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Conference Paper: HPV16 and HPV58 integrations in cervical cancer and premalignant lesions

TitleHPV16 and HPV58 integrations in cervical cancer and premalignant lesions
Authors
Issue Date2011
Publisher27th International Papillomavirus Conference and Clinical Workshop.
Citation
The 27th International Papillomavirus Conference and Clinical Workshop, Berlin, Germany, 17-22 September 2011. In Abstract Book 3, 2011, p. 52, abstract P-24.29 How to Cite?
Abstract
BACKGROUND: Genomic integration of the high-risk human papillomavirus (HPV) DNA into host genome is an important event in the cervical carcinogenesis from premalignant lesions to invasive cervical cancer. The viral DNA integration usually causes the deletion and/or disruption of HPV E2 gene, leading to the up-regulation of E6/7 viral oncoproteins. However, the prognostic value of the viral DNA integration in the prediction of the progression of premalignant lesions is still controversial. HPV16 and HPV58 are the most prevalent high-risk types found in cervical cancer and premalignant lesions in Chinese women, whereas the viral DNA integration status is unknown. OBJECTIVES: To assess the prevalence of HPV16 and HPV58 integrations in cervical cancer and premalignant lesions, as well as their clinical significance. Methods: Genomic DNAs were extracted from 110 HPV16 positive and 48 HPV58 positive cervical samples. HPV infection and genotyping was detected using INNO-LiPA HPV genotyping test. The integration state of the virus was measured by quantitative real-time fluorescent PCR with specific primers targeting E2 and E6 genes of HPV16 and HPV58, and determined by the E2/E6 ratio. RESULTS: HPV16 integration was detected in over 90% of the samples, counting 20 (95.2%) normal cervical samples, 12 (92.3%) ASCUS/low-grade CIN, 22 (95.7%) high-grade CIN and 53 (100%) cancers. Similarly, viral integration was also observed in most of the HPV58 positive samples (44 of 48, 91.7%), including 86.7% normal cervical samples and ASCUS/low-grade CIN, and 100% high-grade CIN and cancers. The integration status of HPV16/58 did not correlate with disease stages and patient survival. CONCLUSIONS: The HPV viral integration in host genome was a common phenomenon in HPV infected normal and cervical disease cases, suggesting that viral DNA integration may occur early in the cervical lesion progression.
DescriptionPoster Session 24 - Transformation and Carcinogenesis I: P-24.29
Persistent Identifierhttp://hdl.handle.net/10722/165572

 

DC FieldValueLanguage
dc.contributor.authorLiu, Sen_US
dc.contributor.authorChan, YKen_US
dc.contributor.authorLeung, Ren_US
dc.contributor.authorJiang, Len_US
dc.contributor.authorLuk, Men_US
dc.contributor.authorLo, Sen_US
dc.contributor.authorFong, Den_US
dc.contributor.authorCheung, Aen_US
dc.contributor.authorLin, Zen_US
dc.contributor.authorNgan, Hen_US
dc.date.accessioned2012-09-20T08:19:57Z-
dc.date.available2012-09-20T08:19:57Z-
dc.date.issued2011en_US
dc.identifier.citationThe 27th International Papillomavirus Conference and Clinical Workshop, Berlin, Germany, 17-22 September 2011. In Abstract Book 3, 2011, p. 52, abstract P-24.29en_US
dc.identifier.urihttp://hdl.handle.net/10722/165572-
dc.descriptionPoster Session 24 - Transformation and Carcinogenesis I: P-24.29-
dc.description.abstractBACKGROUND: Genomic integration of the high-risk human papillomavirus (HPV) DNA into host genome is an important event in the cervical carcinogenesis from premalignant lesions to invasive cervical cancer. The viral DNA integration usually causes the deletion and/or disruption of HPV E2 gene, leading to the up-regulation of E6/7 viral oncoproteins. However, the prognostic value of the viral DNA integration in the prediction of the progression of premalignant lesions is still controversial. HPV16 and HPV58 are the most prevalent high-risk types found in cervical cancer and premalignant lesions in Chinese women, whereas the viral DNA integration status is unknown. OBJECTIVES: To assess the prevalence of HPV16 and HPV58 integrations in cervical cancer and premalignant lesions, as well as their clinical significance. Methods: Genomic DNAs were extracted from 110 HPV16 positive and 48 HPV58 positive cervical samples. HPV infection and genotyping was detected using INNO-LiPA HPV genotyping test. The integration state of the virus was measured by quantitative real-time fluorescent PCR with specific primers targeting E2 and E6 genes of HPV16 and HPV58, and determined by the E2/E6 ratio. RESULTS: HPV16 integration was detected in over 90% of the samples, counting 20 (95.2%) normal cervical samples, 12 (92.3%) ASCUS/low-grade CIN, 22 (95.7%) high-grade CIN and 53 (100%) cancers. Similarly, viral integration was also observed in most of the HPV58 positive samples (44 of 48, 91.7%), including 86.7% normal cervical samples and ASCUS/low-grade CIN, and 100% high-grade CIN and cancers. The integration status of HPV16/58 did not correlate with disease stages and patient survival. CONCLUSIONS: The HPV viral integration in host genome was a common phenomenon in HPV infected normal and cervical disease cases, suggesting that viral DNA integration may occur early in the cervical lesion progression.-
dc.languageengen_US
dc.publisher27th International Papillomavirus Conference and Clinical Workshop.-
dc.relation.ispartofAbstract Book 3 - Basic Scienceen_US
dc.titleHPV16 and HPV58 integrations in cervical cancer and premalignant lesionsen_US
dc.typeConference_Paperen_US
dc.identifier.emailLiu, S: stephasl@hku.hken_US
dc.identifier.emailChan, YK: ykchanc@hku.hken_US
dc.identifier.emailLeung, R: cyleungr@hkucc.hku.hken_US
dc.identifier.emailFong, D: dytfong@hku.hken_US
dc.identifier.emailCheung, A: anycheun@hkucc.hku.hken_US
dc.identifier.emailNgan, H: hysngan@hkucc.hku.hken_US
dc.identifier.authorityLiu, S=rp00372en_US
dc.identifier.authorityChan, YK=rp00453en_US
dc.identifier.authorityFong, D=rp00253en_US
dc.identifier.authorityCheung, A=rp00542en_US
dc.identifier.authorityNgan, H=rp00346en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.hkuros208679en_US
dc.identifier.spage52-
dc.identifier.epage52-
dc.publisher.placeGermany-
dc.customcontrol.immutablesml 130514-

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