title: Mechanisms of trastuzumab resistance and their clinical implications.
abstract: Trastuzumab (Herceptin) is an excellent model of rationally designed targeted cancer treatment. However, less than 35% of patients with ErbB2-positive breast tumors respond to trastuzumab as a single agent, and 2-5% of trastuzumab-treated patients suffer from severe side effects, including cardiac dysfunction. Recent progress in understanding the mechanisms of trastuzumab antitumor function and cellular defects leading to trastuzumab resistance is summarized. Also explored is the potential of combination therapies for reversing trastuzumab resistance.
authors.affiliation: Department of Surgical Oncology, The University of Texas M.D. Anderson Cancer Center, Houston, TX 77030, USA.
authors.forename: Keng-Hsueh
authors.initials: KH
authors.lastname: Lan
authors.forename: Chien-Hsing
authors.initials: CH
authors.lastname: Lu
authors.forename: Dihua
authors.initials: D
authors.lastname: Yu
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000494:pharmacology*; D061067:Antibodies, Monoclonal, Humanized; D000970:Antineoplastic Agents / Q000494:pharmacology; D019008:Drug Resistance, Neoplasm; D006801:Humans; D008954:Models, Biological; D051059:PTEN Phosphohydrolase / Q000378:metabolism; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000378:metabolism; D015398:Signal Transduction; D000068878:Trastuzumab
chemical_list: D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D000970:Antineoplastic Agents; D051059:PTEN Phosphohydrolase; D019869:Phosphatidylinositol 3-Kinases; D018719:Erb-b2 Receptor Tyrosine Kinases; D000068878:Trastuzumab