| pubmed-article:8146136 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8146136 | lifeskim:mentions | umls-concept:C0021344 | lld:lifeskim |
| pubmed-article:8146136 | lifeskim:mentions | umls-concept:C0950124 | lld:lifeskim |
| pubmed-article:8146136 | lifeskim:mentions | umls-concept:C0559522 | lld:lifeskim |
| pubmed-article:8146136 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:8146136 | pubmed:dateCreated | 1994-5-5 | lld:pubmed |
| pubmed-article:8146136 | pubmed:abstractText | Genital human papillomavirus (HPV) infection is a common sexually transmitted disease that at the present time is not effectively controlled or treated. Many infections are inapparent and transient. However, some HPV infections result in persistent lesions that in some cases undergo carcinogenic progression. A subset of genital HPVs, designated high-risk types, are preferentially associated with high-grade dysplasias and carcinomas. About 90% of cervical cancers contain high-risk HPV DNA, most often HPV16. Development of a subunit vaccine against high-risk genital HPVs is a desirable and, it appears, an increasingly feasible long-term goal. The viral E6 and E7 oncoproteins are selectively maintained and expressed in progressed HPV tumors and could potentially be targets for therapeutic vaccines. The L1 major virion structural proteins have recently been shown to self-assemble into virus-like particles when expressed in insect cells. These particles might serve as the basis for a prophylactic vaccine to prevent genital HPV infection. | lld:pubmed |
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| pubmed-article:8146136 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:8146136 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:8146136 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8146136 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:8146136 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:8146136 | pubmed:author | pubmed-author:LowyD RDR | lld:pubmed |
| pubmed-article:8146136 | pubmed:author | pubmed-author:SchillerJ TJT | lld:pubmed |
| pubmed-article:8146136 | pubmed:author | pubmed-author:KirnbauerRR | lld:pubmed |
| pubmed-article:8146136 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8146136 | pubmed:day | 29 | lld:pubmed |
| pubmed-article:8146136 | pubmed:volume | 91 | lld:pubmed |
| pubmed-article:8146136 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8146136 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8146136 | pubmed:pagination | 2436-40 | lld:pubmed |
| pubmed-article:8146136 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:8146136 | pubmed:year | 1994 | lld:pubmed |
| pubmed-article:8146136 | pubmed:articleTitle | Genital human papillomavirus infection. | lld:pubmed |
| pubmed-article:8146136 | pubmed:affiliation | Laboratory of Cellular Oncology, National Cancer Institute, Bethesda, MD 20892. | lld:pubmed |
| pubmed-article:8146136 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8146136 | pubmed:publicationType | Review | lld:pubmed |
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