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KMID : 0375219940090010025
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Journal of Il Sin Christian Hospital
1994 Volume.9 No. 1 p.25 ~ p.44
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A Study on High Risk HPV Infection and p53, EGF-R and bcl-2 Expression in Uterine Cervical Carcinoma
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Abstract
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A study on the high risk HPV-16/18 infection by situ hybridization and on te expression patterns of mutant p53 protein, EGF-R protein, bcl-2 protein and PCNA by immunohistochemical stains was performed with 73 uterine cervical carcinoma tissues,
and the
relation between the protein products of oncogenes and antioncogenes in development and progression in uterine cervical carcinoma was investigated.
@ES The results were as follow.
@EN 1. Koilocytosis of the cervical mucosal epithelium was in 42 (57.5%) of 73 cases of uterine cervical carcinomas.
2. HPV 16/18 was detected in 22 cases(30.1%).
3. mutant p53 protein was in 20 (27.5%) of 73 cases of uterine cervical carcinoma tissues and in 8 (36.4%) of 22 HPV-positive uterine cervical carcinomas.
4. EGF-R was overexpressed in 63 cases(86.5%) and EGF-R was coexpressed in 16(80%) of 20 mutant p53 positive cases.
5. bcl-2 was overexpressed in 56 cases (76.7%) and bcl-2 was coexpressed in 16 (80%) of p53 positive cases.
6. PCNA was increased in all 73 cases (100%) of uterine cervical carcinoma.
It is known that the uterine cervical carcinoma is highly associated with HPV infection and the p53 mutation is rare in cervical cancer cells in contrast to other human cancers. The result of this study is comewhat different from recent reports
from
other countries by relative high incidence of mutant p53 protein in carcinoma tissue, which suggests that the inactivation of wild type p53 functio by appearance of mutant p53 as well as degradation of wild type p53 protein by binding with HPV
viral
oncoprotein are important factors in pathogenesis of uterine cervical carcinoma in Korean women. In addition to transformation of cervical cells by HPV infection, it is supposed that the development of uterine cervical carcinoma is associated
with
pathologic overexpression of EGF-r delevering continuous mitogenic signals to the tumor cells and with bcl-2overexpression resulting in extension of cell survival y prevention of programmed cell death (apoptosis) and increasing risk of other
mutations
of oncongenes and antioncogenes. And it seems that these changes induce the increase of PCNA and cellular proliferating activity. In conclusion, this study study indicates that the loss of function and mutation of p53 by HPV infection and
activation of
EGF-r and bcl 2 are important in development and mutation of P53 by HPV infection and activation of EGF-R and blc-2 are important in development and progression of the uterine cervical carcinoms.
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KEYWORD
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