The Obesity with and without metabolic syndrome as a risk factor for the Breast Cancer

Abstract

Epidemiologic evidences link the breast cancer, typical dependent endocrine tumor, with lifestyle, in particular alimentary habits. The visceral obesity and the gain of body weight are considered responsible for the increase of breast cancer in the postmenopause. In fact, the mammary gland is sensitive to the circulatory estrogen rate and the obesity is usually associated to high rates of free steroids. The effects of estrogens are mediated by the receptors (ER). Studies indicate two types of cancer related to the ER: the first, negative ER is characterized for being more a aggressive and with higher incidence in the premenopause. The second positive ER, which occurs more commonly in the postmenopause. Therefore, the estrogens represent a crucial role in the pathogenesis and the prognosis of the breast cancer. Up to now, there are two types of known ERs, REa and REB (Abrantes M.M, et al., 2003). The genes that codify proteins involved in the biosynthesis, action and metabolization of the estrogens are polymorphics (Cai et al., 2003; Haiman et al., 2003). The polymorphism is a genetic variation of common occurance in the general population, found in frequency higher than 1% (Schor et al., 2004). There are many know polymorphism in the REa gene, some of them which can change the function of the receptor. Out of the existing polymorphism, Pvull, Xbal and GTn. The genotype Xbal could modify the individual risk of breast cancer in women in the menopause (Shin A et al., 2003). According to this, this study will evaluate the casual association among Pvull, Xbal and GTn polymorphic genes in women in the postmenopause with clinical events (obesity and metabolic syndrome). (AU)