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Temporal trends in the incidence of cutaneous malignant melanoma among Caucasians in the San Francisco-Oakland MSA

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Temporal changes in the incidence of cutaneous malignant melanoma (CMM) were examined in the San Franscisco-Oakland (California, United States) Metropolitan Statistical Area (MSA) between 1976 and 1987, using data from the population-based cancer registry. This analysis was conducted after the completion of a project designed to eliminate bias in the reporting of CMM due to changes in medical practice. The incidence of CMM is higher in the San Francisco-Oakland MSA than nationally. From 1976 through 1987, the incidence of invasive CMM increased from 9.8±0.9 to 16.5±1.1 per 100,000 (P=0.0001) among men and from 9.3±0.8 to 12.7±0.9 per 100,000 (P=0.001) among women. Age-specific, histologic-specific, and anatomic site-specific trends were also evaluated. The temporal patterns of CMM suggest that the recent increases are not accounted for solely by ascertainment bias due to reporting practices. The observed trends are consistent with early detection efforts and with changes in the prevalence of risk factors.

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Authors are at the Northern California Cancer Center, Alameda, CA, USA. Dr Holly is also with the Department of Health Research and Policy, Stanford University School of Medicine, and the Department of Epidemiology and Biostatistics, University of California, San Francisco, School of Medicine, USA. Address correspondence to Dr Horn-Ross, Northern California Cancer Center, 1420 Harbor Bay Pkwy, Suite 260, Alameda, CA 94501, USA. This research was supported by contract N01-CN-05224 from the Surveillance, Epidemiology, and End Results Program, National Cancer Institute, contract N01-CP-05681 from the National Cancer Institute, and subcontract 050E-8708 from the California Tumor Registry, California State Department of Health Services.

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Horn-Ross, P.L., Holly, E.A., Brown, S.R. et al. Temporal trends in the incidence of cutaneous malignant melanoma among Caucasians in the San Francisco-Oakland MSA. Cancer Causes Control 2, 299–305 (1991). https://doi.org/10.1007/BF00051669

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  • DOI: https://doi.org/10.1007/BF00051669

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