hormon therapy in breast cancer

Uncontrolled cellular proliferation, aberrant programmed cell death as a consequence of accumulative genetic damages and epigenetic change lead to genetic alterations and the beginning of breast cancer. Breast cancer risk depends on a variation of hormonal and reproductive factors. Amongst the hormonal effects, a main role has been attributed to the estrogens. Seventy per cent of breast cancers are hormone-dependent, they express estrogen receptor (ERα), and their proliferation is influenced by estrogens. The majority of tumours express ERα and thereby inhibiting the ER-signalling pathway by anti-estrogens is a valuable option in treatment of women with ER-ositive(ER+) breast cancer. Recently, studies have demonstrated that hyperactive mitogen-activated protein kinase (MAPK) activity contributes to generation of the ERα- phenotype and that inhibition of MAPK activity can cause re-expression of the ERα and restore sensitivity to endocrine therapies. Because of multiple mode of actions (classical genomic,non-classical genomic and non-genomic), estrogen receptor has important for breast tumor development and has ssignificant therapeutic suggestions. In this review the challenges given in treating ERα- breast cancer, resistant factors to endocrine therapy, understanding and manipulating the cellular mechanisms that effect expression ofERα to restore sensitivity to endocrine therapies and to design novel therapeutics for the treatment of ERα- breast cancers are discussed