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Article: Concordant CpG island methylation in hyperplastic polyposis

TitleConcordant CpG island methylation in hyperplastic polyposis
Authors
Issue Date2002
PublisherAmerican Society for Investigative Pathology. The Journal's web site is located at http://www.amjpathol.org
Citation
American Journal of Pathology, 2002, v. 160 n. 2, p. 529-536 How to Cite?
AbstractThe CpG island methylator phenotype (CIMP) is a newly described mechanism for carcinogenesis in colorectal carcinomas and adenomas characterized by methylation of multiple CpG islands. The causes of CIMP are unknown. We studied CIMP in hyperplastic polyps (HPs), with emphasis on patients with multiple HPs (5 to 10 HPs), large HPs (one HP >1 cm) or hyperplastic polyposis (>20 HPs). Methylation of p16, MINT1, MINT2, MINT31, and hMLH1 was analyzed by methylation-specific polymerase chain reaction in 102 HPs, 8 serrated adenomas, 19 tubular adenomas, and 9 adenocarcinomas from 17 patients, with multiple/large HPs or hyperplastic polyposis and in 16 sporadic HPs from 14 additional patients. Sporadic HPs were CIMP-negative (not methylated at any locus), but 43% of HPs from multiple/large HPs, or hyperplastic polyposis were CIMP-high (two or more methylated loci, P = 0.00001). Methylation among the four loci was correlated within HPs (odds ratio, 3.41; P = 0.002), and the methylation status of HPs within the same patient was also correlated (odds ratio, 5.92; P = 0.0001). CIMP-high HPs were present primarily in patients with a predominance of HPs in the right colon and/or serrated adenomas (P = 0.0009) and were associated with the absence of K-ras proto-oncogene mutations (odds ratio, 5.08; P = 0.03). Our findings of concordant CpG island methylation of HPs in multiple/large HPs or hyperplastic polyposis supports the concept that some patients have a hypermethylator phenotype characterized by methylation of multiple HPs and other colorectal lesions. The hypermethylator phenotype is related to patient-specific factors, such as carcinogenic exposure or genetic predisposition.
Persistent Identifierhttp://hdl.handle.net/10722/49124
ISSN
2015 Impact Factor: 4.206
2015 SCImago Journal Rankings: 2.653
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorChan, OOen_HK
dc.contributor.authorIssa, JPJen_HK
dc.contributor.authorMorris, JSen_HK
dc.contributor.authorHamilton, SRen_HK
dc.contributor.authorRashid, Aen_HK
dc.date.accessioned2008-06-12T06:34:56Z-
dc.date.available2008-06-12T06:34:56Z-
dc.date.issued2002en_HK
dc.identifier.citationAmerican Journal of Pathology, 2002, v. 160 n. 2, p. 529-536en_HK
dc.identifier.issn0002-9440en_HK
dc.identifier.urihttp://hdl.handle.net/10722/49124-
dc.description.abstractThe CpG island methylator phenotype (CIMP) is a newly described mechanism for carcinogenesis in colorectal carcinomas and adenomas characterized by methylation of multiple CpG islands. The causes of CIMP are unknown. We studied CIMP in hyperplastic polyps (HPs), with emphasis on patients with multiple HPs (5 to 10 HPs), large HPs (one HP >1 cm) or hyperplastic polyposis (>20 HPs). Methylation of p16, MINT1, MINT2, MINT31, and hMLH1 was analyzed by methylation-specific polymerase chain reaction in 102 HPs, 8 serrated adenomas, 19 tubular adenomas, and 9 adenocarcinomas from 17 patients, with multiple/large HPs or hyperplastic polyposis and in 16 sporadic HPs from 14 additional patients. Sporadic HPs were CIMP-negative (not methylated at any locus), but 43% of HPs from multiple/large HPs, or hyperplastic polyposis were CIMP-high (two or more methylated loci, P = 0.00001). Methylation among the four loci was correlated within HPs (odds ratio, 3.41; P = 0.002), and the methylation status of HPs within the same patient was also correlated (odds ratio, 5.92; P = 0.0001). CIMP-high HPs were present primarily in patients with a predominance of HPs in the right colon and/or serrated adenomas (P = 0.0009) and were associated with the absence of K-ras proto-oncogene mutations (odds ratio, 5.08; P = 0.03). Our findings of concordant CpG island methylation of HPs in multiple/large HPs or hyperplastic polyposis supports the concept that some patients have a hypermethylator phenotype characterized by methylation of multiple HPs and other colorectal lesions. The hypermethylator phenotype is related to patient-specific factors, such as carcinogenic exposure or genetic predisposition.en_HK
dc.format.extent388 bytes-
dc.format.mimetypetext/html-
dc.languageengen_HK
dc.publisherAmerican Society for Investigative Pathology. The Journal's web site is located at http://www.amjpathol.orgen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject.meshColonic Polyps - genetics - pathologyen_HK
dc.subject.meshColorectal Neoplasms - geneticsen_HK
dc.subject.meshCpG Islands - geneticsen_HK
dc.subject.meshDNA Methylationen_HK
dc.subject.meshIntestinal Polyps - genetics - pathologyen_HK
dc.titleConcordant CpG island methylation in hyperplastic polyposisen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0002-9440&volume=160&issue=2&spage=529&epage=536&date=2002&atitle=Concordant+CpG+island+methylation+in+hyperplastic+polyposisen_HK
dc.identifier.emailChan, OO: aoochan@HKUCC.hku.hken_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.pmid11839573-
dc.identifier.pmcidPMC1850645en_HK
dc.identifier.scopuseid_2-s2.0-0036169109-
dc.identifier.hkuros80838-
dc.identifier.isiWOS:000173733500017-

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