Breast cancer survivors and vitamin D: A review

Hines, Stephanie L.; Jörn, H.; Thompson, Kristine M.; Larson, Jan M.

doi:10.1016/j.nut.2009.08.020

Cited by 39 publications

(28 citation statements)

References 40 publications

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“…Risk factors associated with environment and lifestyle include family history of lung cancer, history of pulmonary diseases, nutrition, air pollution, cigarette smoke, and exposure to radiation, asbestos and radon. Furthermore, recent epidemiological studies have shown that exposure to solar radiation (in particular ultraviolet B (UVB) radiation) and vitamin D intake is connected with decreased incidence of many cancers including lung, breast, prostate and colon cancer [2,3,4,5,6]. The mortality of lung cancer is lowest during the autumn and summer months, which are associated with the highest vitamin D levels in a year [7].…”

Section: Introductionmentioning

confidence: 99%

Vitamin D-Related Gene Polymorphisms, Plasma 25-Hydroxy-Vitamin D, Cigarette Smoke and Non-Small Cell Lung Cancer (NSCLC) Risk

Cheng

Yang

2016

IJMS

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Epidemiological studies regarding the relationship between vitamin D, genetic polymorphisms in the vitamin D metabolism, cigarette smoke and non-small cell lung cancer (NSCLC) risk have not been investigated comprehensively. To search for additional evidence, the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique and radioimmunoassay method were utilized to evaluate 5 single-nucleotide polymorphisms (SNPs) in vitamin D receptor (VDR), 6 SNPs in 24-hydroxylase (CYP24A1), 2 SNPs in 1α-hydroxylase (CYP27B1) and 2 SNPs in vitamin D-binding protein (group-specific component, GC) and plasma vitamin D levels in 426 NSCLC cases and 445 controls from China. Exposure to cigarette smoke was ascertained through questionnaire information. Multivariable linear regressions and mixed effects models were used in statistical analysis. The results showed that Reference SNP rs6068816 in CYP24A1, rs1544410 and rs731236 in VDR and rs7041 in GC were statistically significant in relation to reduction in NSCLC risk (p < 0.001–0.05). No significant connection was seen between NSCLC risk and overall plasma 25-hydroxyvitamin D [25(OH)D] concentrations, regardless of smoking status. However, the mutation genotype of CYP24A1 rs6068816 and VDR rs1544410 were also significantly associated with increased 25(OH)D levels only in both the smoker and non-smoker cases (p < 0.01–0.05). Meanwhile, smokers and non-smokers with mutated homozygous rs2181874 in CYP24A1 had significantly increased NSCLC risk (odds ratio (OR) = 2.14, 95% confidence interval (CI) 1.47–3.43; p = 0.031; OR = 3.57, 95% CI 2.66–4.74; p = 0.019, respectively). Smokers with mutated homozygous rs10735810 in VDR had significantly increased NSCLC risk (OR = 1.93, 95% CI 1.41–2.76; p = 0.015). However, smokers with mutated homozygous rs6068816 in CYP24A1 had significantly decreased NSCLC risk (OR = 0.43, 95% CI 0.27–1.02; p = 0.006); and smokers and non-smokers with mutated homozygous rs1544410 in VDR had significantly decreased NSCLC risk (OR = 0.51, 95% CI 0.34–1.17; p = 0.002; OR = 0.26, 95% CI 0.20–0.69; p = 0.001, respectively). There are significant joint effects between smoking and CYP24A1 rs2181874, CYP24A1 rs6068816, VDR rs10735810, and VDR rs1544410 (p < 0.01–0.05). Smokers with mutated homozygous rs10735810 in VDR had significantly increased NSCLC risk (OR = 1.93, 95% CI 1.41–2.76; p = 0.015). In summary, the results suggested that the lower the distribution of vitamin D concentration, the more the genetic variations in CYP24A1, VDR and GC genes may be associated with NSCLC risk. In addition, there are significant joint associations of cigarette smoking and vitamin D deficiency on NSCLC risk.

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Section: Introductionmentioning

confidence: 99%

Vitamin D-Related Gene Polymorphisms, Plasma 25-Hydroxy-Vitamin D, Cigarette Smoke and Non-Small Cell Lung Cancer (NSCLC) Risk

Cheng

Yang

2016

IJMS

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“…However, the clinical application of 1␣,25(OH) 2 D 3 for inhibition of breast cancer was limited by hypercalcemic toxicity, which was detected in 20 to 30% of patients in clinical trials (Hellström et al, 1990;Deeb et al, 2007). Therefore, numerous synthetic vitamin D 3 analogs have been developed for better anticancer efficacy with lower toxicity (Hines et al, 2010). Our studies demonstrated that Gemini vitamin D analogs inhibited the formation and growth of estrogen receptor-positive mammary tumors in vivo without hypercalcemic toxicity (Lee et al, 2008) and suppressed mammary tumor growth in the ErbB2-overexpressing transgenic mice .…”

Section: Introductionmentioning

confidence: 99%

A Novel Gemini Vitamin D Analog Represses the Expression of a Stem Cell Marker CD44 in Breast Cancer

Lee²,

Smolarek³

et al. 2011

Molecular Pharmacology

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CD44 is a multifunctional transmembrane protein involved in cell proliferation, angiogenesis, invasion, and metastasis. CD44 is identified as a cancer stem cell marker, and the CD44-positive breast cancer cells are enriched in residual breast cancer cell populations after conventional therapies, suggesting that CD44 may be an important target for cancer prevention and therapy. Therefore, we investigated for the inhibitory effect of a novel Gemini vitamin D analog, 1␣,25-dihydroxy-20R-21(3-hydroxy-3-deuteromethyl-4,4,4-trideuterobutyl)-23-yne-26,27-hexafluoro-cholecalciferol (BXL0124), on mammary tumor growth and CD44 expression in MCF10DCIS.com human breast cancer in vitro and in vivo. MCF10DCIS.com cells were injected into mammary fat pads in immunodeficient mice, and BXL0124 was then administered intraperitoneally (0.1 g/kg body weight) or orally (0.03 or 0.1 g/kg body weight) 6 days a week for 5 weeks. At necropsy, mammary tumors and blood were collected for evaluating tumor growth, CD44 expression, and serum calcium level. BXL0124 suppressed mammary tumor growth and markedly decreased the expression of CD44 protein in MCF10DCIS xenograft tumors without causing hypercalcemic toxicity. BXL0124 also inhibited the expression of CD44 protein and mRNA as well as the transcriptional activity of the CD44 promoter in cultured MCF10DCIS.com cells. The repression of CD44 expression induced by BXL0124 was blocked by siRNA vitamin D receptor (VDR), indicating that the regulation of CD44 expression by BXL0124 is a VDRdependent event. The novel Gemini vitamin D analog, BXL0124, represses CD44 expression in MCF10DCIS.com cells in vitro and in xenograft tumors, suggesting an inhibitory role of a Gemini vitamin D derivative on breast cancer stem cells.

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“…On souligne que la supplémentation à la dose quotidienne de 400 UI est ineffi cace puisque les taux sériques ne sont corrigés que chez 15 % des patientes au bout d'un an [23]. La supplémentation doit donc s'effectuer à la dose de 50 000 UI par semaine sur une période initiale d'un à trois mois en fonction des taux sériques de vit 25(OH)D [41], ce qui permet d'atteindre les taux recommandés de 36-40 ng/ml (à ces doses le risque de toxicité qui survient au-delà de 150 ng/ml paraît très faible) [43].…”

Section: Vit D (Niveaux 3-4)unclassified

“…Dans l'état actuel des connaissances, le bénéfi ce majeur de la supplémentation en vit D porte sur le risque d'ostéoporose à long terme [41]. D'autres bénéfi ces sont cependant attendus : dans deux séries avec un effectif limité (29 et • 42 patientes), la supplémentation en vit D à forte dose (50 000 UI/semaine pendant 12 semaines) semble amé-liorer les arthralgies liées au traitement par inhibiteurs Guidelines de l'aromatase, sans toxicité évidente [43,76] ; l'effet sur les arthralgies semble important pour des taux séri-ques de vit D dépassant 66 ng/ml [43] (niveau 4) ; un effet favorable sur le bien-être et les scores de • qualité de vie est suggéré mais n'a été démontré que dans la population générale [41] (niveau 4) ; la supplémentation évite enfi n l'augmentation de la • PTH observée chez les patientes traitées par bisphosphonates et carencées en vit D, mais des doses de 400 UI/j sont insuffi santes [4,72] (niveau 3).…”

Section: Vit D (Niveaux 3-4)unclassified