DNA microsatellite instability in hyperplastic polyps, serrated adenomas, and mixed polyps: a mild mutator pathway for colorectal cancer?

Citation
H. Iino et al., DNA microsatellite instability in hyperplastic polyps, serrated adenomas, and mixed polyps: a mild mutator pathway for colorectal cancer?, J CLIN PATH, 52(1), 1999, pp. 5-9
Citations number
35
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Research/Laboratory Medicine & Medical Tecnology","Medical Research Diagnosis & Treatment
Journal title
JOURNAL OF CLINICAL PATHOLOGY
ISSN journal
0021-9746 → ACNP
Volume
52
Issue
1
Year of publication
1999
Pages
5 - 9
Database
ISI
SICI code
0021-9746(199901)52:1<5:DMIIHP>2.0.ZU;2-8
Abstract
Aim-To investigate the distribution of DNA microsatellite instability (MSI) in a series of hyperplastic polyps, serrated adenomas, and mixed polyps of the colorectum. Methods-DNA was extracted from samples of 73 colorectal polyps comprising t ubular adenomas (23), hyperplastic polyps (21), serrated adenomas (17), and mixed polyps (12). The presence of MSI was investigated at six loci: MYCL, D2S123, F13B, BAT-40, BAT-26, and c-myb T22, using polymerase chain reacti on based methodology. MSI cases were classified as MSI-Low (MSI-L) and MSI- High (MSI-H), based on the number of affected loci. Results-The frequency of MSI increased in tubular adenomas (13%), hyperplas tic polyps (29%), serrated adenomas (53%), and mixed polyps (83%) (Wilcoxon rank sum statistic, p < 0.001). Hyperplastic epithelium was present in nin e of 12 mixed polyps and showed MSI in eight of these. MSI was mostly MSI-L . MSI-H occurred in two serrated adenomas and three mixed polyps. Clonal re lations were demonstrated between hyperplastic and dysplastic epithelium in four of eight informative mixed polyps. Conclusions-The findings support the view that hyperplastic polyps may be f undamentally neoplastic rather than hyperplastic. A proportion of hyperplas tic polyps may serve as a precursor of a subset (10%) of colorectal cancers showing the MSI-L phenotype, albeit through the intermediate step of serra ted dysplasia. This represents a novel and distinct morphogenetic pathway f or colorectal cancer.