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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

Representative genotyping of MDM2-SNP309 by two independent PCR assays for each allele. Lanes 1, 5, and 7: TG heterozygote. Lanes 2, 4, and 6: GG homozygote. Lane 3: TT homozygote. The wild-type (T) and the mutant (G) allele yields 121-bp and 168-bp fragments, respectively.
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fig3: Representative genotyping of MDM2-SNP309 by two independent PCR assays for each allele. Lanes 1, 5, and 7: TG heterozygote. Lanes 2, 4, and 6: GG homozygote. Lane 3: TT homozygote. The wild-type (T) and the mutant (G) allele yields 121-bp and 168-bp fragments, respectively.

Mentions: Figure 3 shows a representative genotyping of MDM-SNP309 by two independent PCR assays. The wild-type (T) and the mutant (G) allele yield 121-bp and 168-bp fragment, respectively. Table 5 shows the frequency of high-risk HPV and MDM2-SNP309 in 195 exfoliated cervical cell samples examined. When TT genotype was compared to TG + GG genotype, 41 patients with HSIL had significantly higher frequency of high-risk HPV than 102 with LSIL and 52 controls; however, there were no statistical significant differences in the TG + GG genotype prevalence and allele frequencies between SILs and controls. No statistical difference was also found in the genotype frequency of MDM2-SNP 309 between SILs and controls among 127 patients without high-risk HPV. However, there was an increased OR for TG + GG genotype in HSIL cases compared to controls among 68 patients with high-risk HPV, as shown in Table 6. Interestingly, 21 cases with HPV types 16 and/or 18 had significantly higher frequency of the TG + GG genotype and G allele than 47 with other types of high-risk HPV, as indicated in Table 7. Moreover, as shown in Figure 4, genotyping of MDM2-SNP309 in 8 cervical squamous carcinoma cell lines revealed that TT genotype was detected only in the SKG-IIIa cell line, whereas the other 7 of 8 (87.5 %) cell lines had TG or GG genotype. In addition, 7 of 8 cell lines except for YUMOTO were positive for high-risk HPV.


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)

Representative genotyping of MDM2-SNP309 by two independent PCR assays for each allele. Lanes 1, 5, and 7: TG heterozygote. Lanes 2, 4, and 6: GG homozygote. Lane 3: TT homozygote. The wild-type (T) and the mutant (G) allele yields 121-bp and 168-bp fragments, respectively.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig3: Representative genotyping of MDM2-SNP309 by two independent PCR assays for each allele. Lanes 1, 5, and 7: TG heterozygote. Lanes 2, 4, and 6: GG homozygote. Lane 3: TT homozygote. The wild-type (T) and the mutant (G) allele yields 121-bp and 168-bp fragments, respectively.
Mentions: Figure 3 shows a representative genotyping of MDM-SNP309 by two independent PCR assays. The wild-type (T) and the mutant (G) allele yield 121-bp and 168-bp fragment, respectively. Table 5 shows the frequency of high-risk HPV and MDM2-SNP309 in 195 exfoliated cervical cell samples examined. When TT genotype was compared to TG + GG genotype, 41 patients with HSIL had significantly higher frequency of high-risk HPV than 102 with LSIL and 52 controls; however, there were no statistical significant differences in the TG + GG genotype prevalence and allele frequencies between SILs and controls. No statistical difference was also found in the genotype frequency of MDM2-SNP 309 between SILs and controls among 127 patients without high-risk HPV. However, there was an increased OR for TG + GG genotype in HSIL cases compared to controls among 68 patients with high-risk HPV, as shown in Table 6. Interestingly, 21 cases with HPV types 16 and/or 18 had significantly higher frequency of the TG + GG genotype and G allele than 47 with other types of high-risk HPV, as indicated in Table 7. Moreover, as shown in Figure 4, genotyping of MDM2-SNP309 in 8 cervical squamous carcinoma cell lines revealed that TT genotype was detected only in the SKG-IIIa cell line, whereas the other 7 of 8 (87.5 %) cell lines had TG or GG genotype. In addition, 7 of 8 cell lines except for YUMOTO were positive for high-risk HPV.

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