Epidemiological studies have suggested a reduced risk of several cancers associated with high vitamin D status. We performed a systematic review with meta-analyses of observational studies of serum 25-hydroxyvitamin D level and colorectal, breast and prostate cancer and colonic adenoma. The literature of December 2009 was searched without language restriction. The meta-regression analysis was done to compute dose-response effects. Because in case-control studies, serum 25-hydroxyvitamin D level is measured after the diagnosis of cancer, separate analyses for case-control and prospective studies were done. We identified 35 independent studies. The seven studies on colorectal adenomas were heterogeneous in terms of endpoint and control for major confounding factors, and we did not perform a meta-analysis of these data. The summary relative risk (SRR) and (95% confidence interval) for a 10 ng/ml increase in serum 25-hydroxyvitamin D was 0.85 (0.79; 0.91) for colorectal cancer (2,630 cases in 9 studies); 0.89 (0.81;0.98) for breast cancer (6,175 cases in 10 studies); and 0.99 (0.95;1.03) for prostate cancer (3,956 cases in 11 studies). For breast cancer, case-control studies (3,030 cases) had major limitations and obtained SRR of 0.83 (0.79; 0.87) whereas SRR of prospective studies (3,145 cases) was 0.97 (0.92; 1.03). For colorectal and breast cancer, differences between cases and controls in the season of blood draw or in overweight/obesity or physical inactivity could not explain the results. In conclusion, a consistent inverse relationship between serum 25-hydroxyvitamin D levels and colorectal cancer was found. No association was found for breast and prostate cancer.Vitamin D can inhibit cell proliferation and promote apoptosis in vitro, and several tissues can locally produce the physiologically active form of vitamin D, 1a,25-dihydroxyvitamin D, which has anticarcinogenic properties.1 In addition, these tissues express the vitamin D receptor (VDR) that enables cellular action of the 1a,25-dihydroxyvitamin D. These basic research findings have strengthened the credibility of the hypothesis largely derived from ecological studies in the USA by which a higher vitamin D status would be associated with a lower risk of cancer. 2The 25-hydroxyvitamin D is the precursor of the physiologically active 1a,25-dihydroxyvitamin. The serum level of 25-hydroxyvitamin D is a result of skin exposure to sunlight, total vitamin D intake, and other factors such as age and skin pigmentation. Serum levels vary with season, with the highest levels in summer and autumn. 25-hydroxyvitamin D has a half-life in the circulatory system of about 2-3 weeks. 3In contrast, serum 1a,25-dihydroxyvitamin D is tightly biochemically regulated, except in situations of extreme deficiency, in keeping with its role in calcium homeostasis. It has a circulating half-time of 5-15 hr and exhibits little seasonal variability.3,4 For these reasons, the serum 25-hydroxyvitamin D is considered as reflecting the vitamin D status better than the serum 1a,25-dihy...

BackgroundNew Zealand and Australia have the highest incidence and mortality rates from cutaneous melanoma in the world. The predominantly fair-skinned New Zealanders and Australians both enjoy sun, tanned skin and the outdoors, and differences in these activities among generations have been important determinants of trends in melanoma mortality.We examined whether New Zealand trends in melanoma mortality mirror those in Australia, through detailed comparison of the trends in both countries from 1968 to 2007.MethodsFive-year age-specific and age-standardised mortality rates were calculated for each country for 5-year time periods. Tests for trends in age-specific rates were performed using the Mantel-Haenszel extension chi-square test. The age-adjusted mortality rate ratios for New Zealand/Australia were plotted against period of death to show relative changes in mortality over time. Age-specific mortality rates were plotted against period and the median year of birth to illustrate age-group and birth cohort effects. To compare the mortality of birth cohorts, age-adjusted melanoma mortality rate ratios were calculated for the birth cohorts in the quin-quennial tables of mortality rates.ResultsThe age-standardised mortality rate for melanoma increased in both sexes in New Zealand and Australia from 1968 to 2007, but the increase was greater in New Zealanders and women in particular. There was evidence of recent significant decreases in mortality in younger Australians and less so in New Zealand women aged under 45 years. Mortality from melanoma increased in successive generations born from about 1893 to 1918. In Australia, a decline in mortality started for generations born from about 1958 but in New Zealand there is possibly a decrease only in generations born since 1968.ConclusionsMortality trends in New Zealand and Australia are discrepant. It is too early to know if the pattern in mortality rates in New Zealand is simply a delayed response to melanoma control activities compared with Australia, whereby we can expect the same downward trend in similar age groups in the next few years. Specific research is needed to better understand and control the increases in mortality and thickness of melanoma in New Zealand.

New Zealand Maori, Pacific, and Asian people develop melanoma less frequently than New Zealand Europeans, but little is known about melanomas that develop in these people. We examined the characteristics of melanoma in these minority ethnic groups in New Zealand. In 2007, all first primary melanomas diagnosed from

Screening aims to detect breast cancer at an earlier stage than would occur if symptoms developed. The characteristics of breast cancer that are detectable at screening depend on both the physical properties of the screening test and specific anatomical features of breast cancer. As a result, breast cancer detected by screening is a select subset of all breast cancer existing in the population. Therefore, biomedical, clinical and epidemiological research into breast cancer using populations with access to screening can result in major bias. The biases, with examples, are explained.

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