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Article: Differential DNA methylation profiles in gynecological cancers and correlation with clinico-pathological data

TitleDifferential DNA methylation profiles in gynecological cancers and correlation with clinico-pathological data
Authors
Issue Date2006
PublisherBioMed Central Ltd. The Journal's web site is located at http://www.biomedcentral.com/bmccancer/
Citation
Bmc Cancer, 2006, v. 6 How to Cite?
AbstractBackground: Epigenetic gene silencing is one of the major causes of carcinogenesis. Its widespread occurrence in cancer genome could inactivate many cellular pathways including DNA repair, cell cycle control, apoptosis, cell adherence, and detoxification. The abnormal promoter methylation might be a potential molecular marker for cancer management. Methods: For rapid identification of potential targets for aberrant methylation in gynecological cancers, methylation status of the CpG islands of 34 genes was determined using pooled DNA approach and methylation-specific PCR. Pooled DNA mixture from each cancer type (50 cervical cancers, 50 endometrial cancers and 50 ovarian cancers) was made to form three test samples. The corresponding normal DNA from the patients of each cancer type was also pooled to form the other three control samples. Methylated alleles detected in tumors, but not in normal controls, were indicative of aberrant methylation in tumors. Having identified potential markers, frequencies of methylation were further analyzed in individual samples. Markers identified are used to correlate with clinico-pathological data of tumors using χ2 or Fisher's exact test. Results: APC and p16 were hypermethylated across the three cancers. MINT31 and PTEN were hypermethylated in cervical and ovarian cancers. Specific methylation was found in cervical cancer (including CDHI, DAPK, MGMT and MINT2), endometrial cancer (CASP8, CDH13, hMLH1 and p73), and ovarian cancer (BRCA1, p14, p15, RIZ1 and TMS1). The frequencies of occurrence of hypermethylation in 4 candidate genes in individual samples of each cancer type (DAPK, MGMT, p16 and PTEN in 127 cervical cancers; APC, CDHI3, hMLHI and p16 in 60 endometrial cancers; and BRCAI, p14, p16 and PTEN in 49 ovarian cancers) were examined for further confirmation. Incidence varied among different genes and in different cancer types ranging from the lowest 8.2% (PTEN in ovarian cancer) to the highest 56.7% (DAPK in cervical cancer). Aberrant methylation for some genes (BRCA1, DAPK, hMLH1, MGMT, p14, p16, and PTEN) was also associated with clinico-pathological data. Conclusion: Thus, differential methylation profiles occur in the three types of gynecologic cancer. Detection of methylation for critical loci is potentially useful as epigenetic markers in tumor classification. More studies using a much larger sample size are needed to define the potential role of DNA methylation as marker for cancer management. © 2006 Yang et al; licensee BioMed Central Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/45492
ISSN
2015 Impact Factor: 3.265
2015 SCImago Journal Rankings: 1.627
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYang, HJen_HK
dc.contributor.authorLiu, VWSen_HK
dc.contributor.authorWang, Yen_HK
dc.contributor.authorTsang, PCKen_HK
dc.contributor.authorNgan, HYSen_HK
dc.date.accessioned2007-10-30T06:27:17Z-
dc.date.available2007-10-30T06:27:17Z-
dc.date.issued2006en_HK
dc.identifier.citationBmc Cancer, 2006, v. 6en_HK
dc.identifier.issn1471-2407en_HK
dc.identifier.urihttp://hdl.handle.net/10722/45492-
dc.description.abstractBackground: Epigenetic gene silencing is one of the major causes of carcinogenesis. Its widespread occurrence in cancer genome could inactivate many cellular pathways including DNA repair, cell cycle control, apoptosis, cell adherence, and detoxification. The abnormal promoter methylation might be a potential molecular marker for cancer management. Methods: For rapid identification of potential targets for aberrant methylation in gynecological cancers, methylation status of the CpG islands of 34 genes was determined using pooled DNA approach and methylation-specific PCR. Pooled DNA mixture from each cancer type (50 cervical cancers, 50 endometrial cancers and 50 ovarian cancers) was made to form three test samples. The corresponding normal DNA from the patients of each cancer type was also pooled to form the other three control samples. Methylated alleles detected in tumors, but not in normal controls, were indicative of aberrant methylation in tumors. Having identified potential markers, frequencies of methylation were further analyzed in individual samples. Markers identified are used to correlate with clinico-pathological data of tumors using χ2 or Fisher's exact test. Results: APC and p16 were hypermethylated across the three cancers. MINT31 and PTEN were hypermethylated in cervical and ovarian cancers. Specific methylation was found in cervical cancer (including CDHI, DAPK, MGMT and MINT2), endometrial cancer (CASP8, CDH13, hMLH1 and p73), and ovarian cancer (BRCA1, p14, p15, RIZ1 and TMS1). The frequencies of occurrence of hypermethylation in 4 candidate genes in individual samples of each cancer type (DAPK, MGMT, p16 and PTEN in 127 cervical cancers; APC, CDHI3, hMLHI and p16 in 60 endometrial cancers; and BRCAI, p14, p16 and PTEN in 49 ovarian cancers) were examined for further confirmation. Incidence varied among different genes and in different cancer types ranging from the lowest 8.2% (PTEN in ovarian cancer) to the highest 56.7% (DAPK in cervical cancer). Aberrant methylation for some genes (BRCA1, DAPK, hMLH1, MGMT, p14, p16, and PTEN) was also associated with clinico-pathological data. Conclusion: Thus, differential methylation profiles occur in the three types of gynecologic cancer. Detection of methylation for critical loci is potentially useful as epigenetic markers in tumor classification. More studies using a much larger sample size are needed to define the potential role of DNA methylation as marker for cancer management. © 2006 Yang et al; licensee BioMed Central Ltd.en_HK
dc.format.extent457659 bytes-
dc.format.extent1784 bytes-
dc.format.extent3017 bytes-
dc.format.mimetypeapplication/pdf-
dc.format.mimetypetext/plain-
dc.format.mimetypetext/plain-
dc.languageengen_HK
dc.publisherBioMed Central Ltd. The Journal's web site is located at http://www.biomedcentral.com/bmccancer/en_HK
dc.relation.ispartofBMC Canceren_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject.meshDNA Methylationen_HK
dc.subject.meshGenital Neoplasms, Female - metabolism - pathologyen_HK
dc.subject.meshOvarian Neoplasms - pathologyen_HK
dc.subject.meshUterine Cervical Neoplasms - pathologyen_HK
dc.subject.meshEndometrial Neoplasms - pathologyen_HK
dc.titleDifferential DNA methylation profiles in gynecological cancers and correlation with clinico-pathological dataen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1471-2407&volume=6&spage=212&epage=&date=2006&atitle=Differential+DNA+methylation+profiles+in+gynecological+cancers+and+correlation+with+clinico-pathological+dataen_HK
dc.identifier.emailLiu, VWS: vwsliu@hkusua.hku.hken_HK
dc.identifier.emailNgan, HYS: hysngan@hkucc.hku.hken_HK
dc.identifier.authorityLiu, VWS=rp00341en_HK
dc.identifier.authorityNgan, HYS=rp00346en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1186/1471-2407-6-212en_HK
dc.identifier.pmid16928264-
dc.identifier.pmcidPMC1560388-
dc.identifier.scopuseid_2-s2.0-33748639077en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33748639077&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume6en_HK
dc.identifier.isiWOS:000240420200001-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridYang, HJ=7408624370en_HK
dc.identifier.scopusauthoridLiu, VWS=7006405113en_HK
dc.identifier.scopusauthoridWang, Y=8678094600en_HK
dc.identifier.scopusauthoridTsang, PCK=7102404070en_HK
dc.identifier.scopusauthoridNgan, HYS=34571944100en_HK
dc.identifier.citeulike814846-

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