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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 p53 codon 72 by PCR-RFLP. Lane 1: Arg/Arg homozygote. Lane 2: Arg/Pro heterozygote. Lane 3: Pro/Pro homozygote. The fragment of 199 bp is the nondigested PCR product from the Pro allele. Fragments of 113 and 86 bp result from BstUI digestion of the Arg allele.
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fig2: Genotyping of p53 codon 72 by PCR-RFLP. Lane 1: Arg/Arg homozygote. Lane 2: Arg/Pro heterozygote. Lane 3: Pro/Pro homozygote. The fragment of 199 bp is the nondigested PCR product from the Pro allele. Fragments of 113 and 86 bp result from BstUI digestion of the Arg allele.

Mentions: As shown in Figure 2, the Arg allele is cleaved by BstUI and yields two small fragments (113 and 86 bp). The Pro allele is not cleaved by BstUI and has a single 199 bp band. The heterozygote contains three bands (199, 113, and 86 bp). Table 3 shows HPV status and polymorphic frequency of p53 codon 72 in 198 samples examined. The 42 patients with HSIL had significantly higher frequency of high-risk HPV than 102 with LSIL and 54 controls, as described above. The differences in the polymorphic frequency of p53 Arg, Arg/Pro, and Pro genotypes between SILs and controls were statistically not significant. When the Arg genotype was compared to the Arg/Pro + Pro genotypes, there was again no statistical difference in the genotype prevalence between SILs and controls with or without high-risk HPV, as shown in Table 4.


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 p53 codon 72 by PCR-RFLP. Lane 1: Arg/Arg homozygote. Lane 2: Arg/Pro heterozygote. Lane 3: Pro/Pro homozygote. The fragment of 199 bp is the nondigested PCR product from the Pro allele. Fragments of 113 and 86 bp result from BstUI digestion of the Arg allele.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig2: Genotyping of p53 codon 72 by PCR-RFLP. Lane 1: Arg/Arg homozygote. Lane 2: Arg/Pro heterozygote. Lane 3: Pro/Pro homozygote. The fragment of 199 bp is the nondigested PCR product from the Pro allele. Fragments of 113 and 86 bp result from BstUI digestion of the Arg allele.
Mentions: As shown in Figure 2, the Arg allele is cleaved by BstUI and yields two small fragments (113 and 86 bp). The Pro allele is not cleaved by BstUI and has a single 199 bp band. The heterozygote contains three bands (199, 113, and 86 bp). Table 3 shows HPV status and polymorphic frequency of p53 codon 72 in 198 samples examined. The 42 patients with HSIL had significantly higher frequency of high-risk HPV than 102 with LSIL and 54 controls, as described above. The differences in the polymorphic frequency of p53 Arg, Arg/Pro, and Pro genotypes between SILs and controls were statistically not significant. When the Arg genotype was compared to the Arg/Pro + Pro genotypes, there was again no statistical difference in the genotype prevalence between SILs and controls with or without high-risk HPV, as shown in Table 4.

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