pubmed-article:12814990 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:12814990 | lifeskim:mentions | umls-concept:C0021344 | lld:lifeskim |
pubmed-article:12814990 | lifeskim:mentions | umls-concept:C0020205 | lld:lifeskim |
pubmed-article:12814990 | lifeskim:mentions | umls-concept:C0012854 | lld:lifeskim |
pubmed-article:12814990 | lifeskim:mentions | umls-concept:C0032520 | lld:lifeskim |
pubmed-article:12814990 | lifeskim:mentions | umls-concept:C1707455 | lld:lifeskim |
pubmed-article:12814990 | lifeskim:mentions | umls-concept:C1709793 | lld:lifeskim |
pubmed-article:12814990 | pubmed:issue | 6 | lld:pubmed |
pubmed-article:12814990 | pubmed:dateCreated | 2003-6-19 | lld:pubmed |
pubmed-article:12814990 | pubmed:abstractText | Studies investigating human papillomavirus (HPV) viral load as a risk factor in the development of squamous intraepithelial lesions (SILs) and cancer have often yielded conflicting results. These studies used a variety of HPV viral quantitation assays [including the commercially available hybrid capture 2 (HC 2) assay], which differ in their ability to account for differences in cervical cell collection, linear dynamic range of viral load quantitation, and determination of type-specific versus cumulative viral load measures. HPV-16 and HPV-18 viral quantitation using real-time PCR assays were performed to determine whether type-specific viral load measurements that adjust for specimen cellularity result in a different association between viral load and prevalent SIL and cancer, compared with HC 2 quantitation (which does not adjust for cellularity or multiple infections). In general, HPV-16 viral load as measured by real-time PCR increased linearly with increasing grade of SIL while HPV-18 measured using similar techniques increased through low-grade SIL (LSIL), with HPV-18 viral load among high-grade SIL and cancers near the level of cytologically normal women. HC 2 viral load, using the clinical 1.0 pg/ml cut point, differentiated cytologically normal women from women with any level of cytological abnormality (normal versus >/=LSIL) but did not change as lesion severity increased. There was no evidence for plateau of HC 2 at high copy numbers, nor was significant variability in total specimen cellularity observed. However, cumulative viral load measurements by HC 2, in the presence of multiple coinfections, overestimated type-specific viral load. Multiple infections were more common among women with no (32%) or LSIL (51%) [versus 23% in high-grade SIL/cancer], partially explaining the lack of a dose response using a cumulative HC2 viral load measure. The nonrandom distribution of multiple infections by case-control status and the apparent differential effect of viral load by genotype warrant caution when using HC 2 measurements to infer viral load associations with SIL and cancer. | lld:pubmed |
pubmed-article:12814990 | pubmed:language | eng | lld:pubmed |
pubmed-article:12814990 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12814990 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:12814990 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12814990 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12814990 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:12814990 | pubmed:month | Jun | lld:pubmed |
pubmed-article:12814990 | pubmed:issn | 1055-9965 | lld:pubmed |
pubmed-article:12814990 | pubmed:author | pubmed-author:HelzlsouerKat... | lld:pubmed |
pubmed-article:12814990 | pubmed:author | pubmed-author:BurkRobert... | lld:pubmed |
pubmed-article:12814990 | pubmed:author | pubmed-author:ShermanMark... | lld:pubmed |
pubmed-article:12814990 | pubmed:author | pubmed-author:SchiffmanMark... | lld:pubmed |
pubmed-article:12814990 | pubmed:author | pubmed-author:HerreroRoland... | lld:pubmed |
pubmed-article:12814990 | pubmed:author | pubmed-author:HildesheimAll... | lld:pubmed |
pubmed-article:12814990 | pubmed:author | pubmed-author:LorinczAttila... | lld:pubmed |
pubmed-article:12814990 | pubmed:author | pubmed-author:GravittPatti... | lld:pubmed |
pubmed-article:12814990 | pubmed:author | pubmed-author:BrattiMaria... | lld:pubmed |
pubmed-article:12814990 | pubmed:author | pubmed-author:RodriguezAna... | lld:pubmed |
pubmed-article:12814990 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:12814990 | pubmed:volume | 12 | lld:pubmed |
pubmed-article:12814990 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:12814990 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:12814990 | pubmed:pagination | 477-84 | lld:pubmed |
pubmed-article:12814990 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
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pubmed-article:12814990 | pubmed:year | 2003 | lld:pubmed |
pubmed-article:12814990 | pubmed:articleTitle | A comparison between real-time polymerase chain reaction and hybrid capture 2 for human papillomavirus DNA quantitation. | lld:pubmed |
pubmed-article:12814990 | pubmed:affiliation | Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland 20892, USA. pgravitt@jhsph.edu | lld:pubmed |
pubmed-article:12814990 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:12814990 | pubmed:publicationType | Comparative Study | lld:pubmed |
pubmed-article:12814990 | pubmed:publicationType | Evaluation Studies | lld:pubmed |
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