Clinical significance of intronic variants in BRAF inhibitor resistant melanomas with altered BRAF transcript splicing View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2017-05-11

AUTHORS

Gulietta M. Pupo, Suzanah C. Boyd, Carina Fung, Matteo S. Carlino, Alexander M. Menzies, Bernadette Pedersen, Peter Johansson, Nicholas K. Hayward, Richard F. Kefford, Richard A. Scolyer, Georgina V. Long, Helen Rizos

ABSTRACT

Alternate BRAF splicing is the most common mechanism of acquired resistance to BRAF inhibitor treatment in melanoma. Recently, alternate BRAF exon 4–8 splicing was shown to involve an intronic mutation, located 51 nucleotides upstream of BRAF exon 9 within a predicted splicing branch point. This intronic mutation was identified in a single cell line but has not been examined in vivo. Herein we demonstrate that in three melanomas biopsied from patients with acquired resistance to BRAF inhibitors, alternate BRAF exon 4–8 splicing is not associated with this intronic branch point mutation. We also confirm that melanoma cells expressing BRAF splicing variants retain exquisite sensitivity to existing FDA-approved MEK inhibitors. More... »

PAGES

17

Identifiers

URI

http://scigraph.springernature.com/pub.10.1186/s40364-017-0098-3

DOI

http://dx.doi.org/10.1186/s40364-017-0098-3

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1085366432

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/28503307


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