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Metformin tablets in usa during 1990 to 1990-1992, a period (1994 1997) when number of studies, including our own, found an association between higher and lower doses of vitamin K and cancer risk. In our current study we analyzed the associations between serum levels of vitamin K and breast, colorectal pancreatic cancer risk among a population-based study population. Methods Study Population The study sample included all women born in the United States during baseline period of 1987--1988, whose mothers or their first-born dependents were registered in the US National Health Interview Survey between 1988 and 1989. At the age of 18 years, women completed a mailed questionnaire about their lifestyle and medical history; a blood sample was obtained from a finger prick in the forearm. A complete set of demographic, clinical, and laboratory information regarding the participants is available at http://www.cdc.gov/nchs/data/nhanes.htm. For the current study, we analyzed data from two prospective cohort studies carried out in the late 1990s and 1999: Nurses' Health Study the II. Both studies follow same cohort of women who were enrolled in 1982 as women two separate prospective cohort studies of female nurses and male physicians that were initiated in 1976 and 1977. The participants completed a baseline questionnaire that included questions about lifestyle and medical history. Data on vitamin K intake in supplements were available from the two studies. In 1989, these women returned a similar questionnaire. In 1993, third wave of the questionnaire included questions on use of vitamin K supplements during the 12-month period before enrollment in the study. primary outcome variable was change in the incidence of breast cancer in women the cohort, and a secondary outcome variable used in the analyses was change incidence of colorectal cancer. This final outcome variable was the for which we reported associations our main analysis, because it was the outcome that most consistent among the original cohort members who have been followed to this date. Although data on use of vitamin K supplements are available for a smaller number of participants in the Nurses' Health Study, our inclusion criteria remained largely unchanged. Assessment of Vitamin K Intake The dietary intake of vitamin K is determined in three ways: self-report of intake or fortified food and vitamin K-fortified supplement use. In the Nurses' Health Study, dietary intake questionnaire has been administered to members of the staff participating hospitals and is used to quantify nutrient intake (23). We used data on the intake of vitamin K from multivitamins, supplements, and fortified foods that were collected through telephone interviews by trained interviewers, with the help of dietary data obtained in the National Health and Nutrition Examination Survey. In the Nurses' Health Study II, dietary data were retrieved from questionnaires mailed by the nurses of participating hospitals. We used the same criteria for estimating vitamin K intake as the Nurses' Health Study except that we chose to use a more flexible definition of dietary intake. Because the information on vitamin K supplement use was collected from questionnaires, we did not consider it in our analyses. Assessment of Hormone-Related Cancer Risk Several hormones play a role in cancer initiation and promotion. The primary estrogen is 17β-estradiol (E2; the 17-α-hydroxylated form of estradiol) (e.g., 17β-estradiol in some hormonal contraceptives), which is synthesized from estrone in the ovary and secreted by other organs (24). E2 can inhibit protein synthesis in both prostate and breast cancer cells, an increase in circulating E2 levels is associated with increased risk of both prostate and breast cancer (25,26). E2 treatment of ovariectomized rats significantly delays tumorigenesis and growth of prostate cancer by reducing protein Best online pharmacy in canada synthesis (27). E2 also increases the activity of enzymes in growth mammary tumor cells (28). E2 treatment of ovariectomized rats increases the growth of mammary tumor cells by increasing the activity of enzymes responsible for growth in the liver, kidney, and adipose tissue, this effect is mediated by estradiol receptors on these cells (29,30). The estrogenic effects of E2 therapy are less clear in the breast cancer setting (e.g., in the use of combined estrogen and tamoxifen, which is a progestin-only therapy) (28). However, evidence suggests that E2, through estrogen-induced suppression of the mammary growth factor MCP-1 (31), might play a role in the prevention and treatment of breast cancer in women (32). Consequently, several studies have assessed the effect of HRT on risk breast and colorectal cancers cancer death (32--36), as well the effect on risk of breast cancer in women during early life, when E2 is.

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