ENDOCRINE RESISTANCE IN HORMONE RECEPTOR POSITIVE ADVANCED BREAST CANCER (A RETROSPECTIVE STUDY)

Abstract

Summary and conclusions B reast cancer is considered the most frequently diagnosed cancer and the second cancer death leading cause in American women (following lung cancer). Despite the advances in the diagnosis and management of breast cancer, 6–10% of affected patients present metastatic breast cancer at diagnosis and 30–40% will develop metastases during the evolution of their disease. Breast cancer comprises a heterogeneous group of tumors with a wide spectrum of morphologically and molecularly different subtypes, resulting in different biological behaviors, presentation, and prognosis. Human breast cancers depend on estrogen and/or progesterone for growth, and these effects are mediated through estrogen receptors (ERs) and progesterone receptors (PRs), respectively. Thus deprivation of estrogen signaling through endocrine-targeted therapy has become the mainstay of treatment in ER𝛼-positive disease. Despite these benefits, endocrine therapy resistance eventually occurs in a large number of patients and represents a significant issue for optimal clinical management. In recent years a large body of work has focused on trying to understand the underlying mechanisms leading to resistance and approaches for their circumvention, as well as developing methods to predict which patients are likely to develop resistance and are therefore in need of additional or alternative therapies The human epidermal growth factor receptor 2 (HER2) genes encode a member of the epidermal growth factor receptor family of receptor tyrosine kinases, and its amplification with resultant overexpression plays a major role in sustaining multiple pathways in cancer growth