The influence of chemokine receptor CCR2 genotypes in the route to cervical carcinogenesis

被引:13
作者
Coelho, Ana
Matos, Ana
Catarino, Raquel
Pinto, Daniela
Sousa, Hugo
Pereira, Deolinda
Medeiros, Rui
机构
[1] Inst Portugues Oncol Francisco Gentil, Dept Mol Oncol & Virol, Oporto, Portugal
[2] Inst Portugues Oncol Francisco Gentil, Dept Gynecol, Oporto, Portugal
[3] Inst Portugues Oncol Francisco Gentil, Dept Med Oncol II, Oporto, Portugal
关键词
cervical cancer; high grade squamous intraepithelial lesions; low-gradesquamous intraepithelial lesions; human papillomavius; immunology; chemokines; CCR2; CCL2; polymorphism;
D O I
10.1159/000106492
中图分类号
R71 [妇产科学];
学科分类号
100211 [妇产科学];
摘要
Invasive squamous cell carcinomas of the cervix arise from earlier, reversible precursor lesions called low- and high-grade squamous intraepithelial lesions ( LSIL and HSIL, respectively). The aim of our study was to analyse the influence of the CCR2-64I polymorphism in the development of SIL due to its preponderant role in the cervical carcinogenesis and in the progression of these lesions to invasive cervical carcinoma. We conducted a case-control study, analyzing 565 Caucasian women from the north of Portugal. The CCR2-64I polymorphism was analysed through polymerase chain reaction followed by restriction fragment length polymorphism. The frequency of GG, GA and AA genotypes was 76.5, 23.5 and 0.0% respectively, in HSIL patients, and 87.8, 11.1 and 1.1% respectively, in the control group. The G allele frequency was 88.2% in the HSIL group and 93.4% in the control group. Regarding the A allele frequency, it was 11.8% in the HSIL group and 6.6% in the control group. Overall, the frequency of A carrier genotypes was higher in HSIL patients than in the control group ( p = 0.013; OR = 2.21; 95% CI: 1.17 4.15), suggesting that CCR2-64I polymorphism might contribute to the establishment of HSIL, through the disruption of the naturally fragile immune response directed towards human papillomavirus infection. Copyright (c) 2007 S. Karger AG, Basel.
引用
收藏
页码:208 / 212
页数:5
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