Journal
JOURNAL OF INVESTIGATIVE DERMATOLOGY
Volume 133, Issue 8, Pages 1928-1929Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/jid.2013.136
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Funding
- NCI NIH HHS [R01 CA160495] Funding Source: Medline
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Despite recent advancements in the treatment of late-stage mutant BRAF (V600E/K) melanomas, a major hurdle continues to be acquired resistance to BRAF inhibitors such as vemurafenib. The mechanisms for resistance have proven to be heterogeneous, emphasizing the need to use broad therapeutic approaches. In this issue, the study Stat3-targeted therapies overcome the acquired resistance to vemurafenib in melanomas by Liu et al. proposes that signal transducer and activator of transcription 3 (STAT3) paired box 3 (PAX3) signaling may be a mechanism that is used by melanomas to resist RAF inhibitors.
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