Abstract
BRAF mutations are one of the many oncogenic drivers described in lung adenocarcinomas and are seen in approximately 3% of cases. The most common BRAF mutation corresponds to a hotspot transversion mutation T1799A at exon 15, which causes a valine to glutamine substitution at residue 600. The other BRAF mutations, classified as non-V600E, are distributed in exons 15 and 11, the most common being G469A in exon 11 (39%). The BRAF inhibitors vemurafenib and dabrafenib, specifically target the BRAFV600E mutant kinase. In this chapter the biology, molecular pathogenesis and clinical characteristics of BRAF mutated lung adenocarcinomas are described.
Original language | English (US) |
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Title of host publication | Lung Cancer |
Subtitle of host publication | Fourth Edition |
Publisher | Wiley-Blackwell |
Pages | 557-563 |
Number of pages | 7 |
ISBN (Electronic) | 9781118468791 |
ISBN (Print) | 9781118468746 |
DOIs | |
State | Published - May 27 2014 |
Keywords
- Adenocarcinoma
- BRAF mutations
- Dabrafenib and mechanisms of resistance
- Dominant negative BRAF
- Lung cancer
- NSCLC
- Vemurafenib
ASJC Scopus subject areas
- General Medicine