title: Resistance to Anti-HER2 Therapies in Breast Cancer.
abstract: HER2 is amplified or overexpressed in 20% to 25% of breast cancers. HER2 is a redundant, robust, and powerful signaling pathway that represents an attractive therapeutic target. Anti-HER2 therapy in the clinic has resulted in significant improvements in patient outcomes and, in recent years, combinations of anti-HER2 therapies have been explored and carry great promise. However, treatment resistance remains a problem. Resistance can be mediated, among others, by pathway redundancy, reactivation, or the utilization of escape pathways. Understanding mechanisms of resistance can lead to better therapeutic strategies to overcome resistance and optimize outcomes.
authors.affiliation: From the Lester and Sue Smith Breast Center and Dan L. Duncan Cancer Center at Baylor College of Medicine, Houston, TX.
authors.forename: Mothaffar F
authors.initials: MF
authors.lastname: Rimawi
authors.affiliation: From the Lester and Sue Smith Breast Center and Dan L. Duncan Cancer Center at Baylor College of Medicine, Houston, TX.
authors.forename: Carmine
authors.initials: C
authors.lastname: De Angelis
authors.affiliation: From the Lester and Sue Smith Breast Center and Dan L. Duncan Cancer Center at Baylor College of Medicine, Houston, TX.
authors.forename: Rachel
authors.initials: R
authors.lastname: Schiff
mesh_terms: D000818:Animals; D000970:Antineoplastic Agents / Q000627:therapeutic use*; D001943:Breast Neoplasms / Q000188:drug therapy* / Q000378:metabolism; D019008:Drug Resistance, Neoplasm; D006801:Humans; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000037:antagonists & inhibitors*; D011960:Receptors, Estrogen / Q000378:metabolism
chemical_list: D000970:Antineoplastic Agents; D019869:Phosphatidylinositol 3-Kinases; D018719:Erb-b2 Receptor Tyrosine Kinases; D011960:Receptors, Estrogen; C508053:ERBB2 protein, human