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Article: TP53 codon 72 polymorphism and cervical cancer: a pooled analysis of individual data from 49 studies

TitleTP53 codon 72 polymorphism and cervical cancer: a pooled analysis of individual data from 49 studies
Authors
Issue Date2009
PublisherThe Lancet Publishing Group. The Journal's web site is located at http://www.elsevier.com/locate/j.lancetoncol
Citation
The Lancet Oncology, 2009, v. 10 n. 8, p. 772-784 How to Cite?
AbstractBackground: Cervical cancer is caused primarily by human papillomaviruses (HPV). The polymorphism rs1042522 at codon 72 of the TP53 tumour-suppressor gene has been investigated as a genetic cofactor. More than 80 studies were done between 1998 and 2006, after it was initially reported that women who are homozygous for the arginine allele had a risk for cervical cancer seven times higher than women who were heterozygous for the allele. However, results have been inconsistent. Here we analyse pooled data from 49 studies to determine whether there is an association between TP53 codon 72 polymorphism and cervical cancer. Methods: Individual data on 7946 cases and 7888 controls from 49 different studies worldwide were reanalysed. Odds ratios (OR) were estimated using logistic regression, stratifying by study and ethnic origin. Subgroup analyses were done for infection with HPV, ethnic origin, Hardy-Weinberg equilibrium, study quality, and the material used to determine TP53 genotype. Findings: The pooled estimates (OR) for invasive cervical cancer were 1·22 (95% CI 1·08-1·39) for arginine homozygotes compared with heterozygotes, and 1·13 (0·94-1·35) for arginine homozygotes versus proline homozygotes. Subgroup analyses showed significant excess risks only in studies where controls were not in Hardy-Weinberg equilibrium (1·71 [1·21-2·42] for arginine homozygotes compared with heterozygotes), in non-epidemiological studies (1·35 [1·15-1·58] for arginine homozygotes compared with heterozygotes), and in studies where TP53 genotype was determined from tumour tissue (1·39 [1·13-1·73] for arginine homozygotes compared with heterozygotes). Null results were noted in studies with sound epidemiological design and conduct (1·06 [0·87-1·29] for arginine homozygotes compared with heterozygotes), and studies in which TP53 genotype was determined from white blood cells (1·06 [0·87-1·29] for arginine homozygotes compared with heterozygotes). Interpretation: Subgroup analyses indicated that excess risks were most likely not due to clinical or biological factors, but to errors in study methods. No association was found between cervical cancer and TP53 codon 72 polymorphism when the analysis was restricted to methodologically sound studies. Funding: German Research Foundation (DFG). © 2009 Elsevier Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/87375
ISSN
2015 Impact Factor: 26.509
2015 SCImago Journal Rankings: 13.940
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorKlug, SJen_HK
dc.contributor.authorRessing, Men_HK
dc.contributor.authorKoenig, Jen_HK
dc.contributor.authorAbba, MCen_HK
dc.contributor.authorAgorastos, Ten_HK
dc.contributor.authorBrenna, SMen_HK
dc.contributor.authorCiotti, Men_HK
dc.contributor.authorDas, BRen_HK
dc.contributor.authorDel Mistro, Aen_HK
dc.contributor.authorDybikowska, Aen_HK
dc.contributor.authorGiuliano, ARen_HK
dc.contributor.authorGudleviciene, Zen_HK
dc.contributor.authorGyllensten, Uen_HK
dc.contributor.authorHaws, ALen_HK
dc.contributor.authorHelland, Aen_HK
dc.contributor.authorHerrington, CSen_HK
dc.contributor.authorHildesheim, Aen_HK
dc.contributor.authorHumbey, Oen_HK
dc.contributor.authorJee, SHen_HK
dc.contributor.authorKim, JWen_HK
dc.contributor.authorMadeleine, MMen_HK
dc.contributor.authorMenczer, Jen_HK
dc.contributor.authorNgan, HYen_HK
dc.contributor.authorNishikawa, Aen_HK
dc.contributor.authorNiwa, Yen_HK
dc.contributor.authorPegoraro, Ren_HK
dc.contributor.authorPillai, MRen_HK
dc.contributor.authorRanzani, Gen_HK
dc.contributor.authorRezza, Gen_HK
dc.contributor.authorRosenthal, ANen_HK
dc.contributor.authorRoychoudhury, Sen_HK
dc.contributor.authorSaranath, Den_HK
dc.contributor.authorSchmitt, VMen_HK
dc.contributor.authorSengupta, Sen_HK
dc.contributor.authorSettheethamIshida, Wen_HK
dc.contributor.authorShirasawa, Hen_HK
dc.contributor.authorSnijders, PJen_HK
dc.contributor.authorStoler, MHen_HK
dc.contributor.authorSuárezRincón, AEen_HK
dc.contributor.authorSzarka, Ken_HK
dc.contributor.authorTachezy, Ren_HK
dc.contributor.authorUeda, Men_HK
dc.contributor.authorvan der Zee, AGen_HK
dc.contributor.authorvon Knebel Doeberitz, Men_HK
dc.contributor.authorWu, MTen_HK
dc.contributor.authorYamashita, Ten_HK
dc.contributor.authorZehbe, Ien_HK
dc.contributor.authorBlettner, Men_HK
dc.date.accessioned2010-09-06T09:28:52Z-
dc.date.available2010-09-06T09:28:52Z-
dc.date.issued2009en_HK
dc.identifier.citationThe Lancet Oncology, 2009, v. 10 n. 8, p. 772-784en_HK
dc.identifier.issn1470-2045en_HK
dc.identifier.urihttp://hdl.handle.net/10722/87375-
dc.description.abstractBackground: Cervical cancer is caused primarily by human papillomaviruses (HPV). The polymorphism rs1042522 at codon 72 of the TP53 tumour-suppressor gene has been investigated as a genetic cofactor. More than 80 studies were done between 1998 and 2006, after it was initially reported that women who are homozygous for the arginine allele had a risk for cervical cancer seven times higher than women who were heterozygous for the allele. However, results have been inconsistent. Here we analyse pooled data from 49 studies to determine whether there is an association between TP53 codon 72 polymorphism and cervical cancer. Methods: Individual data on 7946 cases and 7888 controls from 49 different studies worldwide were reanalysed. Odds ratios (OR) were estimated using logistic regression, stratifying by study and ethnic origin. Subgroup analyses were done for infection with HPV, ethnic origin, Hardy-Weinberg equilibrium, study quality, and the material used to determine TP53 genotype. Findings: The pooled estimates (OR) for invasive cervical cancer were 1·22 (95% CI 1·08-1·39) for arginine homozygotes compared with heterozygotes, and 1·13 (0·94-1·35) for arginine homozygotes versus proline homozygotes. Subgroup analyses showed significant excess risks only in studies where controls were not in Hardy-Weinberg equilibrium (1·71 [1·21-2·42] for arginine homozygotes compared with heterozygotes), in non-epidemiological studies (1·35 [1·15-1·58] for arginine homozygotes compared with heterozygotes), and in studies where TP53 genotype was determined from tumour tissue (1·39 [1·13-1·73] for arginine homozygotes compared with heterozygotes). Null results were noted in studies with sound epidemiological design and conduct (1·06 [0·87-1·29] for arginine homozygotes compared with heterozygotes), and studies in which TP53 genotype was determined from white blood cells (1·06 [0·87-1·29] for arginine homozygotes compared with heterozygotes). Interpretation: Subgroup analyses indicated that excess risks were most likely not due to clinical or biological factors, but to errors in study methods. No association was found between cervical cancer and TP53 codon 72 polymorphism when the analysis was restricted to methodologically sound studies. Funding: German Research Foundation (DFG). © 2009 Elsevier Ltd. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherThe Lancet Publishing Group. The Journal's web site is located at http://www.elsevier.com/locate/j.lancetoncolen_HK
dc.relation.ispartofThe Lancet Oncologyen_HK
dc.subject.meshAdolescenten_HK
dc.subject.meshAdulten_HK
dc.subject.meshAgeden_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGenes, p53en_HK
dc.subject.meshGenetic Predisposition to Diseaseen_HK
dc.subject.meshHumansen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshPapillomavirus Infections - complications - geneticsen_HK
dc.subject.meshPolymorphism, Geneticen_HK
dc.subject.meshUterine Cervical Neoplasms - genetics - virologyen_HK
dc.subject.meshYoung Adulten_HK
dc.titleTP53 codon 72 polymorphism and cervical cancer: a pooled analysis of individual data from 49 studiesen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0140-6736&volume=10&issue=8&spage=&epage=&date=2009&atitle=TP53+codon+72+polymorphism+and+cervical+cancer:+a+pooled+analysis+of+individual+data+from+49+studiesen_HK
dc.identifier.emailNgan, HY:hysngan@hkucc.hku.hken_HK
dc.identifier.authorityNgan, HY=rp00346en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S1470-2045(09)70187-1en_HK
dc.identifier.pmid19625214en_HK
dc.identifier.scopuseid_2-s2.0-67651158989en_HK
dc.identifier.hkuros161721en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-67651158989&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume10en_HK
dc.identifier.issue8en_HK
dc.identifier.spage772en_HK
dc.identifier.epage784en_HK
dc.identifier.isiWOS:000268697700016-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridKlug, SJ=7004363010en_HK
dc.identifier.scopusauthoridRessing, M=34868623000en_HK
dc.identifier.scopusauthoridKoenig, J=7201555429en_HK
dc.identifier.scopusauthoridAbba, MC=6603775921en_HK
dc.identifier.scopusauthoridAgorastos, T=7004201994en_HK
dc.identifier.scopusauthoridBrenna, SM=36939530700en_HK
dc.identifier.scopusauthoridCiotti, M=7005743246en_HK
dc.identifier.scopusauthoridDas, BR=35278158300en_HK
dc.identifier.scopusauthoridDel Mistro, A=7003892467en_HK
dc.identifier.scopusauthoridDybikowska, A=6506226604en_HK
dc.identifier.scopusauthoridGiuliano, AR=7101806090en_HK
dc.identifier.scopusauthoridGudleviciene, Z=12777271600en_HK
dc.identifier.scopusauthoridGyllensten, U=7004953409en_HK
dc.identifier.scopusauthoridHaws, AL=8727372600en_HK
dc.identifier.scopusauthoridHelland, A=7003281104en_HK
dc.identifier.scopusauthoridHerrington, CS=7005129965en_HK
dc.identifier.scopusauthoridHildesheim, A=7005255598en_HK
dc.identifier.scopusauthoridHumbey, O=6602790059en_HK
dc.identifier.scopusauthoridJee, SH=16039275900en_HK
dc.identifier.scopusauthoridKim, JW=34771509800en_HK
dc.identifier.scopusauthoridMadeleine, MM=6701675064en_HK
dc.identifier.scopusauthoridMenczer, J=7005620636en_HK
dc.identifier.scopusauthoridNgan, HY=34571944100en_HK
dc.identifier.scopusauthoridNishikawa, A=7202385314en_HK
dc.identifier.scopusauthoridNiwa, Y=7202582983en_HK
dc.identifier.scopusauthoridPegoraro, R=7004110964en_HK
dc.identifier.scopusauthoridPillai, MR=35278495300en_HK
dc.identifier.scopusauthoridRanzani, G=7004049286en_HK
dc.identifier.scopusauthoridRezza, G=7103351229en_HK
dc.identifier.scopusauthoridRosenthal, AN=7203080137en_HK
dc.identifier.scopusauthoridRoychoudhury, S=7005948721en_HK
dc.identifier.scopusauthoridSaranath, D=7003824918en_HK
dc.identifier.scopusauthoridSchmitt, VM=12752804900en_HK
dc.identifier.scopusauthoridSengupta, S=15067670800en_HK
dc.identifier.scopusauthoridSettheethamIshida, W=6603228769en_HK
dc.identifier.scopusauthoridShirasawa, H=7006189334en_HK
dc.identifier.scopusauthoridSnijders, PJ=35432268100en_HK
dc.identifier.scopusauthoridStoler, MH=7006130106en_HK
dc.identifier.scopusauthoridSuárezRincón, AE=6507852864en_HK
dc.identifier.scopusauthoridSzarka, K=6603402009en_HK
dc.identifier.scopusauthoridTachezy, R=6701593451en_HK
dc.identifier.scopusauthoridUeda, M=7403944211en_HK
dc.identifier.scopusauthoridvan der Zee, AG=55166499500en_HK
dc.identifier.scopusauthoridvon Knebel Doeberitz, M=35477888400en_HK
dc.identifier.scopusauthoridWu, MT=8211122000en_HK
dc.identifier.scopusauthoridYamashita, T=7404185314en_HK
dc.identifier.scopusauthoridZehbe, I=7003448919en_HK
dc.identifier.scopusauthoridBlettner, M=7004331042en_HK
dc.identifier.citeulike5374132-

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