Abstract: Our current understanding of colorectal cancer assumes that its pathogenesis includes a progressive accumulation of genomic changes at multiple stages. Thus, initiating events, such as driver mutations affecting APC or KRAS genes, are followed by additional alterations in specific genes such as p16 and p53 [1] and signalling pathways including WNT, MAPK, GNAS or TGFB that, over time, will shape the genomic conditions that drive a pre-malignant lesion towards cancer [2–4]. Thus, premalignant lesions such as colorectal adenomas feature mutational events in APC, BRAF, KRAS and other genes [2, 5]. As the disease progresses, colorectal adenocarcinoma specimens can also accumulate mutations in genes such as p53 and FBXW7 as well as in MAPK, TGFB, PI3K and DNA mismatch-repair pathways [3]. However, the question of whether somatic mutations accumulate in the adenoma-carcinoma sequence in the same patient remains to be investigated.

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