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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 GSTM1 and GSTT1 by multiplex PCR. Lane 1:  GSTM1 genotype (absence of 215 bp fragment). Lane 2:  GSTT1 genotype (absence of 480 bp fragment). Lane 3:  GSTM1 and GSTT1 genotypes (absence of 215 and 480 bp fragments). Lane 4: present GSTM1 and GSTT1 genotypes. β-globin as a positive control is detected as 268 bp fragment.
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fig1: Genotyping of GSTM1 and GSTT1 by multiplex PCR. Lane 1: GSTM1 genotype (absence of 215 bp fragment). Lane 2: GSTT1 genotype (absence of 480 bp fragment). Lane 3: GSTM1 and GSTT1 genotypes (absence of 215 and 480 bp fragments). Lane 4: present GSTM1 and GSTT1 genotypes. β-globin as a positive control is detected as 268 bp fragment.

Mentions: Figure 1 shows an example for genotyping of GSTM1 and GSTT1. The polymorphic deletion of the GSTM1 and GSTT1 genes was determined by multiplex PCR. The absence of 215 or 480 bp fragment indicated GSTM1 or GSTT1 genotype, respectively. Table 1 shows frequency of high-risk HPV and GSTM1, GSTT1 polymorphisms in 198 exfoliated cervical cell samples examined. The 42 patients with HSIL had significantly higher frequency of high-risk HPV than 102 with LSIL and 54 controls. There was no significant difference in the frequency of GSTM1 genotype between SILs and controls, whereas the 42 patients with HSIL had statistically higher frequency of GSTT1 genotype than 102 with LSIL and 54 controls. As shown in Table 2, the 31 patients with HSIL had also statistically higher frequency of GSTT1 genotype than 28 with LSIL among the 69 patients with 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)

Genotyping of GSTM1 and GSTT1 by multiplex PCR. Lane 1:  GSTM1 genotype (absence of 215 bp fragment). Lane 2:  GSTT1 genotype (absence of 480 bp fragment). Lane 3:  GSTM1 and GSTT1 genotypes (absence of 215 and 480 bp fragments). Lane 4: present GSTM1 and GSTT1 genotypes. β-globin as a positive control is detected as 268 bp fragment.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig1: Genotyping of GSTM1 and GSTT1 by multiplex PCR. Lane 1: GSTM1 genotype (absence of 215 bp fragment). Lane 2: GSTT1 genotype (absence of 480 bp fragment). Lane 3: GSTM1 and GSTT1 genotypes (absence of 215 and 480 bp fragments). Lane 4: present GSTM1 and GSTT1 genotypes. β-globin as a positive control is detected as 268 bp fragment.
Mentions: Figure 1 shows an example for genotyping of GSTM1 and GSTT1. The polymorphic deletion of the GSTM1 and GSTT1 genes was determined by multiplex PCR. The absence of 215 or 480 bp fragment indicated GSTM1 or GSTT1 genotype, respectively. Table 1 shows frequency of high-risk HPV and GSTM1, GSTT1 polymorphisms in 198 exfoliated cervical cell samples examined. The 42 patients with HSIL had significantly higher frequency of high-risk HPV than 102 with LSIL and 54 controls. There was no significant difference in the frequency of GSTM1 genotype between SILs and controls, whereas the 42 patients with HSIL had statistically higher frequency of GSTT1 genotype than 102 with LSIL and 54 controls. As shown in Table 2, the 31 patients with HSIL had also statistically higher frequency of GSTT1 genotype than 28 with LSIL among the 69 patients with 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