TY - JOUR T1 - A Review of the Molecular Mechanisms of EGFR and IGFR Receptors in Tamoxifen Resistance in Breast Cancer TT - JF - mcijournal JO - mcijournal VL - 6 IS - 4 UR - http://mcijournal.com/article-1-360-en.html Y1 - 2022 SP - 6 EP - 16 KW - Breast Neoplasms KW - Estrogen Receptor alpha KW - Epidermal Growth Factor KW - Receptor KW - Insulin-Like Growth Factor KW - Receptor KW - Signal Pathways KW - Tamoxifen N2 - In 1980, tamoxifen was introduced as an effective adjuvant endocrine therapy for breast cancer, resulting in a significant increase in overall survival. Nevertheless, the development of acquired resistance limited the efficacy of tamoxifen therapy. Several molecular mechanisms have been proposed to explain the probable process of tamoxifen resistance. In vitro studies have suggested that alterations in the expression of cytoplasmic growth cascades such as insulin-like growth factor receptor (IGFR) and epidermal growth factor receptor (EGFR) along with associated downstream signaling pathways such as ERK1, ERK2, and ERK6 are the main cause of resistance to tamoxifen. In this review, we investigated the role of estrogen receptor-α (ER-α), EGFR, IGFR, and their downstream signaling pathways in tamoxifen resistance. The present study attempted to find out possible culprits of tamoxifen resistance to improve treatment efficacy in breast cancer patients. M3 10.30699/mci.6.4.32-5 ER -