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HPV integration begins in the tonsillar crypt and leads to the alteration of p16, EGFR and c-myc during tumor formation

DC Field Value Language
dc.contributor.author강숙희-
dc.contributor.author구본석-
dc.contributor.author김세헌-
dc.contributor.author조남훈-
dc.contributor.author최은창-
dc.date.accessioned2014-12-21T16:40:31Z-
dc.date.available2014-12-21T16:40:31Z-
dc.date.issued2007-
dc.identifier.issn0020-7136-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/96136-
dc.description.abstractThe prevalence of human papillomavirus (HPV) infection is high in the oropharyngeal mucosal regions, of which the tonsil is the most commonly affected. There may be a link between HPV and the pathogenesis of tonsillar cancer (TC), because of common anatomical characteristics between cervical and tonsillar cancer. We aimed to clarify whether HPV directly affects the oncogenesis and biologic behavior of TC by making a comparison between infection prevalence, physical status and viral loading numbers, and clinicopathologic prognostic factors. To compare HPV-related molecules between TC and tonsillitis (CFT), p16, survivin, HIF-1α, skp-1, cyclin A, cyclin B1, c-myc and EGFR were investigated. We observed a significant difference in HPV prevalence between 52 TCs and 69 CFTs (73.1% vs. 11.6%), and most of the HPVs were type 16 (87.2%) and nonepisomal (94.1%). Most TCs associated with HPV arose from the tonsillar crypts, and tended to be inverted and poorly differentiated. Compared with HPV-negative TC, HPV-positive TC showed a strong association with p16 overexpression (p < 0.0001), and an inverse association with EGFR amplification (p = 0.0478). HPV-16 integration status was strongly associated with c-myc amplification (p = 0.034) and HIF-1α overexpression (p = 0.022). HPV-16 integration could be directly related to tonsillar carcinogenesis initially in tonsillar crypts, followed by cell cycle aberration such as p16 overexpression related to the G1-S phase.-
dc.description.statementOfResponsibilityopen-
dc.format.extent1418~1425-
dc.relation.isPartOfINTERNATIONAL JOURNAL OF CANCER-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHCarcinoma, Squamous Cell/metabolism-
dc.subject.MESHCarcinoma, Squamous Cell/pathology-
dc.subject.MESHCarcinoma, Squamous Cell/virology*-
dc.subject.MESHCyclin A/genetics-
dc.subject.MESHCyclin A/metabolism-
dc.subject.MESHCyclin A1-
dc.subject.MESHCyclin B/genetics-
dc.subject.MESHCyclin B/metabolism-
dc.subject.MESHCyclin B1-
dc.subject.MESHCyclin-Dependent Kinase Inhibitor p16/genetics*-
dc.subject.MESHDNA, Viral/genetics-
dc.subject.MESHDNA, Viral/metabolism-
dc.subject.MESHErbB Receptors/genetics*-
dc.subject.MESHGene Amplification-
dc.subject.MESHHumans-
dc.subject.MESHHypoxia-Inducible Factor 1, alpha Subunit/genetics-
dc.subject.MESHHypoxia-Inducible Factor 1, alpha Subunit/metabolism-
dc.subject.MESHIn Situ Hybridization, Fluorescence-
dc.subject.MESHInhibitor of Apoptosis Proteins-
dc.subject.MESHMicrotubule-Associated Proteins/genetics-
dc.subject.MESHMicrotubule-Associated Proteins/metabolism-
dc.subject.MESHNeoplasm Proteins/genetics-
dc.subject.MESHNeoplasm Proteins/metabolism-
dc.subject.MESHPapillomaviridae/physiology*-
dc.subject.MESHProto-Oncogene Proteins c-myc/genetics*-
dc.subject.MESHRNA, Messenger/metabolism-
dc.subject.MESHReverse Transcriptase Polymerase Chain Reaction-
dc.subject.MESHS-Phase Kinase-Associated Proteins/genetics-
dc.subject.MESHS-Phase Kinase-Associated Proteins/metabolism-
dc.subject.MESHSurvivin-
dc.subject.MESHTissue Array Analysis-
dc.subject.MESHTonsillar Neoplasms/metabolism-
dc.subject.MESHTonsillar Neoplasms/pathology-
dc.subject.MESHTonsillar Neoplasms/virology*-
dc.subject.MESHTonsillitis/genetics-
dc.subject.MESHTonsillitis/pathology-
dc.subject.MESHTonsillitis/virology*-
dc.subject.MESHVirus Integration/physiology*-
dc.titleHPV integration begins in the tonsillar crypt and leads to the alteration of p16, EGFR and c-myc during tumor formation-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Otorhinolaryngology (이비인후과학)-
dc.contributor.googleauthorSe-Heon Kim-
dc.contributor.googleauthorBon-Seok Koo-
dc.contributor.googleauthorNam Hoon Cho-
dc.contributor.googleauthorEun Chang Choi-
dc.contributor.googleauthorJong Man Kim-
dc.contributor.googleauthorMoo Joo Lee-
dc.contributor.googleauthorKyung Ryul Lee-
dc.contributor.googleauthorHaeryoung Kim-
dc.contributor.googleauthorKyeongmee Park-
dc.contributor.googleauthorSuki Kang-
dc.identifier.doi10.1002/ijc.22464-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00044-
dc.contributor.localIdA00194-
dc.contributor.localIdA00605-
dc.contributor.localIdA03812-
dc.contributor.localIdA04161-
dc.relation.journalcodeJ01092-
dc.identifier.eissn1097-0215-
dc.identifier.pmid17205528-
dc.identifier.urlhttp://onlinelibrary.wiley.com/doi/10.1002/ijc.22464/abstract-
dc.contributor.alternativeNameKang, Suki-
dc.contributor.alternativeNameKoo, Bon Seok-
dc.contributor.alternativeNameKim, Se Heon-
dc.contributor.alternativeNameCho, Nam Hoon-
dc.contributor.alternativeNameChoi, Eun Chang-
dc.contributor.affiliatedAuthorKang, Suki-
dc.contributor.affiliatedAuthorKoo, Bon Seok-
dc.contributor.affiliatedAuthorKim, Se Heon-
dc.contributor.affiliatedAuthorCho, Nam Hoon-
dc.contributor.affiliatedAuthorChoi, Eun Chang-
dc.rights.accessRightsnot free-
dc.citation.volume120-
dc.citation.number7-
dc.citation.startPage1418-
dc.citation.endPage1425-
dc.identifier.bibliographicCitationINTERNATIONAL JOURNAL OF CANCER, Vol.120(7) : 1418-1425, 2007-
dc.identifier.rimsid35454-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Otorhinolaryngology (이비인후과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Pathology (병리학교실) > 1. Journal Papers

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