Meta-analysis of Vitamin D–Binding Protein and Cancer Risk

Tagliabue, Elena; Raimondi, Sara; Gandini, Sara

doi:10.1158/1055-9965.epi-15-0262

Cited by 43 publications

(37 citation statements)

References 61 publications

(60 reference statements)

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“…22,23 A recent meta-analysis examined VDBP levels in relation to the overall risk of multiple cancers (basal cell carcinoma, bladder, breast, colon and rectum, endometrium, liver, esophagus, stomach, melanoma, pancreas, prostate, and kidney) and found borderline decreased risk in individuals with higher VDBP levels. 24 To date, four epidemiologic studies have assessed VDBP levels in relation to prostate cancer risk with mixed findings: one study found an inverse association between VDBP levels and prostate cancer risk in African Americans, 25 whereas the others reported a null association. [26][27][28] Notably, all these studies included both aggressive and non-aggressive diseases, yet none of the studies reported that the association between VDBP levels and prostate cancer risk was modified by disease aggressiveness.…”

Section: Discussionmentioning

confidence: 99%

Circulating 25‐hydroxyvitamin D, vitamin D binding protein and risk of advanced and lethal prostate cancer

Yuan

Shui

Wilson

et al. 2018

Intl Journal of Cancer

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We previously found that higher total 25‐hydroxyvitamin D [25(OH)D] levels were associated with lower risk of lethal prostate cancer. However, the relationships of bioavailable 25(OH)D and vitamin D binding protein (VDBP) with risk of advanced and lethal prostate cancer are unclear. In a prospective case–control study of 156 pairs of advanced prostate cancer cases and controls, we directly measured prediagnostic circulating 25(OH)D and VDBP and calculated bioavailable 25(OH)D using a validated formula. We examined the association of bioavailable 25(OH)D and VDBP levels with risk of advanced and lethal prostate cancer and whether total 25(OH)D levels interacted with VDBP levels to affect the risk. Conditional logistic models were used to calculate odds ratios (ORs) and 95% confidence intervals (CIs). Compared to total 25(OH)D (ptrend = 0.02), bioavailable 25(OH)D levels were not more strongly associated with risk of advanced prostate cancer (ptrend = 0.14). Although VDBP levels were not associated with risk of advanced prostate cancer (ptrend = 0.16), we observed an interaction between total 25(OH)D levels and VDBP levels in relation to risk of advanced prostate cancer (pinteraction = 0.03). Compared to those with total 25(OH)D levels below the median and VDBP levels above the median (at highest risk), men with both levels above the median had a multivariable‐adjusted OR of 0.31 (95% CI, 0.15–0.65) for advanced prostate cancer. We observed similar results when we restricted the analyses to 116 lethal prostate cancer cases and their controls. Our data suggest that VDBP levels may modify the association between total 25(OH)D levels and risk of advanced and lethal prostate cancer.

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Section: Discussionmentioning

confidence: 99%

Circulating 25‐hydroxyvitamin D, vitamin D binding protein and risk of advanced and lethal prostate cancer

Yuan

Shui

Wilson

et al. 2018

Intl Journal of Cancer

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“…DBP levels in the circulation are marginally associated with cancer risk (10). Analysis of matched NAF samples from women with cancer in one breast but not the other identified DBP as increased in the breasts with cancer (20).…”

Section: Discussionmentioning

confidence: 91%

“…The major function of DBP is to bind and transport vitamin D and its metabolites (9). Epidemiologic evidence supports a role for DBP in cancer etiology (10). DBP has been demonstrated to be present in different body fluids (serum, urine, breast milk, ascitic fluid, cerebrospinal fluid, saliva and seminal fluid).…”

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confidence: 99%

Vitamin D3 Treatment Influences PGE2 and TGFβ in Normal and Increased Breast Cancer Risk Women

Qin

Holick

Sörensen³

et al. 2016

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Abstract. Background Preclinical (3) and epidemiological (4) studies suggest that the anti-inflammatory agent celecoxib also reduces BCa risk. Celecoxib inhibits COX2 through direct binding to the molecule, preventing the conversion of arachidonic acid to PGE 2 and other PGs (5). 1,25(OH) 2 D3 is also reported to alter the transforming growth factor (TGF)β pathway, which is important for the prevention and progression of breast carcinogenesis (6).Breast cells have the enzymatic machinery to convert 25(OH)D3 to 1,25(OH) 2 D3 (7). Increasing circulating levels of 25(OH)D3 is thought to result in an increased production of 1,25(OH) 2 D3 locally within breast cells, which, in turn, can affect their proliferation and differentiation (7).Thus, there is potential for a synergistic effect of improving the vitamin D status with celecoxib in the breast, with the local production of 1,25(OH) 2 D3 acting to reduce production of COX2, celecoxib to prevent the conversion of arachidonic acid to PGE 2 and 1,25(OH) 2 D3 also increasing the metabolism of the PGE 2 produced. We previously reported in a preliminary study that 2,000 IU vitamin D (but not vitamin D plus celecoxib) significantly decreased PGE 2 in the breast nipple aspirate fluid (NAF) of normal-risk women (8). To validate our preliminary findings and to determine if they also applied to women at increased breast cancer risk, we now report our findings of a larger cohort of normal-risk women, as well as a cohort of high-risk women who received placebo, 400 IU vitamin D3, 2,000 IU vitamin D3 or 2,000 IU vitamin D3 plus celecoxib. We also evaluated, vitamin D binding 5347

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“…Several studies [80] have investigated serum DBP levels and DBP polymorphisms in association with cancer risk. Humphries [81] has validated DBP as one of the novel biomarkers of human gastric cancer.…”

Section: Vitamin D/vdr and Gastric Cancer: Epidemiological Datamentioning

confidence: 99%

Pathogenic roles of alterations in vitamin D and vitamin D receptor in gastric tumorigenesis

Yang

Zhao

et al. 2017

Oncotarget

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Gastric cancer is currently the second leading cause of cancer-related death worldwide, especially in Japan, Korea and China, and the 5-year survival rate of gastric cancer is less than 30%. Thus, it is important to shed more lights on novel agents to prevent gastric cancer or to improve survival rate of the patients. Vitamin D not only maintains calcium and bone homeostasis, but also mostly inhibits tumor genesis, invasion, and metastasis through activation of vitamin D receptor. Although epidemiological results are not consistent, accumulating evidence from gastric cancer cells, animal models, and clinical trials suggest that vitamin D deficiency may increase the risk and mortality of gastric cancer, but vitamin D supplement might be a safe and economical way to prevent or treat gastric cancer. Here, we reviewed the current studies on vitamin D and its receptor and focused on the pathogenic roles of their alterations in gastric tumorigenesis.

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Meta-analysis of Vitamin D–Binding Protein and Cancer Risk

Cited by 43 publications

References 61 publications

Circulating 25‐hydroxyvitamin D, vitamin D binding protein and risk of advanced and lethal prostate cancer

Circulating 25‐hydroxyvitamin D, vitamin D binding protein and risk of advanced and lethal prostate cancer

Vitamin D3 Treatment Influences PGE2 and TGFβ in Normal and Increased Breast Cancer Risk Women

Pathogenic roles of alterations in vitamin D and vitamin D receptor in gastric tumorigenesis

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