Several epidemiological studies have determined the associations between coffee intake level and skin cancer risk; however, the results were not yet conclusive.,Herein, we conducted a systematic review and meta-analysis of the cohort and case-control studies for the association between coffee intake level and malignant melanoma (MM) risk.,Studies were identified through searching the PubMed and MEDLINE databases (to November, 2015).,Study-specific risk estimates were pooled under the random-effects model.,Two case-control studies (846 MM patients and 843 controls) and five cohort studies (including 844,246 participants and 5,737 MM cases) were identified.,For caffeinated coffee, the pooled relative risk (RR) of MM was 0.81 [95% confidential interval (95% CI) = 0.68-0.97; P-value for Q-test = 0.003; I2 = 63.5%] for those with highest versus lowest quantity of intake.,In the dose-response analysis, the RR of MM was 0.955 (95% CI = 0.912-0.999) for per 1 cup/day increment of caffeinated coffee consumption and linearity dose-response association was found (P-value for nonlinearity = 0.326).,Strikingly, no significant association was found between the decaffeinated coffee intake level and MM risk (pooled RR = 0.92, 95% CI = 0.81-1.05; P-value for Q-test = 0.967; I2 = 0%; highest versus lowest quantity of intake).,This meta-analysis suggested that caffeinated coffee might have chemo-preventive effects against MM but not decaffeinated coffee.,However, larger prospective studies and the intervention studies are warranted to confirm these findings.
The circadian clock controls the timing of the cell cycle in healthy tissues and clock disruption is known to increase tumourigenesis.,Melanoma is one of the most rapidly increasing forms of cancer and the precise molecular circadian changes that occur in a melanoma tumor are unknown.,Using a melanoma zebrafish model, we have explored the molecular changes that occur to the circadian clock within tumors.,We have found disruptions in melanoma clock gene expression due to a major impairment to the light input pathway, with a parallel loss of light-dependent activation of DNA repair genes.,Furthermore, the timing of mitosis in tumors is perturbed, as well as the regulation of certain key cell cycle regulators, such that cells divide arhythmically.,The inability to co-ordinate DNA damage repair and cell division is likely to promote further tumourigenesis and accelerate melanoma development.