Insulin like growth factor and risk of breast cancer

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Summary Background :-Breast cancer is responsible for the death of millions of women worldwide every year. It is widespread in the world and Iraq that become a genuine problem for public health. The etiology of the disease is unknown. Genetic and hormonal factors are involved in the development of breast cancer and progression of the disease. Insulin like growth factor-ӏ (IGF-ӏ) have been implicated as essential in controlling cellular differentiation and tissue regeneration, through mitogenic , anti-apoptotic and increases cell migration so IGF-ӏpromotetumorigenesis. Objective:- To evaluate the role of IGF-ӏ, insulin , estrogen and lipid profile in patients with breast cancer and their contribution to the pathogenesis of breast cancer. Subjects and Methods :- This study included 60 patients with primary breast cancer age range (29-70) years and 60 age matched healthy controls . The subjects were selected from patients attending the Clinic Medical City/Baghdad Teaching Hospital / Oncology unit . Insulin like growth factor-I, insulin and estrogen were measured by ELISA. Results:- Serum insulin like growth factor-I and insulin in breast cancer patients were significantly higher than healthy controls (p 0.05), but there was a significant difference between postmenopausal patients and control group (P<0.01). . Conclusion :- Insulin like growth factor-ӏ and estrogen level increased in the breast cancer in premenopausal patients , these results suggested that levels of serum IGF-I and estrogen together can be used as a predictive markers for breast cancer in the premenopausal women. Key word:- Insulin like growth factor - ӏ , Insulin, Estrogen, Breast cancer I. Introduction:Breast Cancer is widespread that it has become a genuine problem for public health, with about one woman in ten developing it in her lifetime throughout the world. Its incidence increases with age, being uncommon below the age of 30, and its behavior varies from a slowly progressive to a rapidly progressive disease despite all forms of treatment (1). Genetic and hormonal factors that are involved in the development of breast cancer and progression of the disease. Several genetic alterations have been associated with an increased risk of breast cancer development. Mutations in two breast cancer susceptibility genes, BRCA 1 and 2 have been shown to predispose women to breast cancer, however mutations in these genes account for only 5% of breast cancer cases. The factors responsible for the remaining 95% are still obscure. Breast cancer primarily affects women, however, it occasionally affects men. The female to male ratio of breast cancer prevalence is 100:1 Breast cancer accounts for 0.2% of all cancer cases in men (2). Other factors known to be involved in breast cancer development are hormones and growth factors. The finding that breast cancer is rare in males as well as in nonestrogenized women suggests that most, if not all, breast cancers originate as a hormone-dependent disease(3). Insulin like growth factor-I (IGFI) are multifunctional peptides that regulate cell proliferation differentiation and apoptosis attributes important in tumorigenesis (4). (IGFI) is a potent mitogen for both normal and transformed breast epithelial cells and serum IGF-I level is associated with the development of mammary gland hyperplasia and cancer in a primate model, increased expression of insulin like growth factor- I receptor (IGF I R) in the cytoplasm of the benign ductal epithelium is correlated with the risk of breast carcinoma development. Estrogens are critical for the development and normal physiological function of female reproductive tissues including the mammary gland (5). About two-third of breast carcinomas have an estrogen receptor positive status, but 50% of patients respond to anti-estrogen treatment(6). Therefore, oestrogen is believed to increase the risk of breast cancer(7). Insulin promotes the production and activity of (IGF- I) (8), which can promote cell proliferation in an over-nutrition state. The metabolic ramifications of chronic hyperinsulinemia are diverse and complex. It has been demonstrated that the compensatory hyperinsulinemia that characterizes adolescent obesity chronically suppresses hepatic synthesis of insulin like growth factor binding protein- I (IGFBP- I) which in turn