Korean J Obstet Gynecol.
2004 Jul;47(7):1317-1326.
Relationship between HPV Typing and Expressions of p16 and p53 in Cervical Neoplasia
- Affiliations
-
- 1Department of Obstetrics and Gynecology, College of Medicine, Inha University, Incheon, Korea.
- 2Department of Pathology, College of Medicine, Inha University, Incheon, Korea.
- 3Department of Urology, College of Medicine, Soonchunhyong University, Seoul, Korea.
- 4Department of Food Science and Technology, Chung-Ang University, Seoul, Korea.
Abstract
OBJECTIVE
To determine the relationships among the grade of cervical pathology, HPV infection status, p16 expression, and p53 expression in cervical neoplasia.
METHODS
From July of 2002 to June of 2003, authors did HPV typing with HPV Oligonucleotide Microarray DNA Chip (Biomed, Seoul, Korea), p16 and p53 immunochemical staining in cervical tissues obtained from conization or hysterectomy
RESULTS
41 patients were enrolled in this study. There were 16 normal (WNL) patients, 9 CIN patients, 8 microinvasive cancer (MIC) patients, and 8 invasive cervical cancer (ICC) patients. The HPV infection rate in WNL, CIN, MIC and ICC were 0%, 100%, 50% and 50% retrospectively. The expression rate of p16 was 13% in WNL, 67% in CIN, 50% in MIC and 100% in ICC. That of p53 was 0% in WNL, 67% in CIN, 75% in MIC and 100% in ICC. With regard to p16 staining in HPV negative cases, negative staining was 67%, weakly positive was 13% and strongly positive was 21%. But in HPV-infected cases, negative staining of p16 was 29%, weakly positive was 53% and strongly positive was 18%. With regard to p53 staining in HPV negative cases, without HPV infection, negative staining was 62%, weakly positive was 33% and strongly positive was 4%. But in HPV infected cased, negative staining of p53 was 18%, weakly positive was 53% and strongly positive was 29%. Finally, in p16 negative cases, negative staining of p53 was 62%, weakly positive was 38% and strongly positive was 0%. But in p16 weakly positive cases, with weakly positive p16, negative staining of p53 was 33%, weakly positive was 42%, and strongly positive was 25%. In p16 strongly positive cases, negative staining of p53 was 13%, weakly positive was 50% and strongly positive was 38%.
CONCLUSION
There were significant associations among grades of cervical pathology, HPV infection, p16 and p53 expression. Thus there might be some possibilities that expression of p16 and p53 induced by E7 and E6 proteins of HPV can impact on the tumorigenesis.