title: Melanoma Treatments: Advances and Mechanisms.
abstract: Advances in the understanding of the molecular pathogenesis of melanoma and in cancer immunology have led to the rational design and recent clinical implementation of a variety of novel therapies for metastatic melanoma. BRAF and MEK inhibitors that target the MAPK pathway have high rates of clinical response in BRAF-mutant melanoma. Therapies that modulate the immune response to melanoma, including monoclonal antibodies that interfere with pathways that inhibit T-cell function, have been shown to be effective in melanoma. Lessons learned from these encouraging results are driving the development of new treatments for melanoma and other cancers. This review will focus on the science and clinical findings related to targeted therapies that inhibit BRAF or MEK as well as the immunotherapies that block the CTLA-4 or PD-1 pathways. Other experimental and combinatorial therapeutic approaches will also be discussed.
authors.affiliation: Department of Dermatology, Yale-New Haven Hospital, Yale School of Medicine, New Haven, Connecticut.|Department of Internal Medicine, Yale-New Haven Hospital, Yale School of Medicine, New Haven, Connecticut.
authors.forename: Alexander
authors.initials: A
authors.lastname: Marzuka
authors.affiliation: Department of Dermatology, Yale-New Haven Hospital, Yale School of Medicine, New Haven, Connecticut.|Department of Internal Medicine, Yale-New Haven Hospital, Yale School of Medicine, New Haven, Connecticut.
authors.forename: Laura
authors.initials: L
authors.lastname: Huang
authors.affiliation: Department of Pathology, Yale-New Haven Hospital, Yale School of Medicine, New Haven, Connecticut.
authors.forename: Nicholas
authors.initials: N
authors.lastname: Theodosakis
authors.affiliation: Department of Dermatology, Yale-New Haven Hospital, Yale School of Medicine, New Haven, Connecticut.|Department of Pathology, Yale-New Haven Hospital, Yale School of Medicine, New Haven, Connecticut.
authors.forename: Marcus
authors.initials: M
authors.lastname: Bosenberg
mesh_terms: D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D060908:CTLA-4 Antigen / Q000235:genetics / Q000378:metabolism; D006801:Humans; D020930:MAP Kinase Kinase Kinases / Q000037:antagonists & inhibitors / Q000235:genetics*; D008545:Melanoma / Q000188:drug therapy* / Q000235:genetics / Q000473:pathology; D009154:Mutation; D061026:Programmed Cell Death 1 Receptor / Q000235:genetics / Q000378:metabolism; D047428:Protein Kinase Inhibitors / Q000009:adverse effects / Q000627:therapeutic use; D048493:Proto-Oncogene Proteins B-raf / Q000037:antagonists & inhibitors / Q000235:genetics*; D015398:Signal Transduction; D012878:Skin Neoplasms / Q000188:drug therapy* / Q000235:genetics / Q000473:pathology
chemical_list: D000911:Antibodies, Monoclonal; D060908:CTLA-4 Antigen; C105992:PDCD1 protein, human; D061026:Programmed Cell Death 1 Receptor; D047428:Protein Kinase Inhibitors; C482119:BRAF protein, human; D048493:Proto-Oncogene Proteins B-raf; D020930:MAP Kinase Kinase Kinases