How melanomas bypass new therapy

The promise of an exciting new drug that inhibits the mutant B-RAF protein in skin cancer is marred by the fact that most patients relapse within a year. Fresh data hint at how such resistance emerges. See Letters p.968 & p.973 Drug-resistance mechanism in melanoma Clinical trials in melanoma pa...

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Bibliographic Details
Published inNature (London) Vol. 468; no. 7326; pp. 902 - 903
Main Authors Solit, David, Sawyers, Charles L.
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 16.12.2010
Nature Publishing Group
Subjects
631/67/1059/153
631/67/1059/2326
692/699/67/1813/1634
Drug therapy
Humanities and Social Sciences
Melanoma
multidisciplinary
news-and-views
Science
Science (multidisciplinary)
Skin cancer
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Summary:The promise of an exciting new drug that inhibits the mutant B-RAF protein in skin cancer is marred by the fact that most patients relapse within a year. Fresh data hint at how such resistance emerges. See Letters p.968 & p.973 Drug-resistance mechanism in melanoma Clinical trials in melanoma patients carrying B-RAF gene mutations have shown promising results with the B-RAF kinase inhibitor PLX4032, but many patients go on to become resistant. Two papers now uncover possible mechanisms for this resistance. Nazarian et al . report that melanomas can acquire resistance due to mutations of N-RAS or increased expression of PDGFRβ , and Johannessen et al . report resistance due to upregulation of MAP3K8/COT. Each of these mechanisms seems to apply to some patients in the recent PLX4032 trial, yet surprisingly, no secondary B-RAF mutations were observed.
ISSN:0028-0836
1476-4687
DOI:10.1038/468902a