title: The insulin-like growth factor-I receptor (IGF-IR) in breast cancer: biology and treatment strategies.
abstract: Breast cancer is the most common cancer and the second leading cause of cancer-related deaths among women worldwide. Although patients are often diagnosed in the early and curable stages, the treatment of metastatic breast cancer remains a major clinical challenge. The combination of chemotherapy with new targeting agents, such as bevacizumab, is helpful in improving patient survival; however, novel treatment strategies are required to improve clinical outcomes. The insulin-like growth factor-I receptor (IGF-IR) is a tyrosine kinase cell surface receptor which is involved in the regulation of cell growth and metabolism. Previous studies have shown that activation of the IGF-IR signaling pathway promotes proliferation, survival, and metastasis of breast cancer cells. Additionally, overexpression of IGF-IR is associated with breast cancer cell resistance to anticancer therapies. Recently, IGF-IR has been introduced as a marker of stemness in breast cancer cells and there is also accumulating evidence that IGF-IR contributes to the establishment and maintenance of breast cancer epithelial-mesenchymal transition (EMT). Therefore, pharmacological or molecular targeting of IGF-IR could be a promising strategy, in the treatment of patients with breast cancer, particularly in order to circumvent the therapeutic resistance and targeting breast cancer stem/progenitors. Currently, many strategies have been developed for targeting IGF-IR, some have entered clinical trials and some are in preclinical stages for breast cancer therapy. In this review, we will first discuss on the biology of IGF-IR in an attempt to find the role of this receptor in breast cancer and then discuss about therapeutic strategies to target this receptor.
authors.affiliation: Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.|Department of Immunology, School of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
authors.forename: Morteza
authors.initials: M
authors.lastname: Motallebnezhad
authors.affiliation: Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.|Department of Immunology, School of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
authors.forename: Leili
authors.initials: L
authors.lastname: Aghebati-Maleki
authors.affiliation: Department of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.
authors.forename: Farhad
authors.initials: F
authors.lastname: Jadidi-Niaragh
authors.affiliation: Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.|Department of Immunology, School of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
authors.forename: Hamid
authors.initials: H
authors.lastname: Nickho
authors.affiliation: Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
authors.forename: Hosein
authors.initials: H
authors.lastname: Samadi-Kafil
authors.affiliation: Hematology and Oncology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
authors.forename: Karim
authors.initials: K
authors.lastname: Shamsasenjan
authors.affiliation: Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. yousefime@tbzmed.ac.ir.|Department of Immunology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran. yousefime@tbzmed.ac.ir.
authors.forename: Mehdi
authors.initials: M
authors.lastname: Yousefi
mesh_terms: D052242:Adiponectin / Q000502:physiology; D001943:Breast Neoplasms / Q000401:mortality / Q000473:pathology / Q000628:therapy*; D019008:Drug Resistance, Neoplasm; D058750:Epithelial-Mesenchymal Transition; D005260:Female; D006801:Humans; D011836:Radiation Tolerance; D017526:Receptor, IGF Type 1 / Q000037:antagonists & inhibitors / Q000502:physiology*; D011960:Receptors, Estrogen / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology
chemical_list: D052242:Adiponectin; D011960:Receptors, Estrogen; D017526:Receptor, IGF Type 1
keywords: Breast cancer; Insulin-like growth factor (IGF); Insulin-like growth factor-I receptor (IGF-IR); Targeting