Please use this identifier to cite or link to this item: http://hdl.handle.net/1822/62001

TitleKRAS and BRAF mutations and MSI status in precursor lesions of colorectal cancer detected by colonoscopy
Author(s)Yamane, L. S.
Scapulatempo-Neto, C.
Alvarenga, L.
Oliveira, C. Z.
Berardinelli, G. N.
Almodova, E.
Cunha, T. R.
Fava, G.
Colaiacovo, W.
Melani, A.
Fregnani, J. H.
Reis, R. M.
Guimarães, D. P.
KeywordsAdenocarcinoma
Adenoma
Aged
Aged, 80 and over
Colonic Polyps
Colonoscopy
Colorectal Neoplasms
Female
Humans
Male
Middle Aged
Mutation
Proto-Oncogene Proteins
Proto-Oncogene Proteins B-raf
Proto-Oncogene Proteins p21(ras)
ras Proteins
Microsatellite Instability
serrated polyp
KRAS
BRAF
colorectal cancer
Issue dateOct-2014
PublisherSpandidos Publications
JournalOncology Reports
CitationYamane, L. S., Scapulatempo-Neto, C., Alvarenga, L., Oliveira, C. Z., Berardinelli, G. N., Almodova, E., ... & Fregnani, J. H. (2014). KRAS and BRAF mutations and MSI status in precursor lesions of colorectal cancer detected by colonoscopy. Oncology reports, 32(4), 1419-1426
Abstract(s)Colorectal cancer (CRC) is one of the most frequent cancers worldwide. Adenoma is the main precursor lesion and, recently, the serrated polyps were described as a group of colorectal lesions with malignant potential. The morphologic and biologic characterizations of serrated polyps remain limited. The aim of the present study was to determine the frequency of KRAS and BRAF mutations and microsatellite instability (MSI) in CRC precursor lesions, to evaluate the association between molecular, pathologic and morphologic alterations in precursor lesions and to compare with the alterations detected in CRC. A series of 342 precursor lesions were removed from 155 patients during colonoscopy. After morphologic classification, molecular analysis was performed in 103 precursor lesions, and their genetic profile compared with 47 sporadic CRCs. Adenomas were the main precursor lesions (70.2%). Among the serrated polyps, the main precursor lesion was hyperplastic polyps (HPs) (82.4%), followed by sessile serrated adenomas (12.7%) and traditional serrated adenomas (2.0%). KRAS mutations were detected in 13.6% of the precursor lesions, namely in adenomas and in HPs, but in no serrated adenoma. BRAF mutations were found in 9 (8.7%) precursor lesions, mainly associated with serrated polyps and absent in adenomas (P<0.001). High MSI (MSI-H) was absent in precursor lesions. In the 47 CCR cases, 46.8% exhibited KRAS mutation, 6.5% BRAF mutations and 10.6% MSI-H. This study confirms the role of KRAS and BRAF mutations in CRC carcinogenesis, a crucial step in implementing CRC screening strategies.
TypeArticle
URIhttp://hdl.handle.net/1822/62001
DOI10.3892/or.2014.3338
ISSN1021-335X
e-ISSN1791-2431
Publisher versionhttps://www.spandidos-publications.com/10.3892/or.2014.3338
Peer-Reviewedyes
AccessRestricted access (UMinho)
Appears in Collections:ICVS - Artigos em Revistas Internacionais com Referee

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