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A polymorphism at codon 72 of gene p53 results in the presence of either arginine or proline at this position. We investigated the distribution of p53 codon 72 polymorphism in cervical cancer patients and a control group of healthy women from Poland. Our results do not confirm the hypothesis that the p53 codon polymorphism could play a role as a factor for squamous carcinoma of the cervix.
The relationship between HPV (Human Papillomavirus) and cervical carcinoma is very strong, causal, constant, specific and universal. HPV infection precedes the occurrence of preinvasive carcinoma and the evidence for biological probability of such relationship does not leave any doubt. Out of high-risk HPV types, the most often occurring in cervical infections types 16 and 18 were placed in the first group of human carcinogens. However, HPV infection is not the only factor of malignant neoplasm development. Neuroplastic transformation of cervical epithelium requires the presence of cofactors. In recent years, higher role is ascribed to the influences of steroid hormones, including estradiol and progesterone. In normal and neoplastic cells of uterine cervix, the occurrence of receptors for steroid hormones was described. In the regulatory region of oncogenic HPV hormone response elements were found. Receptors combined with steroid hormones functioning as transcription factors may influence the expression of viral oncogens E6 and E7 through stimulation of proliferation and transformation. The aim of this study was to analyse the influence of 17ß-estradiol on the amount of proteins E6 and E7 HPV 18 and to evaluate the transcript E6/E7 after incubation of HeLa line cells with 17ß-estradiol. The results revealed stimulating influence of the hormone on the expression of proteins and mRNA at concentrations of lx10-7M. At high concentrations of 1x10- 4M, estradiol was inhibiting transcription and expression of oncoproteins.
 Cervical carcinogenesis is a complex problem with papillomavirus widely accepted as a causative agent. Integration of a human papillomavirus (HPV) of the high-risk type into the host cell genome is one of the major contributing factors to cervical malignant transformation. In this study, the correlation of CMV, EBV, HSV-1, HSV-2, HHV-6 and HHV-7 infections with the physical status of the HPV genome in cervical cancer and precancerous cervical lesions was investigated in sixty HPV-16-positive women. Cervical secretion samples were submitted to DNA extraction and analyzed by PCR. HPV-16 DNA was confirmed in genotyping with the reverse hybridization line probe assay. Multiplex PCR with specific primers for the E2/E6 genes was used to assess the viral integration status of HPV-16. Our results show that CMV DNA was more frequently present in samples with mixed forms of HPV-16 than in the episomal form (P < 0.025). Such a correlation was also observed in the case of EBV (P < 0.005). The presence of CMV resulted in a six-fold (OR 6.069; 95% CI 1.91-19.22; P = 0.002), while EBV caused a seven-fold (OR 7.11; 95% CI 1.70-29.67; P = 0.007) increase in the risk of the integrated or mixed HPV-16 genome occurrence. Our data suggest that coinfection with herpesviruses, especially CMV and EBV, may be involved in the integration of the HPV-16 genome and may contribute to the development of cervical cancer.
Human papillomavirus (HPV) is widely accepted as a causative agent of cervical cancer. The distribution and prevalence of HPV types depend on geographic region and demographic factors. The aim of this study was to investigate the relationship between the presence of various HPV types and the outcome of cytological examination. Cervical smears were obtained from 125 women from southern Poland: low grade squamous intraepithelial lesions (LSIL) — 44, high grade squamous intraepithelial lesions (HSIL) — 12, cervical carcinoma — 27 and 42 women without abnormality in cytology as a control group. DNA was extracted from the smears and broad-spectrum HPV DNA amplification and genotyping was performed with the SPF 10 primer set and reverse hybridisation line probe assay (INNO-LiPA HPV Genotyping, Innogenetics). HPV DNA was detected in approximately 72% cases, more frequently in women with squamous intraepithelial lesions and cervical carcinoma than in the control group (P <0.0005). The most frequent type found was HPV 16 (37%), followed by HPV 51 (28%) and HPV 52 (17%). A single HPV type was detected in 51% positive cases, more frequently in cervical cancer specimens. Multiple HPV infection was dominant in women with LSIL and normal cytology. Prevalence of HPV 16 increased with the severity of cervical smear abnormality. For women HPV 16 positive, the relative risk (odds ratio) of the occurrence of HSIL and cervical cancer versus LSIL was 14.4 (95% CI, 3.0–69.2; P=0.001) and 49.4 (95% CI, 6.5–372.8; P<0.001), respectively. Genotyping of HPV will allow better classification of women with cervical abnormalities into different risk groups and could be useful in therapy.
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