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| Vitamin D expression is decreased in: Breast, CRC, Prostate, Lung, Melanoma, GBM, Pancreatic cancer. (Poor prognosis, with decreased overall survival). Vitamin D expression is increased in RCC, Thyroid, Ovarian, Endometrial, Cervical cancers (***Better prognosis, with increased overall survival). See VDR and CYP27B1. CYP27B1 is the enzyme responsible for converting 25‐hydroxyvitamin D into its active form, 1,25‐dihydroxyvitamin D (calcitriol). As with VDR, CYP27B1 expression in tumors has been investigated for its potential prognostic significance in various cancers. What Vitamin D Reflects in Cancer Low 25(OH)D commonly indicates: -Reduced host resilience (frailty, sarcopenia risk) -Impaired immune regulation (innate and adaptive) -Higher inflammatory tone -Less favorable tumor microenvironment signaling Vitamin D status therefore integrates nutrition, inflammation, and immune competence. How Vitamin D Is Used Clinically A) Prognosis (Primary Use) -Low vitamin D associates with worse outcomes across several cancers (observational consistency). -Deficiency correlates with advanced disease and higher mortality. B) Treatment Tolerance & Supportive Care -Adequate levels support bone health, muscle function, and may reduce treatment-related complications. -Correction of deficiency is standard supportive care in many oncology settings. C) Immune Context (Adjunct) -VDR signaling modulates cytokine balance, dendritic cell function, and T-cell responses. -Status helps interpret immune readiness, but is not an immunotherapy selector. Vitamin D is a meaningful host-state biomarker in oncology. Low levels signal reduced physiological and immune reserve and are associated with poorer outcomes. While it does not guide tumor-specific therapy, maintaining adequate vitamin D is clinically relevant for prognosis, tolerance, and supportive care—making it an important component of the host biomarker layer. |
| Prostate Cancer: Alterations in genes such as ERG, SPOP, MYC, androgen receptor (AR), and CHD1, drive PCa progression. TP53 is the most commonly mutated gene in human cancer. HH↑, GLI-1↑, SHH↑ P53↓ The loss of p53 and/or other tumor suppressor genes, reduced capacity for DNA repair, the dysfunction of telomerase activity, and changes in the pathways that govern the growth of cells also mediate the progression of Pca. It has been well documented that Ca2+ influx and MDR1 upregulation are highly associated with GEM metabolism in human pancreatic carcinoma. Increased Growth factor IGF-1/IGF-1R axis activation mediated by both PI3K/Akt or RAF/MEK/ERK system and AR expression remains important in the development and progression of prostate cancer. It has been demonstrated that prostate cancer cells are relatively sensitive to heat stress. Long non-coding RNA MALAT1 has been reported as an oncogenic target in multiple types of cancers, including PC. |
| - | Trial, | Pca, | NA |
Query results interpretion may depend on "conditions" listed in the research papers. Such Conditions may include : -low or high Dose -format for product, such as nano of lipid formations -different cell line effects -synergies with other products -if effect was for normal or cancerous cells
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:22 Cells:% prod#:% Target#:851 State#:% Dir#:2
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