Sepideh Mansouri - Recombinant Proteins Department, Breast Cancer Research Center, Motamed Cancer Institute, ACECR, Tehran, Iran
Tannaz Samadi - Recombinant Proteins Department, Breast Cancer Research Center, Motamed Cancer Institute, ACECR, Tehran, Iran
Azin Teymourzadeh - Recombinant Proteins Department, Breast Cancer Research Center, Motamed Cancer Institute, ACECR, Tehran, Iran
Keivan Majidzadeh-A - Recombinant Proteins Department, Breast Cancer Research Center, Motamed Cancer Institute, ACECR, Tehran, Iran
Leila Farahmand - Recombinant Proteins Department, Breast Cancer Research Center, Motamed Cancer Institute, ACECR, Tehran, Iran

In ۱۹۸۰, 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 ERK۱, ERK۲, and ERK۶ 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.

Breast Neoplasms, Estrogen Receptor alpha, Epidermal Growth Factor, Receptor, Insulin-Like Growth Factor, Receptor, Signal Pathways, Tamoxifen