preview: RAF around the Edges — The Paradox of BRAF Inhibitors — NEJM

RAF around the Edges — The Paradox of BRAF Inhibitors

N Engl J Med 2012; 366:271-273January 19, 2012

This article has no abstract; the first 100 words appear below.

The recent success of BRAF inhibitors represents a great stride forward for melanoma research. When used to treat patients with melanoma who harbor the BRAF V600E mutation, these inhibitors lead to the remission of even advanced lesions. However, resistance to BRAF inhibitors emerges within months. Of added concern is the development of secondary tumors, most commonly cutaneous squamous-cell carcinomas and keratoacanthomas, in response to BRAF inhibition.¹ In this issue of the Journal, Su et al. found that BRAF inhibition leads to increased MAPK (mitogen-activated protein kinase) signaling and secondary tumor development when another oncogene, HRAS, is activated.² This is due . . .