The effect of 1,25-dihydroxyvitamin D3 on lymphoma cell lines and expression of vitamin D receptor in lymphoma

Hickish, Tamas; Cunningham, David; Colston, K. W.; Millar, B. Cherie; Sandle, J; Mackay, Alan; Soukop, M.; Sloane, J P

doi:10.1038/bjc.1993.406

Cited by 75 publications

(57 citation statements)

References 32 publications

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“…Until recently, the strongest evidence came from the observation that the induction of vitamin D 3 synthesis in the skin by UVR 27 could have a protective effect against lymphoma development. This hypothetical mechanism is supported by the observation that vitamin D 3 promotes differentiation and inhibits proliferation of lymphoma cells in vitro, 28 and by the strong expression of the vitamin D receptor on HL tumor cells. 29 However, a pooled analysis of 10 cohort studies found no association between prediagnostic serum 25-hydroxyvitamin D levels and risk of NHL or its major histologic subtypes.…”

supporting

confidence: 53%

Exposure to UV radiation and risk of Hodgkin lymphoma: a pooled analysis

Monnereau

Glaser

Schupp

et al. 2013

Blood

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• Our pooled analysis found an inverse association between several measures of UVR exposure and Hodgkin lymphoma. • Significant UVR-related inverse associations of EBV-positive HL with a doseresponse relationship support etiologic heterogeneity in HL.Ultraviolet radiation (UVR) exposure has been inversely associated with Hodgkin lymphoma (HL) risk, but only inconsistently, only in a few studies, and without attention to HL heterogeneity. We conducted a pooled analysis of HL risk focusing on type and timing of UVR exposure and on disease subtypes by age, histology, and tumor-cell Epstein-Barr virus (EBV) status. Four case-control studies contributed 1320 HL cases and 6381 controls. We estimated lifetime, adulthood, and childhood UVR exposure and history of sunburn and sunlamp use. We used 2-stage estimation with mixed-effects models and weighted pooled effect estimates by inverse marginal variances. We observed statistically significant inverse associations with HL risk for UVR exposures during childhood and adulthood, sunburn history, and sunlamp use, but we found no significant doseresponse relationships. Risks were significant only for EBV-positive HL (pooled odds ratio, 0.56; 95% confidence interval, 0.35 to 0.91 for the highest overall UVR exposure category), with a significant linear trend for overall exposure (P 5 .03). Pooled relative risk estimates were not heterogeneous across studies. Increased UVR exposure may protect against HL, particularly EBV-positive HL. Plausible mechanisms involving UVR induction of regulatory T cells or the cellular DNA damage response suggest opportunities for new prevention targets. (Blood. 2013;122(20):3492-3499)

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supporting

confidence: 53%

Exposure to UV radiation and risk of Hodgkin lymphoma: a pooled analysis

Monnereau

Glaser

Schupp

et al. 2013

Blood

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“…Experimental studies show that the active form of vitamin D, 1,25D 3 , has anti-proliferative and pro-differentiation effects on cells that possess vitamin D receptors, 49 including lymphocytes 50 and lymphoma cell lines. 51 There is also evidence that 1,25D 3 induces apoptosis and inhibits angiogenesis and tumour spread. 49,52 There is evidence too that plasma concentration of vitamin D is inversely associated with risk of colorectal and prostate cancers, [53][54][55][56] and some evidence that sun exposure may protect against these cancers.…”

Section: Resultsmentioning

confidence: 99%

Sun exposure may protect against non‐Hodgkin lymphoma: A case‐control study

Hughes

Armstrong

Vajdic

et al. 2004

Intl Journal of Cancer

139

103

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“…36,37 Further supporting a role for vitamin D in protection from cancer is the finding that genetic polymorphisms in the vitamin D receptor are associated with different mortality rates for breast, 38 colon, 39,40 prostate, 41 and rectal carcinomas. 42 The addition of vitamin D to cells from prostate carcinoma, 43 colon carcinoma, 34 melanoma, 44 NHL, 45 ovarian carcinoma, 46 and renal carcinoma 47 decreases the proliferation of these cells or induces differentiation in other cell types such as colonic HT 29 cells 48 and endometrial carcinoma cell lines. 49 Previous studies examining the effect of solar UV-B on malignancy used other measures of solar radiation including average annual solar radiation and SO 2 2,12 and haze.…”

Section: Discussionmentioning

confidence: 99%

An estimate of premature cancer mortality in the U.S. due to inadequate doses of solar ultraviolet‐B radiation

Grant

2002

Cancer

659

441

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BACKGROUNDThere are large geographic gradients in mortality rates for a number of cancers in the U.S. (e.g., rates are approximately twice as high in the northeast compared with the southwest). Risk factors such as diet fail to explain this variation. Previous studies have demonstrated that the geographic distributions for five types of cancer are related inversely to solar radiation. The purpose of the current study was to determine how many types of cancer are affected by solar radiation and how many premature deaths from cancer occur due to insufficient ultraviolet (UV)‐B radiation.METHODSUV‐B data for July 1992 and cancer mortality rates in the U.S. for between 1970–1994 were analyzed in an ecologic study.RESULTSThe findings of the current study confirm previous results that solar UV‐B radiation is associated with reduced risk of cancer of the breast, colon, ovary, and prostate as well as non‐Hodgkin lymphoma. Eight additional malignancies were found to exhibit an inverse correlation between mortality rates and UV‐B radiation: bladder, esophageal, kidney, lung, pancreatic, rectal, stomach, and corpus uteri. The annual number of premature deaths from cancer due to lower UV‐B exposures was 21,700 (95% confidence interval [95% CI], 20,400–23,400) for white Americans, 1400 (95% CI, 1100–1600) for black Americans, and 500 (95% CI, 400–600) for Asian Americans and other minorities.CONCLUSIONSThe results of the current study demonstrate that much of the geographic variation in cancer mortality rates in the U.S. can be attributed to variations in solar UV‐B radiation exposure. Thus, many lives could be extended through increased careful exposure to solar UV‐B radiation and more safely, vitamin D3 supplementation, especially in nonsummer months. Cancer 2002;94:1867–75. © 2002 American Cancer Society.DOI 10.1002/cncr.10427

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The effect of 1,25-dihydroxyvitamin D3 on lymphoma cell lines and expression of vitamin D receptor in lymphoma

Cited by 75 publications

References 32 publications

Exposure to UV radiation and risk of Hodgkin lymphoma: a pooled analysis

Exposure to UV radiation and risk of Hodgkin lymphoma: a pooled analysis

Sun exposure may protect against non‐Hodgkin lymphoma: A case‐control study

An estimate of premature cancer mortality in the U.S. due to inadequate doses of solar ultraviolet‐B radiation

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