Epstein-Barr Virus and p16INK4A Methylation in Squamous Cell Carcinoma and Precancerous Lesions of the Cervix Uteri
Journal of Korean Medical Science
;
: 636-642, 2005.
Article
in English
| WPRIM
| ID: wpr-147613
ABSTRACT
Methylation of p16 is an important mechanism in cervical carcinogenesis. However, the relationship between cervical squamous cell carcinoma (SCC) and Epstein-Barr virus (EBV) remains controversial. Here, we explored whether EBV infection and/or p16 gene inactivation would play any role in cervical carcinogenesis. Eighty-two specimens included 41 invasive SCCs, 30 cervical intraepithelial neoplasm (CIN; CIN 1, 11 cases, CIN II, 3 cases, CIN III 16 cases) and 11 nonneoplastic cervices. EBV was detected by polymerase chain reaction (PCR) for EBNA-1 and in situ hybridization for EBER-1. The p16 methylation-status and the expression of p16 protein were studied by methylation-specific PCR and immunohistochemistry, respectively. The materials were divided into four groups 1) nonneoplastic cervices, 2) CIN I, 3) CIN II-III and 4) invasive SCCs. p16 methylation and p16 immunoexpressions increased in CIN and invasive SCCs than nonneoplastic tissue. p16-methylation and p16-immunoreactivities were higher in the EBV-positive group (p=0.009, p<0.001) than in the EBV-negative group. EBV was detected more frequently in CIN and SCCs than nonneoplastic cervices. In conclusion, a correlation between p16 methylation, p16 immunoreactivity and the detection of EBV strongly suggested that the cooperation of EBV and p16 gene may play a synergic effect on cell cycle deregulation.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Precancerous Conditions
/
DNA, Viral
/
RNA, Viral
/
Comparative Study
/
Immunohistochemistry
/
Carcinoma, Squamous Cell
/
Uterine Cervical Neoplasms
/
Polymerase Chain Reaction
/
In Situ Hybridization
/
Herpesvirus 4, Human
Limits:
Female
/
Humans
Language:
English
Journal:
Journal of Korean Medical Science
Year:
2005
Type:
Article
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