Selenium, estradiol 17 beta, nitrites, and human breast cancer.
Breast cancer is the most common cancer in women in the United States. Although there is a large body of studies dealing with selenium, estrogens and nitrites in relation to cancer, most of them are correlated singly and the dynamics of carcinogenesis are overly simplified. The epidemiologic and etiologic effects of selenium, estrogens and nitrites in human breast cancer are traced in their important dimensions. A hypothesis for the interaction of these factors, especially in relation to the erythrocyte is presented within a multi-stage focus of carcinogenesis. A biochemical process for breast cell carcinogenesis in general is postulated and the erythrocyte interaction with breast cancer is diagramed. An enzyme "X" is postulated (estradiase) as a facilitator in vivo of the necessary biochemical conversion of estradiol 17 to a carcinogen.
D001940:Breast / Q000098:blood supply; D001943:Breast Neoplasms / Q000139:chemically induced / Q000209:etiology*; D002273:Carcinogens; D004912:Erythrocytes / Q000502:physiology; D004958:Estradiol / Q000378:metabolism*; D005260:Female; D005979:Glutathione Peroxidase / Q000378:metabolism; D006801:Humans; D009573:Nitrites / Q000009:adverse effects*; D012643:Selenium / Q000009:adverse effects*
D002273:Carcinogens; D009573:Nitrites; D004958:Estradiol; D005979:Glutathione Peroxidase; D012643:Selenium