{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,9]],"date-time":"2026-07-09T09:17:38Z","timestamp":1783588658906,"version":"3.55.0"},"reference-count":152,"publisher":"MDPI AG","issue":"14","license":[{"start":{"date-parts":[[2026,7,9]],"date-time":"2026-07-09T00:00:00Z","timestamp":1783555200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Nutrients"],"abstract":"<jats:p>Leukemia represents a heterogeneous group of hematologic malignancies characterized by the dysregulated proliferation, differentiation, and survival of hematopoietic cells. Vitamin D (VD), a fat-soluble secosteroid hormone, is increasingly recognized not only as a regulator of calcium\u2013phosphate metabolism but also as an important immune\u2013metabolic modulator involved in hematopoietic homeostasis, inflammatory signaling, and cellular fate determination. Growing evidence suggests that VD deficiency may influence leukemogenesis, disease progression, treatment responsiveness, and supportive-care outcomes in patients with leukemia. Mechanistic studies indicate that the active metabolite, 1,25-dihydroxyvitamin D3 (calcitriol), modulates leukemic cell biology by activating the vitamin D receptor (VDR) and regulating genomic and non-genomic signaling pathways, including MAPK, PI3K\/AKT\/mTOR, JAK\/STAT, NF-\u03baB, and \u03b2-catenin. Through these pathways, VD may affect transcriptional programs governing proliferation, differentiation, apoptosis, autophagy, immune regulation, and treatment resistance. Clinical and observational studies suggest that low 25-hydroxyvitamin D levels may be associated with adverse outcomes in selected leukemia subtypes, including poorer treatment responses, shorter overall survival and relapse-free survival, and shorter time to treatment. However, the available data remain heterogeneous, and causality has not been established. This review provides an integrated translational synthesis of VD deficiency in leukemia, linking molecular mechanisms with subtype-specific clinical evidence and supportive-care implications. Although VD supplementation should not be considered an independent anti-leukemic therapy, individualized assessment and correction of deficiency may represent a rational, low-toxicity component of supportive care. Further prospective and interventional studies are needed to define optimal supplementation strategies, identify responsive patient subgroups, and clarify the clinical relevance of VD status in leukemia.<\/jats:p>","DOI":"10.3390\/nu18142227","type":"journal-article","created":{"date-parts":[[2026,7,9]],"date-time":"2026-07-09T08:50:56Z","timestamp":1783587056000},"page":"2227","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Vitamin D Deficiency in Leukemia: Implications for Pathophysiology, Treatment, and Supportive Care"],"prefix":"10.3390","volume":"18","author":[{"ORCID":"https:\/\/orcid.org\/0009-0004-9326-436X","authenticated-orcid":false,"given":"Zahra","family":"Eskandari","sequence":"first","affiliation":[{"name":"Department of Hematology, Faculty of Allied Medicine, Bushehr University of Medical Sciences, Bushehr 7514633341, Iran"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7365-6014","authenticated-orcid":false,"given":"Ireneusz","family":"Ryszkiel","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Metabolic Diseases and Angiology, Faculty of Health Sciences in Katowice, Medical University of Silesia, Zio\u0142owa 45\/47, 40-635 Katowice, Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0001-0703-6511","authenticated-orcid":false,"given":"Amirhossein Faghih","family":"Ojaroodi","sequence":"additional","affiliation":[{"name":"Student Research Committee, Tabriz University of Medical Sciences, Tabriz 5165665931, Iran"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1703-9847","authenticated-orcid":false,"given":"Haniyeh","family":"Bazavar","sequence":"additional","affiliation":[{"name":"Department of Hematology, Zanjan University of Medical Science, Zanjan 4513956184, Iran"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0612-9978","authenticated-orcid":false,"given":"Shayan","family":"Keramat","sequence":"additional","affiliation":[{"name":"VAS-European Independent Foundation in Angiology\/Vascular Medicine, Via GB Grassi 74, 20157 Milan, Italy"},{"name":"Support Association of Patients of Buerger\u2019s Disease, Buerger\u2019s Disease NGO, Mashhad 9183785195, Iran"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6939-9898","authenticated-orcid":false,"given":"Agata","family":"Stanek","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Metabolic Diseases and Angiology, Faculty of Health Sciences in Katowice, Medical University of Silesia, Zio\u0142owa 45\/47, 40-635 Katowice, Poland"},{"name":"VAS-European Independent Foundation in Angiology\/Vascular Medicine, Via GB Grassi 74, 20157 Milan, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2026,7,9]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","unstructured":"Tebbi, C.K. 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