Scott Davis, PhD
Scott Davis, PhD, is Professor and Chair of the Department of Epidemiology in the School of Public Health at the University of Washington and a Full Member in the Program in Epidemiology of the Division of Public Health Sciences at the Fred Hutchinson Cancer Research Center. He obtained his undergraduate degree in Biology and Chemistry from the University of New Mexico, a Master of Science in Community Health from the University of Rochester, and a Ph.D. in Epidemiology from the University of Washington. He served as a Research Associate in Epidemiology at the Radiation Effects Research Foundation in Hiroshima, Japan, from 1983-1985. Dr. Davis was a Special Fellow of the Leukemia Society of American from 1986-1987, and the recipient of a Research Career Development Award from the National Cancer Institute from 1988-1993. He is an elected member of the American Epidemiological Society, and a Fellow of the American College of Epidemiology. He served as a member of the BEIR (Biological Effects of Ionizing Radiation) VII Committee of the National Academy of Sciences, and is the only foreign epidemiologist elected member (Academician) of the Russian Academy of Medical Sciences. He has served as a member of the National Cancer Institute Board of Scientific Counselors for Clinical Sciences and Epidemiology.
His primary research focus is radiation epidemiology. For more than a decade he has directed two major research activities investigating the effects of ionizing radiation on human health. One is a series of studies in the Russian Federation of the effects of radiation exposure from the Chernobyl Power Station. These studies have focused on the risk of thyroid cancer and leukemia among children in the Bryansk Oblast, and recently have expanded to include the molecular characterization of thyroid cancer cases and a large-scale study of breast cancer. The second is a long-term follow up study of thyroid disease in persons exposed to atmospheric releases of radiation from the Hanford Nuclear Site in eastern Washington State (the Hanford Thyroid Disease Study). He has also conducted several epidemiologic studies of the possible health effects associated with exposure to power frequency magnetic fields, focusing on the risk of leukemia and breast cancer. Recently this work has expanded to include investigations of the effects of exposure to light-at-night and circadian disruption, including night shift work, on melatonin and reproductive hormones important in the etiology of breast and other hormone-related cancer. He has also maintained a long-standing interest in the etiology of the leukemias and lymphomas, and has directed epidemiologic studies of Hodgkin’s disease, non-Hodgkin’s lymphoma, and multiple myeloma.
Brief abstract of talk:
There is increasing interest in the possibility that disruption of normal circadian rhythm may increase the risk of developing cancer. Persons who engage in night shift work may exhibit altered nighttime melatonin levels and reproductive hormone profiles that could increase the risk of hormone-related diseases, including breast and prostate cancer. Epidemiologic studies are beginning to suggest that women who work at night, and who experience sleep deprivation, circadian disruption, and exposure to light-at-night are at an increased risk of breast cancer, and possibly colorectal cancer as well. Similar findings are beginning to appear regarding prostate cancer in men. Several studies have been conducted in Seattle to investigate the effects of factors that can disrupt circadian rhythm and alter normal nocturnal production of melatonin and reproductive hormones of relevance to breast cancer etiology. Studies completed to date have found: 1) an increased risk of breast cancer associated with indicators of exposure to light-at-night and night shift work; 2) decreased nocturnal urinary levels of 6-sulphatoxymelatonin associated with exposure to 60-Hz magnetic fields in the bedroom the same night; 3) a decrease in nocturnal urinary concentration of 6-sulphatoxymelatonin, but little increase in the urinary concentration of luteinizing hormone, follicle stimulating hormone, and estradiol in a sample of healthy women of reproductive age; and 4) decreased levels of urinary 6-sulphatoxymelatonin, and increased urinary concentrations of the reproductive hormones listed above in healthy women of reproductive age. A similar study of hormone levels in men who work the night shift is nearing completion. This study in men will also begin to investigate whether alterations in the primary genes thought to regulate the human circadian clock are associated with the hormone profiles identified, and the ability to adapt to night shift work. A number of biological mechanisms have been proposed to explain the findings to date. This presentation will summarize the evidence for direct action of melatonin as well as indirect action of circadian disruption on hypothesized pathways in cancer etiology. It is anticipated that collectively these studies will enhance our understanding of the role of circadian disruption in the etiology of cancer.
Updated on January 24, 2011