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 Detalle_Publicacion

Colorectal adenomas contain multiple somatic mutations that do not coincide with synchronous adenocarcinoma specimens

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.

Otras publicaciones de la misma revista o congreso con autores/as de la Universidad de Cantabria

 Fuente: PLoS One. 2015 Mar 16;10(3):e0119946

Editorial: Public Library of Science

 Año de publicación: 2015

Nº de páginas: 12

Tipo de publicación: Artículo de Revista

 DOI: 10.1371/journal.pone.0119946

ISSN: 1932-6203

Proyecto español: Grant PI12/00357, RETICS, SAF2008-03871

Autores/as

MARTÍNEZ, NEREA

FIDEL ANGEL FERNANDEZ FERNANDEZ

MARTA M. MAYORGA FERNANDEZ

DERDAK, SOPHIA

BELTRÁN, SERGI

THAIDY MORENO RODRIGUEZ

ALMARÁZ, CARMEN

GONZALO DE LAS HERAS CASTAÑO

BAYÉS, MÓNICA

GUT, IVO

MIGUEL ANGEL PIRIS PINILLA