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Mutation in KRAS, BRAF and PIK3CA are commonly present in colorectal cancer (CRC). KRAS and BRAF form part of the mitogen-activated protein kinase (MAPK) signalling pathway and KRAS lies immediately upstream of BRAF. Consequently, KRAS and BRAF mutations are mutually exclusive with mutation in either one causing activation of MAPK signalling.1 PIK3CA forms part of the phosphatidylinositide‐3‐kinase PI3K signalling pathway, and several studies have shown a significant association of KRAS and PIK3CA mutation in several cancer types including CRC.1–3 At face value, there would appear to be positive co-selection of MAPK and PI3K signalling activation implying synergy between these two pathways. If this were true, then a similar positive association would be expected between mutation of BRAF and PIK3CA. To date, less consistent or no association of BRAF and PIK3CA mutation has been reported.1 3 4 However, it is well established that BRAF mutation is strongly associated with microsatellite instability (MSI) in CRC. We therefore sought to test the association between mutation of BRAF and PIK3CA …
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