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HPV-16 DNA (hpv-16 + dna)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Establishment of the 1st World Health Organization international standards for human papillomavirus type 16 DNA and type 18 DNA

INTERNATIONAL JOURNAL OF CANCER, Issue 12 2010
Dianna E. Wilkinson
Abstract A World Health Organization collaborative study was conducted to evaluate candidate international standards for human papillomavirus (HPV) Type 16 DNA (NIBSC code 06/202) and HPV Type 18 DNA (NIBSC code 06/206) for use in the amplification and detection steps of nucleic acid-based assays. The freeze-dried candidate international standards were prepared from bulk preparations of cloned plasmid containing full-length HPV-16 or HPV-18 genomic DNA. Nineteen laboratories from 13 countries participated in the study using a variety of commercial and in-house quantitative and qualitative assays. The data presented here indicate that, upon freeze-drying, there is no significant loss in potency for the candidate HPV-18 DNA and a slight loss in potency for the candidate HPV-16 DNA; although this is likely not scientifically relevant when assay precision is considered. In general, the individual laboratory mean estimates for each study sample were grouped ±,2 log10 around the theoretical HPV DNA concentration of the reconstituted ampoule (1 × 107 HPV genome equivalents/mL). The agreement between laboratories is improved when potencies are made relative to the candidate international standards, demonstrating their utility in harmonizing amplification and detection steps of HPV-16 and ,18 DNA assays. Degradation studies indicate that the candidate international standards are extremely stable and suitable for long-term use. Based on these findings, the candidate standards were established as the 1st WHO international standards for HPV-16 DNA and HPV-18 DNA, each with a potency of 5 × 106 international units (IU) per ampoule or 1 × 107 IU mL,1 when reconstituted as directed. [source]

Human papillomavirus seropositivity and risks of head and neck cancer

INTERNATIONAL JOURNAL OF CANCER, Issue 4 2007
Elaine M. Smith
Abstract We examined antibody response to VLP HPV-16, HPV-16 E6 and E7 antibodies as potential seromarkers of HPV-related head and neck cancer (HNC). The study included 204 HNC cases and 326 controls evaluated for HPV presence in sera using ELISAs for anti-HPV VLP antibodies and HPV-16 E6 and/or E7 antibodies, and in tumor tissue using PCR and DNA sequencing. Anti-HPV-16 VLP was detected in 33.8% of cases and 22.4% of controls, anti-E6 in 20.6% of cases and 0.9% of controls and anti-E7 in 18.6% of cases and 0.6% of controls. HPV-16 DNA was detected in 26.1% of tumors. The adjusted risk of HNC was elevated among those seropositive for HPV-16 VLP (odds ratio (OR) = 1.7, 1.1,2.5), E6 (OR = 32.8, 9.7,110.8) or E7 (OR = 37.5, 8.7,161.2). Compared to HPV DNA-negative/seronegative cases, tumor HPV-16 cases had increased risk of detection with anti-VLP antibodies (OR = 6.8, 3.1,14.9). The odds were more pronounced among cases seropositive for E6 (OR = 69.0, 19.3,247) or E7 (OR = 50.1, 14.7,171). Antibodies against E6 or E7 were associated with risk of cancer in the oral cavity (OR = 5.1, 1.2,22.4) and oropharynx (OR = 72.8, 16.0,330), and with disease characteristics: stage, grade and nodal status. Anti-E6 and/or E7 antibodies were found in 74% of tumor HPV-16 positive cases but in only 5% of tumor HPV-negative cases (K =0.7, 0.6,0.8) suggesting good correlation between the serologic marker and HPV tumor status. Antibodies to HPV-16 E6 and/or E7 represent a more specific biomarker than anti-HPV-16 VLP of an HPV-related HNC. Because of the survival advantage of HPV-related HNC, HPV-16 E6/E7 detection may be useful in therapy targeted for HPV-related tumors. © 2006 Wiley-Liss, Inc. [source]

The prognostic significance of HPV-16 genome status of the lymph nodes, the integration status and p53 genotype in HPV-16 positive cervical cancer: a long term follow up

BJOG : AN INTERNATIONAL JOURNAL OF OBSTETRICS & GYNAECOLOGY, Issue 2 2003
Zoltán Hernádi
Objective Prognostic evaluation of HPV-16 genome status of the pelvic lymph nodes, the integration status of HPV-16 and p53 codon 72 polymorphism in cervical cancer. Design Prospective cohort study. Setting Department of Gynaecological Oncology, University of Debrecen, Hungary. Sample Thirty-nine patients with HPV-16 positive cervical cancer. Methods Primary tumour specimens of 39 cervical cancer patients with HPV-16 positive primary tumour were subjected to multiplex polymerase chain reaction using HPV-16 E1/E2, E7 and p53 codon 72 allele-specific primers. Pelvic lymph nodes of the same patients were also tested for the presence of HPV-16 DNA and for its integration status using HPV-16 E7 and E1/E2 ORF specific primers, respectively. Main outcome measures Progression-free survival. Results Metastatic lymph nodes carried HPV-16 DNA more frequently than nodes with no evidence of disease (100.0% vs 35.7%, P= 0.001). Cases with HPV-16 positive nodes had higher recurrence rate than those with HPV-16 negative nodes (42.9% vs 11.1%, P= 0.009). There was no difference between cases with and without histologically proven nodal disease with regard to integration status of HPV-16 DNA in the primary tumour (integrated 90.9% vs 71.4%, episomal 9.1% vs 21.4%, mixed 0% vs 7.1%) and p53 codon 72 polymorphism (Arg/Arg 54.5% vs 67.9%, Pro/Pro 0 vs 7.1%, Arg/Pro 45.5% vs 21.4%). Conclusion Regardless of the presence of nodal metastasis, HPV-16 status of the nodes is a significant predictor of recurrent disease. HPV-16 integration status and p53 codon 72 genotype do not seem to have a bearing on disease outcome in cervical cancer with HPV-16 positive primary. [source]

Enhancer-promoter Activity of Human Papillomavirus Type 16 Long Control Regions Isolated from Cell Lines SiHa and CaSki and Cervical Cancer Biopsies

CANCER SCIENCE, Issue 3 2000
Takuyo Kozuka
Expression of human papillomavirus 16 (HPV-16) oncogenes is markedly higher in cervical cancer cells than in precancerous cells, and the elevated expression is believed to be required for the malignant phenotypes. We compared cancer cell lines CaSki (with 200 to 400 copies of HPV-16 DNA per cell) and SiHa (with one to two copies of HPV-16 DNA per cell) for the E7 expression in cells and the enhancer-promoter activity of the isolated viral long control region (LCR). Although these parameters per cell were 10-fold higher in CaSki than in SiHa, the levels of the E7 mRNA and protein per HPV DNA copy were 10- to 20-fold higher in SiHa than in CaSki. Characterization of the isolated LCRs showed that, whereas the LCR from CaSki resembled the prototype in structure and activity, the LCR from SiHa, with a deletion of 38 base pairs, enhanced transcription from P97 as assayed by using a plasmid capable of expressing luciferase. The upregulation appeared to be due to removal of one of the silencer YY1-binding sites. Furthermore, we isolated and characterized LCRs from 51 cervical cancer patients' biopsies. Among them, one with a deletion including YY1-binding sites and the other with a substitution in a YY1-motif were found to enhance the transcription. These findings suggest that mutation affecting YY1-motifs in the LCR is one of the mechanisms enhancing the viral oncogene expression in the course of progression of cancer cells. [source]