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Genetic Polymorphism of Cancer Susceptibility Genes and HPV Infection in Cervical Carcinogenesis.

Nunobiki O, Ueda M, Toji E, Yamamoto M, Akashi K, Sato N, Izuma S, Torii K, Tanaka I, Okamoto Y, Noda S - Patholog Res Int (2011)

Bottom Line: It is widely accepted that specific human papillomavirus (HPV) types are the central etiologic agent of cervical carcinogenesis.However, a number of infected women do not develop invasive lesions, suggesting that other environmental and host factors may play decisive roles in the persistence of HPV infection and further malignant conversion of cervical epithelium.Although many previous reports have focused on HPV and environmental factors, the role of host susceptibility to cervical carcinogenesis is largely unknown.

View Article: PubMed Central - PubMed

Affiliation: Department of Medical Technology, Kobe Tokiwa University, 6-2 2 chome, Ohtanicho, Nagataku, Hyogo, Kobe 653-0838, Japan.

ABSTRACT
It is widely accepted that specific human papillomavirus (HPV) types are the central etiologic agent of cervical carcinogenesis. However, a number of infected women do not develop invasive lesions, suggesting that other environmental and host factors may play decisive roles in the persistence of HPV infection and further malignant conversion of cervical epithelium. Although many previous reports have focused on HPV and environmental factors, the role of host susceptibility to cervical carcinogenesis is largely unknown. Here, we review the findings of genetic association studies in cervical carcinogenesis with special reference to polymorphisms of glutathione-S-transferase (GST) isoforms, p53 codon 72, murine double-minute 2 homolog (MDM2) gene promoter 309, and FAS gene promoter -670 together with HPV types including our recent research results.

No MeSH data available.


Related in: MedlinePlus

Genotyping of Fas gene promoter -670 in 8 cervical squamous carcinoma cell lines by PCR-RFLP. The AA genotype was detected only for QG-U, whereas the GA genotype for SKG-I, OMC-1, and YUMOTO, and the GG genotype for SKG-II, SKG-IIIa, SKG-IIIb, and QG-H cell lines, respectively.
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Related In: Results  -  Collection


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fig6: Genotyping of Fas gene promoter -670 in 8 cervical squamous carcinoma cell lines by PCR-RFLP. The AA genotype was detected only for QG-U, whereas the GA genotype for SKG-I, OMC-1, and YUMOTO, and the GG genotype for SKG-II, SKG-IIIa, SKG-IIIb, and QG-H cell lines, respectively.

Mentions: Figure 5 shows an example for genotyping of Fas gene promoter -670 in exfoliated cervical cell samples. The fragments of 232 and 188 bps indicated the AA and GG genotypes, respectively. The GA genotype contained these two bands. Table 8 shows the frequency of high-risk HPV and Fas promoter -670 polymorphism in 279 samples examined. When AA genotype was compared to GA + GG genotype, 49 patients with HSIL had significantly higher frequency of high-risk HPV and GA + GG genotype than 167 with LSIL and 63 controls. G allele frequency was also higher in HSIL than in LSIL and controls. There was no statistical difference in the GA + GG genotype prevalence between SILs and controls among 183 patients without high-risk HPV as shown in Table 9. However, there was an increased odds ratio (OR) for GA + GG genotype in HSIL cases compared to controls among 96 patients with high-risk HPV. As shown in Figure 6, genotyping of Fas gene promoter -670 in 8 cervical squamous carcinoma cell lines revealed that AA genotype was detected only in the QG-U cell line, whereas the other 7 of 8 (87.5 %) cell lines had GA or GG genotype.


Genetic Polymorphism of Cancer Susceptibility Genes and HPV Infection in Cervical Carcinogenesis.

Nunobiki O, Ueda M, Toji E, Yamamoto M, Akashi K, Sato N, Izuma S, Torii K, Tanaka I, Okamoto Y, Noda S - Patholog Res Int (2011)

Genotyping of Fas gene promoter -670 in 8 cervical squamous carcinoma cell lines by PCR-RFLP. The AA genotype was detected only for QG-U, whereas the GA genotype for SKG-I, OMC-1, and YUMOTO, and the GG genotype for SKG-II, SKG-IIIa, SKG-IIIb, and QG-H cell lines, respectively.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3108378&req=5

fig6: Genotyping of Fas gene promoter -670 in 8 cervical squamous carcinoma cell lines by PCR-RFLP. The AA genotype was detected only for QG-U, whereas the GA genotype for SKG-I, OMC-1, and YUMOTO, and the GG genotype for SKG-II, SKG-IIIa, SKG-IIIb, and QG-H cell lines, respectively.
Mentions: Figure 5 shows an example for genotyping of Fas gene promoter -670 in exfoliated cervical cell samples. The fragments of 232 and 188 bps indicated the AA and GG genotypes, respectively. The GA genotype contained these two bands. Table 8 shows the frequency of high-risk HPV and Fas promoter -670 polymorphism in 279 samples examined. When AA genotype was compared to GA + GG genotype, 49 patients with HSIL had significantly higher frequency of high-risk HPV and GA + GG genotype than 167 with LSIL and 63 controls. G allele frequency was also higher in HSIL than in LSIL and controls. There was no statistical difference in the GA + GG genotype prevalence between SILs and controls among 183 patients without high-risk HPV as shown in Table 9. However, there was an increased odds ratio (OR) for GA + GG genotype in HSIL cases compared to controls among 96 patients with high-risk HPV. As shown in Figure 6, genotyping of Fas gene promoter -670 in 8 cervical squamous carcinoma cell lines revealed that AA genotype was detected only in the QG-U cell line, whereas the other 7 of 8 (87.5 %) cell lines had GA or GG genotype.

Bottom Line: It is widely accepted that specific human papillomavirus (HPV) types are the central etiologic agent of cervical carcinogenesis.However, a number of infected women do not develop invasive lesions, suggesting that other environmental and host factors may play decisive roles in the persistence of HPV infection and further malignant conversion of cervical epithelium.Although many previous reports have focused on HPV and environmental factors, the role of host susceptibility to cervical carcinogenesis is largely unknown.

View Article: PubMed Central - PubMed

Affiliation: Department of Medical Technology, Kobe Tokiwa University, 6-2 2 chome, Ohtanicho, Nagataku, Hyogo, Kobe 653-0838, Japan.

ABSTRACT
It is widely accepted that specific human papillomavirus (HPV) types are the central etiologic agent of cervical carcinogenesis. However, a number of infected women do not develop invasive lesions, suggesting that other environmental and host factors may play decisive roles in the persistence of HPV infection and further malignant conversion of cervical epithelium. Although many previous reports have focused on HPV and environmental factors, the role of host susceptibility to cervical carcinogenesis is largely unknown. Here, we review the findings of genetic association studies in cervical carcinogenesis with special reference to polymorphisms of glutathione-S-transferase (GST) isoforms, p53 codon 72, murine double-minute 2 homolog (MDM2) gene promoter 309, and FAS gene promoter -670 together with HPV types including our recent research results.

No MeSH data available.


Related in: MedlinePlus