Fruits and vegetables and cervical cancer: a systematic review and meta-analysis.

We conducted a meta-analysis to examine the association of fruits and vegetables intake with the occurrence of cervical intraepithelial neoplasia (CIN) and invasive cancer. MEDLINE, LILACS, Scopus, Cochrane Library, and Web of Science databases and gray literature on Google Scholar were searched before December 17, 2018. Odds ratio (OR) or relative risk (RR) estimates for the highest vs. the lowest intake of intake and 95% confidence intervals (CI) from the included studies were pooled using fixed and random-effects models. We found 18 studies: 17 case-control studies (n = 9,014 cases, n = 29,088 controls) and one cohort study (n = 299,651). No association was observed for CIN. The pooled adjusted ORs (95% CI) for cervical cancer were 0.61 (95% CI 0.52-0.73) for vegetables and 0.80 (95% CI 0.70-0.93) for fruits. However, no association was observed when the pooled effect was estimated among studies that adjusted for human papillomavirus (HPV). Consumption of vegetables and fruits was not associated with incidence of cervical cancer among studies that controlled for HPV infection. The level of evidence is limited because only one cohort study was included in the analysis.

HPV testing with cytology triage for cervical cancer screening in routine practice.

OBJECTIVE: The purpose of this study was to evaluate the feasibility and effectiveness of Viral Testing Alone with Pap (Papanicolaou) Triage for Screening Cervical Cancer in Routine Practice (VASCAR) in a publicly funded university-affiliated hospital in Montreal, Canada. STUDY DESIGN: Women who are 30-65 years old are screened with the Hybrid Capture-2 assay. Women with negative results are retested at 3-year intervals; women with positive results are triaged with conventional cytologic methods. Women with Papanicolaou positive test results (≥atypical squamous cells of undetermined significance) are referred to colposcopy; women with Papanicolaou negative test results are retested with Hybrid Capture-2 assay and a Papanicolaou test in 1 year. Results were compared with a historic era (annual cytology with ≥atypical squamous cells of undetermined significance threshold for colposcopy referral) in the 3 years before VASCAR. RESULTS: VASCAR included 23,739 eligible women, among whom 1646 women (6.9%) tested positive for the human papillomavirus (HPV). Because of the need for subsequent sampling for cytologic testing, follow-up evaluation for cytologic triage was relatively poor; only 46% and 24% of HPV-positive women were Papanicolaou-triaged and underwent biopsy, respectively. Protocol violations occurred mainly in the early phases of implementation (12%). Detection of high-grade cervical intraepithelial neoplasia increased nearly 3-fold (rate ratio, 2.78; 95% confidence interval [CI], 2.1-3.7) during VASCAR, mostly because of a doubling in the rate of high-grade cervical intraepithelial neoplasia (34.0%; 95% CI, 21.2-48.8) compared with the historic cytology-only era (16.3%; 95% CI, 13.2-19.8). VASCAR reduced the median time to colposcopy from a positive screen from 11 months (95% CI, 10.48-11.50) to 3 months (95% CI, 2.64-3.80). CONCLUSION: VASCAR is feasible; however, it requires cosampling for HPV and cytology and for continuous education of healthcare providers of the HPV-Papanicolaou triage protocol. Efficacy in disease detection and reduction in time to colposcopy referrals compared with the historic cytology era is encouraging but should be considered preliminary because of the small number of patients who were tested.

Generic microtiter plate assay for triaging clinical specimens prior to genotyping of human papillomavirus DNA via consensus PCR.

A generic human papillomavirus (HPV) probe assay was compared to the Linear Array to detect HPV DNA in 1,013 clinical specimens. The sensitivity, specificity, and negative predictive value of the assay were 99.5% (95% confidence interval [CI], 98.4% to 99.9%), 58.6% (95% CI, 53.9% to 63.1%), and 98.9% (95% CI, 96.5% to 99.8%), respectively. This assay conveniently identifies HPV-positive specimens.

High grade cervical lesions are caused preferentially by non-European variants of HPVs 16 and 18.

The intratypic variability of HPVs 16 and 18 has been extensively studied and has been used as an important tool in epidemiological studies of viral transmission, persistence and progression to clinically relevant cervical lesions. Infections by non-European variants of HPVs 16 and 18 are associated with an increased risk for the development of high grade squamous intraepithelial lesions (HSIL). Our aim was to correlate the intratypic molecular variability of both HPV types and risk of persistent infection and lesion outcome in a cohort study conducted in Brazil. We characterized molecular variants of HPV types 16 and 18 by sequencing a fragment of the LCR, and of the E6 and L1 genes, for HPV-16 variants only. For both types, European variants composed the most prevalent and diverse group. Persistent infections with HPV-18 were associated with continuous detection of European variants. However, risk for simultaneous detection of HSIL and HPV DNA was higher in women harboring non-European variants of HPV-16. The same trend was observed with HSIL detected during follow-up. Our study confirms the association between non-European variants and risk of cervical neoplasia, and highlights the importance of their geographic distribution for cervical cancer risk assessment.

Different P105 promoter activities among natural variants of human papillomavirus type 18.

Association between non-European variants of human papillomavirus (HPV) type 16 (HPV-16) and HPV-18 and cervical lesions has been suggested. To compare the P105 promoter activity among 6 HPV-18 variants, their complete long control regions (LCRs), as well as that of HeLa cells, were cloned upstream of the luciferase gene and transiently transfected in C33 cells. Whereas the B18-2 European variant showed the lowest promoter activity, the Asian-Amerindian variant, B18-3, had the highest activity. All variants tested were more active than the P97 HPV-16 prototype promoter. Differences in the LCR that impact P105 promoter activity could be responsible for the observed variability in oncogenic potential.