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BRAF gene is not mutated in mismatch repair-proficient or -deficient plasma cell dyscrasias

Leukemia volume 18, pages 658–659 (2004)Cite this article

TO THE EDITOR

The RAS–RAF–MEK–ERK–MAP kinase pathway mediates cellular responses to growth signals, and oncogenic mutations of RAS are found in about 15% of human cancer. Recently, another member of this pathway BRAF, which is one of three RAF serine/threonine kinases regulated by binding RAS, has also been shown to possess activating mutations in different types of solid tumours.1 In colorectal tumours, BRAF mutations were found in 32 of 330 samples, and there was a highly significant incidence in tumours shown to be mismatch repair (MMR) deficient.2 In fact, the V599E mutation, found in exon 15 of the BRAF gene is the most frequent nucleotide substitution so far described in MMR-deficient tumours.

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  1. Northern Institute for Cancer Research, Medical School, Framlington Place, Newcastle upon Tyne, UK

    M Velangi, E Matheson, P Taylor, G Jackson, A G Hall & J A E Irving

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  1. M Velangi
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  2. E Matheson
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  3. P Taylor
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  4. G Jackson
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  5. A G Hall
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  6. J A E Irving
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Correspondence to J A E Irving.

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Velangi, M., Matheson, E., Taylor, P. et al. BRAF gene is not mutated in mismatch repair-proficient or -deficient plasma cell dyscrasias. Leukemia 18, 658–659 (2004). https://doi.org/10.1038/sj.leu.2403286

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  • DOI: https://doi.org/10.1038/sj.leu.2403286

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