The high prevalence of HPV 53 in CIN 3 and as a stand-alone genotype in the patient with invasive cervical cancer warrants that its clinical significance be further revisited among HIV-infected women.
We performed a case-control association study to evaluate the association between common polymorphisms in MTHFR (C677T and A1298C) and the Arg72Pro polymorphism in the p53 gene and the risk for cervical intraepithelial neoplasia (CIN) or invasive cervical cancer (ICC) in Mexican HPV-infected women.
In conformity with other study groups, our findings do not support the hypothesis that the p53 polymorphism at codon 72 is important in determining an increased risk of developing HPV-associated SIL or invasive cervical cancer in Central Europeans.
With the use of two separate methods for codon 72 allelotyping and accounting for a number of the issues raised in previously published reports, there is no increased risk for invasive cervical cancer associated with arginine homozygosity at codon 72 of p53.
We performed a case-control association study to evaluate the association between common polymorphisms in MTHFR (C677T and A1298C) and the Arg72Pro polymorphism in the p53 gene and the risk for cervical intraepithelial neoplasia (CIN) or invasive cervical cancer (ICC) in Mexican HPV-infected women.
Statistical analysis between the groups of cases with cervical intraepithelial neoplasia or invasive cervical cancer and the control group did not reveal any statistically significant difference in the frequency of the MTHFRC677T polymorphism.
For those with OHR HPV and low-grade cytology (considered to be a single low-grade category in Australia incorporating ASC-US and LSIL), we evaluated (1) the 20-year risk of invasive cervical cancer assuming this group are referred for 12-month follow-up vs. colposcopy, and compared this to the risk in women with low-grade cytology under the current program (i.e. an accepted benchmark risk for 12-month follow-up in Australia); (2) the population-level impact of the whole program, assuming this group are referred to 12-month surveillance vs. colposcopy; and (3) the cost-effectiveness of immediate colposcopy compared to 12-month follow-up.
Our data provide evidence for the involvement of intron 1 EGFR variants and intron 24 ERBB4 variants in modulating risk for the development of in situ and invasive cervical cancer.
Using hierarchical clustering of histology-cytology groups based on HPV genotype distributions, we could plainly distinguish in this referral population 5 increasingly severe diagnostic groups of HPV-positive women: (i) HPV-positive women with <CIN2 histology and normal cytology, (ii) HPV positive women with <CIN2 histology and ASC or LSIL cytology; (iii) CIN2, including histologic CIN2 and HSIL cytology with any histology <CIN2; (iv) CIN3; and (v) invasive cervical cancer.
For those with OHR HPV and low-grade cytology (considered to be a single low-grade category in Australia incorporating ASC-US and LSIL), we evaluated (1) the 20-year risk of invasive cervical cancer assuming this group are referred for 12-month follow-up vs. colposcopy, and compared this to the risk in women with low-grade cytology under the current program (i.e. an accepted benchmark risk for 12-month follow-up in Australia); (2) the population-level impact of the whole program, assuming this group are referred to 12-month surveillance vs. colposcopy; and (3) the cost-effectiveness of immediate colposcopy compared to 12-month follow-up.
Using hierarchical clustering of histology-cytology groups based on HPV genotype distributions, we could plainly distinguish in this referral population 5 increasingly severe diagnostic groups of HPV-positive women: (i) HPV-positive women with <CIN2 histology and normal cytology, (ii) HPV positive women with <CIN2 histology and ASC or LSIL cytology; (iii) CIN2, including histologic CIN2 and HSIL cytology with any histology <CIN2; (iv) CIN3; and (v) invasive cervical cancer.
Peripheral blood samples from patients with invasive cervical cancer (ICC, n=144) and non-cancer controls (NCC, n=179) were used to detect three biallelic IL-10 promoter polymorphisms at -1082, -819, and -592 sites by polymerase chain reaction-restriction fragment length polymorphism assay using MnlI, MaeIII and RsaI, respectively.
The aim of this study was to explore the association of the CCR2-64I polymorphism with the risk of developing invasive cervical cancer (ICC) from squamous intraepithelial lesions (SILs).
Genotyping for CCR2-V64I was done by PCR-SSP in a case-control study of 446 women (106 black African and 340 mixed-ancestry) with histologically confirmed invasive cervical cancer and 1432 controls (322 black African and 1110 mixed-ancestry) group-matched (1:3) by age, ethnicity and domicile status.
Between August 1994 and December 2018, patients with invasive cervical cancer were treated using minimally-invasive surgery at the Universities of Jena, Charité Berlin (Campus CCM and CBF) and Cologne and Asklepios Clinic Hamburg.
We collected cervical samples from 262 women from the general population and 241 tumor samples from women with invasive cervical cancer in Mozambique and tested them for HPV genotyping by the SPF(10)-LiPA(25) PCR system.