These authors contributed equally to this work.
Recurrent BRAF kinase fusions in melanocytic tumors offer an opportunity for targeted therapy
Version of Record online: 19 AUG 2013
© 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
Pigment Cell & Melanoma Research
Volume 26, Issue 6, pages 845–851, November 2013
How to Cite
Botton, T., Yeh, I., Nelson, T., Vemula, S. S., Sparatta, A., Garrido, M. C., Allegra, M., Rocchi, S., Bahadoran, P., McCalmont, T. H., LeBoit, P. E., Burton, E. A., Bollag, G., Ballotti, R. and Bastian, B. C. (2013), Recurrent BRAF kinase fusions in melanocytic tumors offer an opportunity for targeted therapy. Pigment Cell & Melanoma Research, 26: 845–851. doi: 10.1111/pcmr.12148
- Issue online: 24 OCT 2013
- Version of Record online: 19 AUG 2013
- Accepted manuscript online: 24 JUL 2013 08:50AM EST
- Manuscript Accepted: 19 JUL 2013
- Manuscript Received: 10 JUN 2013
- National Institutes of Health. Grant Numbers: R01 CA131524, P01 CA025874
Figure S1. Array CGH profiles for all cases.
Figure S2. BRAF Break-apart FISH on the C0902 cell line.
Figure S3. Genomic structure of the BRAF fusions.
Figure S4. Detection of the AGK-BRAF fusion in the C0902 cell line using an anti-phospho-BRAF antibody.
Figure S5. No paradoxical effect of vemurafenib in the C0902 cell line.
Table S1. Sequence of the genomic breakpoints and number of supporting reads.
Table S2. Characterization of the cohort.
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