File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Genetic abnormalities and HPV status in cervical and vulvar squamous cell carcinomas

TitleGenetic abnormalities and HPV status in cervical and vulvar squamous cell carcinomas
Authors
Issue Date2005
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/cancergene
Citation
Cancer Genetics And Cytogenetics, 2005, v. 157 n. 1, p. 42-48 How to Cite?
AbstractCervical and vulvar cancers are diseases of the female lower genital tract, and high-risk human papillomavirus (HPV) infection is the most important risk factor for the development of both cancers. However, it is clear that additional genetic events are necessary for tumor progression, particularly in HPV-negative cases. We detected the presence of high-risk HPV16 and HPV18 genomes by gene-specific polymerase chain reaction and searched for common genetic imbalances by comparative genomic hybridization (CGH) in 28 cervical and 8 vulvar tumor samples and 7 cancer cell lines. The presence of the HPV genome was detected in 25/28 (89%) cervical tumors and 6/8 (75%) vulvar tumors. CGH of cervical and vulvar tumor samples revealed a consistent pattern of genetic changes in both cancers. Frequent gains were found in 1q, 3q, 5p, and 8q, and less consistent losses were detected in 2q, 3p, 4p, and 11p. Notably, a high-level amplification of 3q was found in 9/28 (32%) cervical tumors and 1/8 (12.5%) vulvar tumors, indicating a pivotal role of gain of 3q in cervical and vulvar carcinogenesis. Furthermore, gains of 5p identified in 9/28 (32%) cervical tumors and 3/8 (37.5%) vulvar tumors were seldom described, particularly in vulvar tumors. Our findings suggest that cervical and vulvar carcinomas bear similar chromosomal alteration hot spots that largely coincide with common genomic lesions during tumor progression, besides the initiation by infection and integration of oncogenic HPV. © 2005 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/173277
ISSN
2012 Impact Factor: 1.929
2013 SCImago Journal Rankings: 0.872
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorHuang, FYen_HK
dc.contributor.authorKwok, YKYen_HK
dc.contributor.authorLau, ETen_HK
dc.contributor.authorTang, MHYen_HK
dc.contributor.authorNg, TYen_HK
dc.contributor.authorNgan, HYSen_HK
dc.date.accessioned2012-10-30T06:29:01Z-
dc.date.available2012-10-30T06:29:01Z-
dc.date.issued2005en_HK
dc.identifier.citationCancer Genetics And Cytogenetics, 2005, v. 157 n. 1, p. 42-48en_HK
dc.identifier.issn0165-4608en_HK
dc.identifier.urihttp://hdl.handle.net/10722/173277-
dc.description.abstractCervical and vulvar cancers are diseases of the female lower genital tract, and high-risk human papillomavirus (HPV) infection is the most important risk factor for the development of both cancers. However, it is clear that additional genetic events are necessary for tumor progression, particularly in HPV-negative cases. We detected the presence of high-risk HPV16 and HPV18 genomes by gene-specific polymerase chain reaction and searched for common genetic imbalances by comparative genomic hybridization (CGH) in 28 cervical and 8 vulvar tumor samples and 7 cancer cell lines. The presence of the HPV genome was detected in 25/28 (89%) cervical tumors and 6/8 (75%) vulvar tumors. CGH of cervical and vulvar tumor samples revealed a consistent pattern of genetic changes in both cancers. Frequent gains were found in 1q, 3q, 5p, and 8q, and less consistent losses were detected in 2q, 3p, 4p, and 11p. Notably, a high-level amplification of 3q was found in 9/28 (32%) cervical tumors and 1/8 (12.5%) vulvar tumors, indicating a pivotal role of gain of 3q in cervical and vulvar carcinogenesis. Furthermore, gains of 5p identified in 9/28 (32%) cervical tumors and 3/8 (37.5%) vulvar tumors were seldom described, particularly in vulvar tumors. Our findings suggest that cervical and vulvar carcinomas bear similar chromosomal alteration hot spots that largely coincide with common genomic lesions during tumor progression, besides the initiation by infection and integration of oncogenic HPV. © 2005 Elsevier Inc. All rights reserved.en_HK
dc.languageengen_US
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/cancergeneen_HK
dc.relation.ispartofCancer Genetics and Cytogeneticsen_HK
dc.subject.meshAdulten_US
dc.subject.meshAgeden_US
dc.subject.meshCarcinoma, Squamous Cell - Genetics - Virologyen_US
dc.subject.meshChromosome Aberrationsen_US
dc.subject.meshFemaleen_US
dc.subject.meshGenotypeen_US
dc.subject.meshHumansen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshNucleic Acid Hybridizationen_US
dc.subject.meshPapillomaviridae - Classification - Isolation & Purificationen_US
dc.subject.meshUterine Cervical Neoplasms - Genetics - Virologyen_US
dc.subject.meshVulvar Neoplasms - Genetics - Virologyen_US
dc.titleGenetic abnormalities and HPV status in cervical and vulvar squamous cell carcinomasen_HK
dc.typeArticleen_HK
dc.identifier.emailTang, MHY: mhytang@hkucc.hku.hken_HK
dc.identifier.emailNgan, HYS: hysngan@hkucc.hku.hken_HK
dc.identifier.authorityTang, MHY=rp01701en_HK
dc.identifier.authorityNgan, HYS=rp00346en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.cancergencyto.2004.06.002en_HK
dc.identifier.pmid15676146-
dc.identifier.scopuseid_2-s2.0-12844279917en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-12844279917&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume157en_HK
dc.identifier.issue1en_HK
dc.identifier.spage42en_HK
dc.identifier.epage48en_HK
dc.identifier.isiWOS:000226955600007-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridHuang, FY=8644138400en_HK
dc.identifier.scopusauthoridKwok, YKY=8247106700en_HK
dc.identifier.scopusauthoridLau, ET=36006491400en_HK
dc.identifier.scopusauthoridTang, MHY=8943401300en_HK
dc.identifier.scopusauthoridNg, TY=7402229853en_HK
dc.identifier.scopusauthoridNgan, HYS=34571944100en_HK
dc.identifier.citeulike6948470-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats