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• W2610281631 abstract "Colonic polyps may arise from BRAF inhibitor treatment of melanoma, possibly due to paradoxical activation of the mitogen-activated protein (MAP)-kinase pathway. In an alternative evidence based scenario, tubular colonic adenomas with APC gene mutations have also been identified in the context of BRAF inhibitor treatment, in the absence of mutations of MAPK genes. A minority of colorectal cancers develop by an alternative serrated polyp pathway. This article postulates a novel hypothesis, that the established phenotypic and molecular characteristics of serrated colonic polyps/CRC offer an intriguing insight into the pathobiology of BRAF inhibitor induced colonic polyps. Serrated polyps are characterized by a CpG island methylation phenotype, MLH1 silencing and cellular senescence. They also have BRAF mutations. The contention is that BRAF inhibitor induced polyps mimic the afore-described histology and molecular features of serrated polyps with the exception that instead of the presence of BRAF mutations they induce C-RAF homodimers and B-RAF: C-RAF heterodimers." @default.
• W2610281631 created "2017-05-12" @default.
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• W2610281631 date "2017-01-01" @default.
• W2610281631 modified "2023-10-14" @default.
• W2610281631 title "BRAF inhibitor treatment of melanoma causing colonic polyps: An alternative hypothesis" @default.
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• W2610281631 doi "https://doi.org/10.3748/wjg.v23.i17.3022" @default.
• W2610281631 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5423039" @default.
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