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Journal of Clinical Pathology 2004;57:1084-1088; doi:10.1136/jcp.2004.018507
Copyright © 2004 by the BMJ Publishing Group Ltd & Association of Clinical Pathologists.
Journal of Clinical Pathology 2004;57:1084-1088
© 2004 BMJ Publishing Group Ltd & Association of Clinical Pathologists

ORIGINAL ARTICLE

Comparative molecular pathology of sporadic hyperplastic polyps and neoplastic lesions from the same individual

P Zauber1, M Sabbath-Solitare2, S Marotta2, A Zauber3, T Bishop4

1 Department of Medicine, Saint Barnabas Medical Center, Livingston, NJ 07039, USA
2 Department of Pathology, Saint Barnabas Medical Center
3 Department of Epidemiology and Biostatistics, Memorial Sloan-Kettering Cancer Center, New York City, NY 10021, USA
4 Genetic Epidemiology Division, Cancer Research UK Clinical Centre in Leeds, St James’s University Hospital, Leeds LS9 7TF, UK

Correspondence to:
Correspondence to:
Dr N P Zauber
22 Old Short Hills Road, Livingston, NJ 07039 USA; Pzauber{at}aol.com

Aim: The biology of colorectal hyperplastic polyps is of considerable relevance, because recent evidence suggests that under certain circumstances hyperplastic polyps may be precursors of neoplasms. The aim of this study was to assess and compare the clinical and molecular characteristics of hyperplastic polyps and neoplastic lesions removed from patients without the hyperplastic polyposis syndrome.

Methods: One hundred and twenty six patients were identified through a series of genetic epidemiological studies. Each patient had at least one neoplastic lesion and one hyperplastic polyp; there was a total of 147 hyperplastic polyps. All lesions were evaluated for K-ras mutations, loss of heterozygosity (LOH) of the adenomatous polyposis coli (APC) gene, and microsatellite instability.

Results: K-ras mutation was detected in 15 (10%) hyperplastic polyps, all from the rectosigmoid colon. No hyperplastic polyp had APC LOH or microsatellite instability. Patients with adenomas or carcinomas showing K-ras mutations were not more likely to have hyperplastic polyps with K-ras mutations. The average number of adenomas did not differ between those patients with hyperplastic polyps with K-ras mutations and those without K-ras mutations. There was no association between the hyperplastic polyp and the adenoma regarding the colon segments from which the two lesions were removed.

Conclusions: The sporadic hyperplastic polyp is a lesion with limited molecular change and no relation to patients’ neoplastic lesions.

Abbreviations: APC, adenomatous polyposis coli; CI, confidence interval; HPS, hyperplastic polyposis syndrome; LOH, loss of heterozygosity; OR, odds ratio; PCR, polymerase chain reaction; SSCP, single stranded conformational polymorphism

Keywords: hyperplastic polyps; colonic adenomas; K-ras mutations; microsatellite instability; loss of heterozygosity


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This article has been cited by other articles:

  • Young, J., Jass, J. R. (2006). The case for a genetic predisposition to serrated neoplasia in the colorectum: hypothesis and review of the literature.. Cancer Epidemiol. Biomarkers Prev. 15: 1778-1784 [Abstract] [Full Text]  

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