COMMENTARY

Unprecedented Treatment Options in Melanoma

Antoni Ribas, MD, PhD; Louise M. Perkins, PhD

Disclosures

June 10, 2013

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In This Article

Introductions

Antoni Ribas, MD, PhD: I am Antoni Ribas, Professor of Medicine at the University of California, Los Angeles, and Director of the Tumor Immunology Program at the Jonsson Comprehensive Cancer Center. Welcome to this edition of Medscape Oncology Insights, presented in association with the Melanoma Research Alliance. Today we are here to discuss the recent developments in melanoma, presented at the 2013 Annual Meeting of the American Society of Clinical Oncology (ASCO®). With me is Dr. Louise Perkins, who is the Chief Science Officer at the Melanoma Research Alliance. Hello, Louise.

Louise M. Perkins, PhD: Hi, Toni.

Unprecedented Benefits Continue to Roll Out

Dr. Ribas: There seems to be continued excitement in melanoma. It was thought to be difficult to top from the previous years. What do you see as the highlights of this year?

Dr. Perkins: This year's ASCO meeting is really just incredible, a testimony to all of the hard work that you and your colleagues have invested over many years. Yesterday's session on immunotherapies and checkpoint blockade inhibitors in melanoma was truly one of the highlights of the meeting. The apparent clinical activity that was demonstrated, with many different approaches specifically targeting PD-1 pathway, is amazing. There are at least 3 different options that are in relatively mature development, for use either alone, in sequence with, or in combination with the existing approved agent ipilimumab, and on the heels of the approval of 2 new agents just this week (dabrafenib and trametinib) this is amazing progress for melanoma. I would love to hear some of your comments about what happened yesterday.

Dr. Ribas: In the past 3-4 years we have seen melanoma progress from being the prototype of a cancer that was resistant to everything; it was what people would give as an example of the untreatable cancer. Not much worked -- chemotherapy didn't work, radiotherapy didn't work -- and now it's the poster child of drug development. They have had to make the sessions in this meeting (and in the past several years) bigger and bigger, as more people attend to see what is going on. It has been a great story of applying science to patients, of understanding the biology of the cancer with the driver mutation of BRAF, and how that is telling the cancer to be a cancer cell and then blocking it with a BRAF inhibitor. This has given unprecedented benefits, but now that we are blocking twice at BRAF and MEK, it will have even more benefits because we are getting better initial responses, more durable response with fewer side effects. The pharmacological activity of the BRAF inhibitors can transactivate some cells in a paradoxical way that is prevented by the MEK inhibitor.

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