Purpose Sunburns are an important risk factor for melanoma and those occurring in childhood are often cited as posing the greatest risk. We conducted a meta-analysis to quantify the magnitude of association for melanoma and sunburns during childhood, adolescence, adulthood and over a lifetime. Methods After reviewing over 1300 article titles and evaluating 270 articles in detail, we pooled ORs from 51 independent study populations for “ever” sunburned and risk of cutaneous melanoma. Among these, 26 studies reported results from dose-response analyses. Dose-response analyses were examined using both fixed-effects models and Bayesian random-effects models. Results An increased risk of melanoma was seen with increasing number of sunburns for all time-periods (childhood, adolescence, adulthood and lifetime). In an attempt to understand how risk between life-periods compares, we also report these same linear models on a scale of 5 sunburns per decade for each life-period. The magnitude of risk for 5 sunburns per decade is highest for adult and lifetime sunburns. Conclusions Overall, these results show an increased risk of melanoma with increasing number of sunburns during all life-periods, not just childhood. Prevention efforts should focus on reducing sunburns during all life-periods.

Studies of self-reported sexually transmitted infections (STI) suggesting an association with prostate cancer may reflect underreporting of such infections among nondiseased subjects. To reduce such bias, we studied archived sera in a cohort of U.S. military personnel known to have high rates of both STIs and prostate cancer. Using a nested case-control design, serum samples from 534 men who served on active duty between September 1, 1993 and September 1, 2003 were examined. Controls were individually matched to cases based on date of serum collection, date of birth, branch of service, military rank, marital status, and race. Each of the 267 case-control pairs had two serum samples: a recent serum sample, taken ∼1 year before the case's prostate cancer diagnosis, and an earlier serum sample, taken ∼8 years before diagnosis. Each serum specimen was studied for antibodies against human papillomavirus, herpes simplex virus-2 (HSV-2), and Chlamydia trachomatis. Logistic regression accounted for matching and potential confounding factors. Study data indicated no association between prostate cancer and serologic evidence of infections just before the reference date. However, a statistically significant association between prostate cancer and serologic evidence of HSV-2 infection was detected in the earlier sample (odds ratio, 1.60; 95% confidence interval, 1.05-2.44). The strength of this association increased when analyses were restricted to sera collected at least 60 months before diagnosis (odds ratio, 2.04; 95% confidence interval, 1.26-3.29; 204 pairs). If this association is causal, then our findings would suggest a long latency period for prostate cancer development after HSV-2 infection. (Cancer Epidemiol Biomarkers Prev 2009;18(10):2665-71)