Affiliation

• ¹Cutaneous Biology Research Center, Massachusetts General Hospital, Charlestown, Massachusetts, USA
• ²Department of Dermatology, Massachusetts General Hospital, Boston, Massachusetts, USA
• ³Department of Biomedical Engineering, Johns Hopkins University, Baltimore, Maryland, USA

Corresponding Author

David E. Fisher, MD, PhD, Department of Dermatology, East Cutaneous Biology Research Center, Massachusetts General Hospital, Building 149, 3^rd Floor, 13^th Street Charlestown, MA 02129, USA. Tel: (+1) 617-643-5428; E-mail: dfisher3@partners.org

Citation

Fisher, D.E., et al. Melanoma Immunotherapy: Mechanisms and Opportunities. (2015) Invest Dermatol Venereol Res 1(2): 33-39.

Copy rights

© 2015 Fisher, D.E. This is an Open access article distributed under the terms of Creative Commons Attribution 4.0 International License.

Keywords

Abstract

  Immune checkpoint blockade via inhibition of Cytotoxic T Lymphocyte Antigen 4 (CTLA-4) and Programmed Cell Death 1 Receptor (PD-1) has demonstrated significant clinical benefits in treating melanoma and other types of cancers and has since become a very progressive field in cancer research. Despite durable tumor regression observed in some patients, response rates to CTLA-4 and PD-1 still have room for improvement. There are many additional immune modulatory pathways, including inhibitory molecules expressed on tumor cells and secretion of pro-inflammatory cytokines by lymphatic cells that could potentially be targeted to enhance the anti-tumor responses to PD-1 and CTLA-4. Here, we review the current status of CTLA-4 and PD-1 inhibitors in the treatment of melanoma and several therapeutic targets and strategies that may synergize with checkpoint blockades.