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Suggested Citation:"References." Institute of Medicine. 2002. Cancer and the Environment: Gene-Environment Interaction. Washington, DC: The National Academies Press. doi: 10.17226/10464.
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Suggested Citation:"References." Institute of Medicine. 2002. Cancer and the Environment: Gene-Environment Interaction. Washington, DC: The National Academies Press. doi: 10.17226/10464.
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Suggested Citation:"References." Institute of Medicine. 2002. Cancer and the Environment: Gene-Environment Interaction. Washington, DC: The National Academies Press. doi: 10.17226/10464.
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Suggested Citation:"References." Institute of Medicine. 2002. Cancer and the Environment: Gene-Environment Interaction. Washington, DC: The National Academies Press. doi: 10.17226/10464.
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Suggested Citation:"References." Institute of Medicine. 2002. Cancer and the Environment: Gene-Environment Interaction. Washington, DC: The National Academies Press. doi: 10.17226/10464.
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Suggested Citation:"References." Institute of Medicine. 2002. Cancer and the Environment: Gene-Environment Interaction. Washington, DC: The National Academies Press. doi: 10.17226/10464.
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Suggested Citation:"References." Institute of Medicine. 2002. Cancer and the Environment: Gene-Environment Interaction. Washington, DC: The National Academies Press. doi: 10.17226/10464.
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Suggested Citation:"References." Institute of Medicine. 2002. Cancer and the Environment: Gene-Environment Interaction. Washington, DC: The National Academies Press. doi: 10.17226/10464.
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Suggested Citation:"References." Institute of Medicine. 2002. Cancer and the Environment: Gene-Environment Interaction. Washington, DC: The National Academies Press. doi: 10.17226/10464.
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Suggested Citation:"References." Institute of Medicine. 2002. Cancer and the Environment: Gene-Environment Interaction. Washington, DC: The National Academies Press. doi: 10.17226/10464.
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Suggested Citation:"References." Institute of Medicine. 2002. Cancer and the Environment: Gene-Environment Interaction. Washington, DC: The National Academies Press. doi: 10.17226/10464.
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110 CANCER AND THE ENVIRONMENT Dorgan JF, Stanczyk FZ, Longcope C, Stephenson HEJ, Chang L, Miller R, Franz C, Falk RT, Kahle L. 1997. Relationship of serum dehyroepiandrosterone (DHEA), DHEA sulfate, and 5- androstene-3 beta, 17 beta-diol to risk of breast cancer in postmenopausal women. Cancer Epidemiology, Biomarkers, and Prevention 6:177–181. Elmore LW, Hancock AR, Chang SF, Wang XW, Chang S, Callahan CP, Geller DA, Will H, Harris CC. 1997. Hepatitis B virus X protein and p53 tumor suppressor interactions in the modulation of apoptosis. Proceedings of the National Academy of Sciences 94:14707–14712. Eto I, Krumdieck CL. 1986. Role of vitamin B12 and folate deficiencies in carcinogenesis. Advances in Experimental Medicine and Biology 206:313–330. Evans MK, Taffe BG, Harris CC, Bohr VA. 1993. DNA strand bias in the repair of the p53 gene in normal human and xeroderma pigmentosum group C fibroblasts. Cancer Research 53:5377– 5381. Everson RB, Wehr CM, Erexson GL, MacGregor JT. 1988. Association of marginal folate depletion with increased human chromosomal damage in vivo: Demonstration by analysis of micro- nucleated erythrocytes. Journal of the National Cancer Institute 80:525–529. Fearon ER. 1997. Human cancer syndromes: Clues to the origin and nature of cancer. Science 278:1043–1050. Feigelson HS, Coetzee GA, Kolonel LN, Ross RK, Henderson BE. 1997. A polymorphism in the CYP17 gene increases the risk of breast cancer. Cancer Research 57:1063–1065. Fenech M, Rinaldi J. 1994. The relationship between micronuclei in human lymphocytes and plasma levels of vitamin C, vitamin E, vitamin B12 and folic acid. Carcinogenesis 15:1405–1411. Ferraroni M, La Vecchia C, D’Avanzo B, Negri E, Franceschi S, Decarli A. 1994. Selected micro- nutrient intake and the risk of colorectal cancer. British Journal of Cancer 70:1150–1155. Fong KM, Sekido Y, Minna JD. 1999. Molecular pathogenesis of lung cancer. Journal of Thoracic and Cardiovascular Surgery 118:1136–1152. Forrester K, Lupold SE, Ott VL, Chay CH, Band V, Wang XW, Harris CC. 1995. Effects of p53 mutants on wild-type p53-mediated transactivation are cell type dependent. Oncogene 10:2103– 2111. Forrester K, Ambs S, Lupold SE, Kapust RB, Spillare EA, Weinberg WC, Felley-Bosco E, Wang XW, Geller DA, Billiar TR, Harris CC. 1996. Nitric oxide-induced p53 accumulation and regulation of inducible nitric oxide synthase (NOS2) expression by wild-type p53. Proceedings of the National Academy of Sciences 93:2442–2447. Friedell GH, Tucker TC, Ross FE. 1999. The impact of poverty and education on lung and cervical cancer in Appalachian Kentucky. Journal of Registry Management 26:125–127. Frosst P, Blom HJ, Milos R, Goyette P, Sheppard CA, Matthews RG, Boers GJH, den Heijer M, Kluijtmans LAJ, van den Heuvel LP, Rozen R. 1995. A candidate genetic risk factor for vascular disease: A common mutation in methylenetetrahydrofolate reductase (letter). Nature Genetics 10:111–113. Gertig DM, Hunter DJ. 1998. Genes and environment in the etiology of colorectal cancer. Seminars in Cancer Biology 8:285–298. Giovannucci E, Stampfer MJ, Colditz GA, Rimm EB, Trichopolous D, Rosner BA, Speizer FE, Willett WC. 1993. Folate, methionine, and alcohol intake and risk of colorectal adenoma. Journal of the National Cancer Institute 85:875–884. Giovannucci E, Rimm EB, Ascherio A, Stampfer MJ, Colditz GA, Willett WC. 1995. Alcohol, low- methionine–low-folate diets, and risk of colon cancer in men. Journal of the National Cancer Institute 87:265–273. Giovannucci E, Stampfer MJ, Colditz GA, Hunter DJ, Fuchs C, Rosner BA, Speizer FE, Willett WC. 1998. Multivitamin use, folate, and colon cancer in women in the Nurses’ Health Study. Annals of Internal Medicine 129:517–524.

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The Roundtable on Environmental Health Sciences, Research, and Medicine wanted to address the link between environmental factors and the development of cancer in light of recent advances in genomics. They asked what research tools are needed, how new scientific information can be applied in a timely manner to reduce the burden of cancer, and how this can be flexible enough to treat the individual.

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