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Null Results in Brief |
1 Genetics Branch, Center for Cancer Research, and 2 Nutritional Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland; 3 Office of Clinical and Regulatory Affairs, National Center for Complementary and Alternative Medicine, and 4 Genetic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, 5 Office of Centers, Training, and Resources, National Cancer Institute, NIH, Bethesda, Maryland; 6 Cancer Institute, Chinese Academy of Medical Sciences, Beijing, China; and 7 Mayo Clinic College of Medicine, Rochester, Minnesota
Requests for reprints: Ilan R. Kirsch, Amgen, 1201 Amgen Court West, AW1-J 4144, Seattle, WA 98119-3105. Phone: 206-265-7316; Fax: 206-216-5930. E-mail: lkirsch{at}amgen.com or You-Lin Qiao, Cancer Institute, Chinese Academy of Medical Sciences, Panjiayian, Chaoyang District, P.O. Box 2258, Beijing 100021, P.R. China. Phone: 86-10-6778-1331, ext. 8982; Fax: 86-10-6771-3648. E-mail: qiaoy{at}public.bta.net.cn
Selenium is a promising cancer chemoprevention agent. A recent randomized controlled chemoprevention trial found that selenomethionine (SeMet) supplementation for 10 months favorably effected a change in esophageal dysplasia grade among participants who started the trial with mild dysplasia. To further explore the role of SeMet in this trial, we compared gene expression profiles by treatment group using Affymetrix HU 133A chips in before/after supplementation paired normal esophageal biopsies from a subset of 29 trial participants, 16 who received SeMet, and 13 who received placebo. Using P < 0.001 as a cutoff, 11 differentially expressed genes were found in the SeMet supplementation group but these genes did not include either known selenoprotein genes or genes previously shown to be modulated by selenium treatment. Because the number of differentially expressed genes (n = 11) was less than expected by chance (n = 18), we concluded that SeMet supplementation had no measurable effect on gene expression in the normal squamous esophagus of these subjects with dysplasia. (Cancer Epidemiol Biomarkers Prev 2006;15(5):1046-7)
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