• 1,25(OH)(2)D(3)
• Cancer
• Carcinogenesis
• Obesity
• VDR
• Vitamin D

• Humans
• Receptors, Calcitriol/metabolism
• Receptors, Calcitriol/genetics
• Obesity/drug therapy
• Obesity/metabolism
• Neoplasms/drug therapy
• Neoplasms/metabolism
• Animals
• Vitamin D/therapeutic use
• Vitamin D/metabolism
• Vitamin D/pharmacology
• Vitamin D Deficiency/drug therapy
• Vitamin D Deficiency/complications
• Molecular Targeted Therapy

• Vitamin D and cancer
• Vitamin D and cancer controversy
• Vitamin D in an oncogenic environment

• Humans
• Vitamin D
• Neoplasms/prevention & control
• Animals
• Vitamin D Deficiency

• Colitis
• histology
• mucosa
• stem cell
• vitamin D3

• Digestive System Neoplasms/diagnosis
• Receptors, Calcitriol/genetics
• Prognosis
• Survival Rate

• Apoptosis
• Colorectal cancer
• Cyclin D1
• Invasion
• Vitamin D receptor
• Wnt/β-catenin

• Bovine
• Endometrial epithelial cells
• IWR-1
• Lipopolysaccharide
• Vitamin D3
• Wnt signaling pathway

• Animals
• Cattle
• Cell Proliferation
• Cholecalciferol/pharmacology
• Epithelial Cells/metabolism
• Female
• Lipopolysaccharides/pharmacology
• Proliferating Cell Nuclear Antigen/metabolism
• Wnt Signaling Pathway/genetics
• beta Catenin/metabolism

• 25-Hydroxyvitamin D
• Colorectal neoplasms
• Vitamin D
• Vitamin D deficiency

Thyroid cancer is the most common endocrine malignancy and exhibits rising incidence. Annual incidence varies by sex, age, and geographical location. It has been reported that impairment of vitamin D signalling promotes thyroid cancer progression. Recent studies have shown that vitamin D, a fat-soluble vitamin that acts as both a nutrient and a hormone, may have utility in the prevention of autoimmune thyroid-related diseases. However, the precise role of vitamin D in the pathobiology of thyroid cancer is controversial. Previous studies have suggested that elevated serum vitamin D levels have a protective role in thyroid cancer. However, there is also evidence demonstrating no inverse relationship between vitamin D levels and the occurrence of thyroid cancer. Furthermore, recent data provide evidence that circulating vitamin D concentration is inversely correlated with disease aggressiveness and poor prognosis, while evidence of an association with tumour initiation remains weak. Nevertheless, a variety of data support an anti-tumorigenic role of vitamin D and its potential utility as a secondary chemopreventive agent. In this review, we highlighted recent findings regarding the association of vitamin D status with the risk of thyroid cancer, prognosis, potential mechanisms, and possible utility as a chemopreventive agent.

• Hashimoto Disease/complications
• Humans
• Thyroid Neoplasms
• Vitamin D
• Vitamin D Deficiency/complications
• Vitamins/therapeutic use

• Cancer
• Environmental chemicals
• Food additive
• Mixtures
• Pesticides

• Animals
• Cholecalciferol
• Colorectal Neoplasms
• Humans
• Pancreatic Neoplasms
• Pesticides/toxicity
• Zebrafish

• P30 CA051008 NCI NIH HHS

The protective effects of vitamin D and calcium on colorectal neoplasms are known. Bone mineral density (BMD) may be a reliable biomarker that reflects the long-term anticancer effect of vitamin D and calcium. This study aimed to evaluate the association between BMD and colorectal adenomas including high-risk adenoma.

A multicenter, cross-sectional, case-control study was conducted among participants with average risk of colorectal cancer who underwent BMD and screening colonoscopy between 2015 and 2019. The main outcome was the detection of colorectal neoplasms. The variable under consideration was low BMD (osteopenia/osteoporosis). The logistic regression model included baseline demographics, components of metabolic syndrome, fatty liver disease status, and aspirin and multivitamin use.

A total of 2,109 subjects were enrolled. The mean age was 52.1±10.8 years and 42.6% were male. The adenoma detection rate was 43%. Colorectal adenoma and high-risk adenoma were both more prevalent in subjects with low BMD than those with normal BMD (48.2% vs 38.8% and 12.1% vs 9.1%). In the univariate analysis, old age, male sex, smoking, metabolic components, fatty liver, and osteoporosis were significantly associated with the risk of adenoma and high-risk adenoma. In the multivariate analysis, osteoporosis was independently associated with risk of colorectal adenoma (odds ratio [OR], 1.65; 95% confidence interval [CI], 1.11 to 2.46; p=0.014) and high-risk adenoma (OR, 1.94; 95% CI, 1.14 to 3.29; p=0.014).

Osteoporosis is an independent risk factor of colorectal adenoma and high-risk adenoma.

• Disease activity index
• Inflammatory bowel disease
• Multipotent stem cell
• Vitamin D
• Wnt pathway

• ApaI
• BsmI
• Gastric cancer
• Kashmiri Population
• TaqI
• VDR polymorphism

• carcinogenesis
• cell death
• inflammation immunomodulation
• signaling pathways
• therapeutic implications
• vitamin D

Expression of forkhead box P3 (FOXP3), a key regulator of T-cell function, in the tumor immune microenvironment is related to survival in classic Hodgkin lymphoma (CHL). Vitamin D receptor (VDR), a transcription factor agonists have been shown to induce FOXP3 expression in T-cells and enhance recruitment of these cells to the inflammatory sites. VDR expression is CHL has been described. However, there is no data on expression of VDR in context of quantity of FOXP3 positive cells in CHL.

We examined and correlated immunohistochemical expression of VDR and FOXP3 along with clinical and pathology findings in 29 cases of CHL.

VDR was expressed in Hodgkin Reed-Sternberg (HRS) cells and background lymphocytes and FOXP3 was expressed in background lymphocytes. 82% of CHL cases, regardless of the subtype, expressed VDR and in majority of the cases, VDR expression was directly proportional to the quantity of FOXP3 expressing lymphocytes in the tumor microenvironment. In cases with higher clinical stage (III/IV), only 28.5% of cases diffusely expressed VDR and FOXP3 compared to 71.4% showing focal positivity. Whereas in cases with lower clinical stages (I/II), the expression pattern of VDR and FOXP3 was almost similar (41.6% diffuse versus 33.3% focal). Interestingly, focal VDR and FOXP3 expression pattern was significantly higher among males. Mixed cellularity cases showed predilection for focal VDR and FOXP3 expression (80% cases); whereas nodular sclerosis subtype had focal and diffuse VDR and FOXP3 expression patterns in similar proportion. Cases with diffuse VDR and FOXP3 expression were less likely to have bone marrow involvement. Epstein Barr virus- encoded small RNA (EBER) positive cases were predominantly focally positive (80%) for VDR and FOXP3.

In summary, quantity of FOXP3 positive T-cells in CHL microenvironment seems to correlate with VDR expression. Clinical stage show a trend of inverse correlation with expression of VDR and quantity of FOXP3 positive T-cells. These findings suggest that VDR could be a possible prognostic and therapeutic target in CHL.

• FOXP3
• Hodgkin lymphoma
• Lymphoma
• Nutrition
• VDR
• Vitamin D

• Colorectal cancer
• prognosis
• progression
• vitamin D receptor

• aspirin
• calcium
• chemoprevention
• colorectal cancer
• metformin

• Child
• Child, Preschool
• China/ethnology
• Female
• Humans
• Male
• Models, Genetic
• Polymorphism, Restriction Fragment Length
• Receptors, Calcitriol/genetics
• Risk Factors
• Urolithiasis/ethnology
• Urolithiasis/genetics

• The Natural Science Foundatin of Guangdong Province
• Science and Technology Planning Project of Guangdong Province, China

• Clear cell papillary renal cell carcinoma
• Vitamin D receptor

• Animals
• Anti-Inflammatory Agents/pharmacology
• Anti-Inflammatory Agents/therapeutic use
• Antineoplastic Agents/pharmacology
• Antineoplastic Agents/therapeutic use
• Antioxidants/pharmacology
• Antioxidants/therapeutic use
• Gene Expression Regulation, Neoplastic/drug effects
• Hormones/metabolism
• Humans
• Metabolic Networks and Pathways/drug effects
• Neoplasms/drug therapy
• Neoplasms/genetics
• Neoplasms/metabolism
• Neoplasms/pathology
• Receptors, Calcitriol/metabolism
• Vitamin D/metabolism
• Vitamin D/pharmacology
• Vitamin D/therapeutic use

Vitamin D is implicated in the etiology of cancers of the gastrointestinal tract, usually characterized by alteration in the APC/β-catenin/TCF tumor suppressor pathway. The vitamin D receptor (VDR) is also implicated in cardiovascular and skin diseases as well as in immunity. Activated VDR can indirectly alter β-catenin nuclear localization and directly suppress β-catenin/TCF mediated transcriptional activity. We treated VDR null mice with the carcinogen azoxymethane (AOM) and generated mice bearing a mutated APC (hypomorph) on a VDR null background (Apc^1638N/+Vdr^−/−). VDR null mice do not develop GI or extra-colonic tumors but loss of VDR decreased intestinal tumor latency and increased progression to adenocarcinoma in both models. AOM treatment of VDR null mice also caused squamous cell carcinoma of the anus. Although levels and distribution of total or activated β-catenin in the epithelial component of tumors were unaffected by loss of VDR, β-catenin dependent cyclin D1 expression was affected suggesting a direct VDR effect on β-catenin co-activator activity. Extra-colonic mucosa manifestations in Apc^1638N/+Vdr^−/− animals included increased nuclear β-catenin in submucosal stromal cells, spleno- and cardiomegaly and large epidermoid cysts characteristic of the FAP variant, Gardner's syndrome. Consistent with this, SNPs in the VDR, vitamin D binding protein and CYP24 as well as mutations in APC distal to codon 850 were strongly associated with Gardners syndrome in a cohort of 457 FAP patients, This work suggests that alterations in the vitamin D/VDR axis are important in Gardner's syndrome, as well as in the etiology of anal cancer.

• anal cancer
• azoxymethane
• colon cancer
• gardner’s syndrome
• vitamin D receptor

• CYP27B1
• cancer
• cardiovascular
• immune system
• skin
• vitamin D

• Analogue
• Calcitriol
• Colorectal cancer
• Gemini
• Vitamin D

• Animals
• Antigens, CD
• Antineoplastic Agents/chemistry
• Antineoplastic Agents/pharmacology
• Apoptosis/drug effects
• Binding Sites
• Cadherins/genetics
• Cadherins/metabolism
• Cell Movement/drug effects
• Colorectal Neoplasms/drug therapy
• Colorectal Neoplasms/genetics
• Colorectal Neoplasms/metabolism
• Colorectal Neoplasms/pathology
• Disease Progression
• Gene Expression Regulation, Neoplastic
• HCT116 Cells
• Humans
• Ligands
• Mice
• Mice, Nude
• Molecular Docking Simulation
• Protein Binding
• Protein Interaction Domains and Motifs
• Receptors, Calcitriol/antagonists & inhibitors
• Receptors, Calcitriol/chemistry
• Receptors, Calcitriol/genetics
• Receptors, Calcitriol/metabolism
• Vitamin D/analogs & derivatives
• Vitamin D/chemistry
• Vitamin D/pharmacology
• Xenograft Model Antitumor Assays
• bcl-2-Associated X Protein/genetics
• bcl-2-Associated X Protein/metabolism
• beta Catenin/genetics
• beta Catenin/metabolism

Vitamin D activity is controlled by vitamin D receptors (VDRs), which are affected by different genetic polymorphisms, including TaqI and Apal restriction fragment length polymorphisms (RFLPs), which have been reported to be associated with several diseases. The aim of this study was to determine the frequency and the association of VDR gene polymorphisms with idiopathic nephrotic syndrome (INS) and steroid responsiveness in Kuwaiti children.

Genotypes of the VDR TaqI gene polymorphism and the Apal gene polymorphism were analyzed using polymerase chain reaction-RFLP in 78 INS patients and 56 matched controls.

A total of 78 INS (62 steroid sensitive [SS] and 16 steroid resistant [SR]) patients with a mean age of 6.5±3.1 years were studied. Male:female ratio was 2:1. The TT genotype of VDR–TaqI polymorphism was detected in 41% of the INS patients compared to 42% of the controls (P=0.816). The heterozygous TC genotype was detected in 33% of INS patients compared to 46% of the controls (P=0.462). The CC genotype was detected in 25.6% of INS patients and 21% of the controls (P=0.719). The C-allele frequency, in its homozygous and heterozygous forms, was 71% in INS patients compared to 63% in the controls (P=0.342). Similarly, no significant difference was detected in terms of VDR–Apal polymorphism in INS patients compared to the controls for all the three genotypes (P=0.76, P=0.207, and P=0.364, respectively, for GG, GT, and TT genotypes). The T-allele frequency, in its homozygous and heterozygous forms, was 89% in INS patients compared to 93% in the controls (P=0.076). No significant difference was found in any of the allele frequencies between SS and SR subgroups when compared with each other or when compared to the controls.

Our data do not support the use of VDR–TaqI or –Apal gene polymorphisms as genetic markers of INS nor do they predict steroid responsiveness in children with the disease.

• genotype
• idiopathic nephrotic syndrome
• polymorphism
• steroid resistant
• steroid sensitive

1,25 dihydroxyvitamin D (1,25(OH)₂D), the active metabolite of vitamin D, and calcium regulate epidermal differentiation. 1,25(OH)₂D exerts its effects through the vitamin D receptor (VDR), a transcription factor in the nuclear hormone receptor family, whereas calcium acts through the calcium sensing receptor (Casr), a membrane bound member of the G protein coupled receptor family. We have developed mouse models in which the Vdr and Casr have been deleted in the epidermis (^epidVdr^−∕− and ^epidCasr^−∕−). Both genotypes show abnormalities in calcium induced epidermal differentiation in vivo and in vitro, associated with altered hedgehog (HH) and β–catenin signaling that when abnormally expressed lead to basal cell carcinomas (BCC) and trichofolliculomas, respectively. The Vdr^−∕− mice are susceptible to tumor formation following UVB or chemical carcinogen exposure. More recently we found that the keratinocytes from these mice over express long non-coding RNA (lncRNA) oncogenes such as H19 and under express lncRNA tumor suppressors such as lincRNA-21. Spontaneous tumors have not been observed in either the ^epidVdr^−∕− or ^epidCasr^−∕−. But in mice with epidermal specific deletion of both Vdr and Casr (^epidVdr^−∕−/^epidCasr^−∕− [DKO]) tumor formation occurs spontaneously when the DKO mice are placed on a low calcium diet. These results demonstrate important interactions between vitamin D and calcium signaling through their respective receptors that lead to cancer when these signals are disrupted. The roles of the β–catenin, hedgehog, and lncRNA pathways in predisposing the epidermis to tumor formation when vitamin D and calcium signaling are disrupted will be discussed.

• UVB
• calcium sensing receptor
• hedgehog
• long non coding RNA
• squamous cell carcinoma
• vitamin D receptor
• β–catenin

Snail1 is a zinc-finger transcription factor, which plays a role in colorectal cancer development by silencing E-cadherin expression and inducing epithelialmesenchymal transition (EMT). During EMT tumour cells acquire a mesenchymal phenotype that is responsible for their invasive activities. Consequently, Snail1 expression in colorectal cancer is usually associated with progression and metastasis. Some studies revealed that about 77% of colon cancer samples display Snail1 immunoreactivity both in activated fibroblasts and in carcinoma cells that have undergone EMT. Therefore, expression of this factor in the stroma may indicate how many cells possess the abilities to escape from the primary tumour mass, invade the basal lamina and colonise distant target organs. Blocking snail proteins activity has the potential to avert cancer cell metastasis by interfering with such cellular processes as remodelling of the actin cytoskeleton, migration and invasion, which are clearly associated with the aggressive phenotype of the disease. Moreover, the link between factors from the snail family and cancer stem cells suggests that inhibitory agents may also prove their potency as inhibitors of cancer recurrence.

• Snail1
• VDR
• Wnt signalling
• calcitriol
• colorectal cancer

• Colon cancer
• Inflammation
• Snail1
• Snail2
• Vitamin D receptor

• Antineoplastic Combined Chemotherapy Protocols/pharmacology
• Cell Movement/drug effects
• Cell Proliferation/drug effects
• Colonic Neoplasms/drug therapy
• Colonic Neoplasms/metabolism
• Colonic Neoplasms/pathology
• Drug Synergism
• HT29 Cells
• Humans
• Receptors, Calcitriol/metabolism
• Retinoid X Receptor alpha/metabolism
• Silybin
• Silymarin/administration & dosage
• Silymarin/pharmacology
• Snail Family Transcription Factors
• Transcription Factors/metabolism
• Tumor Necrosis Factor-alpha/metabolism
• Vitamin D/administration & dosage
• Vitamin D/analogs & derivatives
• Vitamin D/pharmacology

• R03 CA176738 NCI NIH HHS
• CA176738 NCI NIH HHS

• Calcitriol
• Vitamin D analogues
• cancer prevention

• Animals
• Antineoplastic Agents/chemistry
• Antineoplastic Agents/therapeutic use
• Breast Neoplasms/diagnosis
• Breast Neoplasms/epidemiology
• Breast Neoplasms/prevention & control
• Chemoprevention/trends
• Clinical Trials as Topic
• Colorectal Neoplasms/diagnosis
• Colorectal Neoplasms/epidemiology
• Colorectal Neoplasms/prevention & control
• Female
• Growth Inhibitors/chemistry
• Growth Inhibitors/therapeutic use
• Humans
• Immunologic Factors/chemistry
• Immunologic Factors/therapeutic use
• Male
• Neoplasms/diagnosis
• Neoplasms/epidemiology
• Neoplasms/prevention & control
• Prostatic Neoplasms/diagnosis
• Prostatic Neoplasms/epidemiology
• Prostatic Neoplasms/prevention & control
• Vitamin D/analogs & derivatives
• Vitamin D/therapeutic use

• DNA damage repair
• LncRNA
• calcium
• catenin
• caténine
• epidermis
• hedgehog
• long ARNnc
• réparation du dommage à l’ADN
• épiderme

Colorectal cancer incidence has been rising strongly in parallel with economic development. In the past few decades, much has been learned about the lifestyle, dietary and medication risk factors for this malignancy. With respect to lifestyle, compelling evidence indicates that prevention of weight gain and maintenance of a reasonable level of physical activity can positively influence in lowering the risk. Although there is controversy about the role of specific nutritional factors, consideration of dietary pattern as a whole appears useful for formulating recommendations. Though quite often recommended, the role for many supplements, including omega-3, vitamin D, folate, and vitamin B6, remains unsettled. Only calcium and vitamin D supplementation appear to add a modest benefit, particularly in those with a low daily intake. With regard to chemoprevention, medications such as aspirin and nonsteroidal anti-inflammatory drugs, and postmenopausal hormonal replacement for women might be associated with substantial reductions in colorectal cancer risk, though their utility is affected by their side effect profile. However, the role of agents such as statins, bisphosphonates and antioxidants have yet to be determined. Ultimately, primary prevention strategies focusing on modifying environmental, lifestyle risk factors, and chemopreventive drugs are options that have already been tested, and may impact on colon cancer incidence.

• Primary prevention
• Colorectal cancer
• Physical activity
• Diet
• Chemoprevention

• Anticarcinogenic Agents/administration & dosage
• Colorectal Neoplasms/diagnosis
• Colorectal Neoplasms/epidemiology
• Colorectal Neoplasms/prevention & control
• Diet/adverse effects
• Dietary Supplements
• Exercise
• Female
• Humans
• Incidence
• Life Style
• Male
• Nutritional Status
• Primary Prevention/methods
• Recommended Dietary Allowances
• Risk Assessment
• Risk Factors
• Risk Reduction Behavior
• Sex Factors

• vitamin d
• vitamin d receptor
• cyp27b1
• cyp24a1
• cancer

• Animals
• Humans
• Neoplasms/drug therapy
• Neoplasms/epidemiology
• Neoplasms/pathology
• Neoplasms/physiopathology
• Neoplasms/prevention & control
• Vitamin D/physiology
• Vitamin D/therapeutic use
• Vitamins/physiology
• Vitamins/therapeutic use

• P01 AR039448 NIAMS NIH HHS
• P41 RR001614 NCRR NIH HHS
• R01 AR038386 NIAMS NIH HHS
• R01 AR050023 NIAMS NIH HHS

Autoimmunity has been associated with vitamin D deficiency and resistance, with gene polymorphisms related to vitamin D metabolism frequently described in affected patients. High doses of vitamin D3 may conceivably compensate for inherited resistance to its biological effects. This study aimed to assess the efficacy and safety of prolonged high-dose vitamin D3 treatment of patients with psoriasis and vitiligo. Nine patients with psoriasis and 16 patients with vitiligo received vitamin D3 35,000 IU once daily for six months in association with a low-calcium diet (avoiding dairy products and calcium-enriched foods like oat, rice or soya “milk”) and hydration (minimum 2.5 L daily). All psoriasis patients were scored according to “Psoriasis Area and Severity Index” (PASI) at baseline and after treatment. Evaluation of clinical response of vitiligo patients required a quartile grading scale. All patients presented low vitamin D status (serum 25(OH)D3 ≤ 30 ng/mL) at baseline. After treatment 25(OH)D3 levels significantly increased (from 14.9 ± 7.4 to 106.3 ± 31.9 ng/mL and from 18.4 ± 8.9 to 132.5 ± 37.0 ng/mL) and PTH levels significantly decreased (from 57.8 ± 16.7 to 28.9 ± 8.2 pg/mL and from 55.3 ± 25.0 to 25.4 ± 10.7 pg/mL) in patients with psoriasis and vitiligo respectively. PTH and 25(OH)D3 serum concentrations correlated inversely. The PASI score significantly improved in all nine patients with psoriasis. Fourteen of 16 patients with vitiligo had 25–75% repigmentation. Serum urea, creatinine and calcium (total and ionized) did not change and urinary calcium excretion increased within the normal range. High-dose vitamin D3 therapy may be effective and safe for vitiligo and psoriasis patients.

• 25(OH)D3
• autoimmunity
• calcium
• high dose
• psoriasis
• toxicity
• treatment
• vitamin D
• vitiligo

• Asian People/genetics
• Carcinoma/blood
• Carcinoma/genetics
• Case-Control Studies
• Colorectal Neoplasms/blood
• Colorectal Neoplasms/epidemiology
• Colorectal Neoplasms/genetics
• Female
• Genetic Predisposition to Disease
• Genotype
• Humans
• Jordan
• Male
• Polymorphism, Genetic
• Receptors, Calcitriol/genetics
• Risk Factors
• Vitamin D/analogs & derivatives
• Vitamin D/blood
• Vitamin D Deficiency/blood
• Vitamin D Deficiency/epidemiology

Colorectal cancer (CRC) is the third cause of cancer-related morbidity and mortality in America following lung cancer and stomach cancer. In China and other Asian countries, increasingly Westernized diets have led to a high incidence of CRC. The vitamin D receptor (VDR) can mediate 1,25(OH)₂D₃ to regulate cell growth and differentiation in a variety of normal tissues or tumor tissues. VDR gene polymorphisms are closely related to the occurrence and development of CRC. This article summarizes the recent progress in understanding the relationship between VDR and CRC in terms of the structure and function of VDR, mechanisms of CRC inhibition, correlation between VDR polymorphisms and CRC, and the development of analogs of VDR ligands.

• Vitamin D receptor
• 1,25-dihydroxyvitamin D₃
• Colorectal cancer

The Wnt/β-catenin signaling pathway is abnormally activated in most colorectal cancers and in a proportion of other neoplasias. This activation initiates or contributes to carcinogenesis by regulating the expression of a large number of genes in tumor cells. The active vitamin D metabolite 1α,25-dihydroxyvitamin D₃ (1,25(OH)₂D₃) inhibits Wnt/β-catenin signaling by several mechanisms at different points along the pathway. Additionally, paracrine actions of 1,25(OH)₂D₃ on stromal cells may also repress this pathway in neighbouring tumor cells. Here we review the molecular basis for the various mechanisms by which 1,25(OH)₂D₃ antagonizes Wnt/β-catenin signaling, preferentially in human colon carcinoma cells, and the consequences of this inhibition for the phenotype and proliferation rate. The effect of the vitamin D system on Wnt/β-catenin signaling and tumor growth in animal models will also be commented in detail. Finally, we revise existing data on the relation between vitamin D receptor expression and vitamin D status and the expression of Wnt/β-catenin pathway genes and targets in cancer patients.

• cancer
• vitamin d
• calcium
• cyp27b1
• 1α-hydroxylase
• cyp24a1
• 24-hydroxylase
• cyp27a1
• cyp2r1
• 25-hydroxylase
• calcium sensing receptor
• casr
• colorectal cancer
• proliferation
• methylation
• epigenetics
• splice variants
• cox-2
• wnt

• Animals
• Calcium/physiology
• Cell Transformation, Neoplastic
• Humans
• Mixed Function Oxygenases/metabolism
• Neoplasms/enzymology
• Neoplasms/metabolism
• Neoplasms/pathology
• Rats
• Vitamin D/blood
• Vitamin D/physiology

• P 22200 Austrian Science Fund FWF

• 25-hydroxy-vitamin D
• Vitamin D
• cancer
• immunity
• inflammation

• Animals
• Apoptosis/drug effects
• Biomarkers/metabolism
• Cell Differentiation/drug effects
• Cell Line, Transformed
• Cell Lineage/drug effects
• Cell Proliferation/drug effects
• Cell Shape/drug effects
• Cells, Cultured
• Cellular Senescence/drug effects
• Colony-Forming Units Assay
• Fibroblast Growth Factor-23
• Gene Expression Regulation/drug effects
• Humans
• Immunohistochemistry
• Immunophenotyping
• Mesenchymal Stem Cells/cytology
• Mesenchymal Stem Cells/drug effects
• Mesenchymal Stem Cells/enzymology
• Mesenchymal Stem Cells/metabolism
• Mice
• Multipotent Stem Cells/cytology
• Multipotent Stem Cells/drug effects
• Multipotent Stem Cells/metabolism
• Reactive Oxygen Species/metabolism
• Receptors, Calcitriol/metabolism
• Time Factors
• Vitamin D/analogs & derivatives
• Vitamin D/pharmacology
• beta-Galactosidase/metabolism