"National Science Centre","doi-asserted-by":"publisher","award":["UMO-2020\/37\/B\/N24\/03920 and UMO-2021\/41\/B\/NZ7\/03786."],"award-info":[{"award-number":["UMO-2020\/37\/B\/N24\/03920 and UMO-2021\/41\/B\/NZ7\/03786."]}],"id":[{"id":"10.13039\/501100004281","id-type":"DOI","asserted-by":"publisher"}]},{"award":["UMO-2020\/37\/B\/N24\/03920 and UMO-2021\/41\/B\/NZ7\/03786."],"award-info":[{"award-number":["UMO-2020\/37\/B\/N24\/03920 and UMO-2021\/41\/B\/NZ7\/03786."]}],"id":[{"id":"https:\/\/ror.org\/03ha2q922","id-type":"ROR","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cancers"],"abstract":"<jats:p>Ketogenic metabolic therapy (KMT), typically implemented as a ketogenic diet (KD), has re-emerged as a potential adjuvant strategy in oncology. Its rationale is grounded in the metabolic reprogramming of cancer cells, including their reliance on glucose and lipid substrates and the signaling functions of ketone bodies. Despite extensive preclinical evidence of anti-proliferative and immunomodulatory effects, clinical translation in cancer therapy has been slow and inconsistent. This review critically examines the mechanistic basis, experimental and clinical evidence, and translational challenges of KMT across epithelial cancers. We emphasize that \u201cketogenic interventions\u201d comprise mechanistically distinct modalities, including classical KD, fasting, fasting-mimicking diets, and exogenous ketone supplementation, which are frequently conflated yet differ substantially in their endocrine and metabolic contexts. Across clinical studies, KMT is generally feasible and associated with improvements in quality of life and metabolic parameters; however, robust evidence for the survival benefit of KMT remains limited and heterogeneous. Mechanistically, ketone bodies exert both metabolic and signaling functions, including inhibition of histone deacetylases, lysine \u03b2-hydroxybutyrylation, and receptor-mediated effects. Tumor responses are highly context-dependent: ketolytic capacity, governed by enzymes such as OXCT1, can render ketones either a metabolic vulnerability or an alternative fuel for cancer cells. KMT can modify the complex tumor microenvironment, exerting potentially opposing effects on cancer cells, immune cell populations, fibroblasts, and adipocytes. We argue that the central limitation of the field is not a lack of biological activity, but of insufficient integration of tumor-intrinsic metabolism, host physiology, and microenvironmental context. KD\/KMT should therefore be regarded not as a universal anticancer therapy, but as a stratified metabolic intervention, whose progress will depend on biomarker-guided patient selection, improved experimental models, and rational combination strategies within a \u201cpress-pulse\u201d therapeutic framework.<\/jats:p>","DOI":"10.3390\/cancers18162600","type":"journal-article","created":{"date-parts":[[2026,8,12]],"date-time":"2026-08-12T12:53:48Z","timestamp":1786539228000},"page":"2600","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Ketogenic Diet as an Adjuvant in Epithelial Cancers: Mechanisms, Model Systems, and Translational Opportunities"],"prefix":"10.3390","volume":"18","author":[{"given":"Timo","family":"Ylikomi","sequence":"first","affiliation":[{"name":"Faculty of Medicine and Health Technology, Tampere University, Kalevantie 4, 33100 Tampere, Finland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9034-301X","authenticated-orcid":false,"given":"Matthias","family":"Nees","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, Medical University of Lublin, ul. Witolda Chod\u017aki St. 1, 20-093 Lublin, Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2026,8,12]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"760","DOI":"10.1016\/S1470-2045(24)00152-9","article-title":"Overall Survival Benefits of Cancer Drugs Initially Approved by the US Food and Drug Administration on the Basis of Immature Survival Data: A Retrospective Analysis","volume":"25","author":"Naci","year":"2024","journal-title":"Lancet Oncol."},{"key":"ref_2","doi-asserted-by":"crossref","first-page":"j4530","DOI":"10.1136\/bmj.j4530","article-title":"Availability of Evidence of Benefits on Overall Survival and Quality of Life of Cancer Drugs Approved by European Medicines Agency: Retrospective Cohort Study of Drug Approvals 2009-13","volume":"359","author":"Davis","year":"2017","journal-title":"BMJ"},{"key":"ref_3","doi-asserted-by":"crossref","first-page":"4095","DOI":"10.1200\/JCO.22.00535","article-title":"Overall Survival, Progression-Free Survival, and Tumor Response Benefit Supporting Initial US Food and Drug Administration Approval and Indication Extension of New Cancer Drugs, 2003\u20132021","volume":"40","author":"Michaeli","year":"2022","journal-title":"J. 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