[Expression of FHIT genes in CIN and cervical carcinoma and the relationship between FHIT gene and p53 and HPV16/18].
OBJECTIVE
To investigate the role and significance of FHIT genes depletion, p53 overexpression and HPV16/18 infection in cervical intraepithelial neoplasia (CIN) and cervical carcinoma (CC).


METHODS
Tumor samples taken from 52 cases of CIN and 69 cases of CC were processed by immunohistochemistry (SP) to determine the expression of FHIT genes and p53 protein, by in situ hybridization to detect HPV16/18 infection, and were compared with those in 18 cases of normal cervical tissues as control.


RESULTS
(1) The FHIT expression was positive in normal cervical tissue with no depletion occurred, and was 30.8% in CIN. It was significantly higher in CIN III and carcinoma groups than that in normal and CIN I/II groups (P < 0.01). The depleted expression of FHIT in infiltrating cervical carcinoma group was 66.7% (46/69), significantly higher than that in normal and CIN groups (P < 0.01). Along with the decreasing of cell differentiation, the negative rate of FHIT raised. (2) The positive expression of p53 in CC group was 56.5% (39/69) and the HPV16/18 was 84.1% (58/69), both higher than that in CIN and normal groups (P < 0.05). (3) In CIN and CC groups, the positive rate of p53 in cases with positive or negative FHIT expression was similar (P > 0.05). (4) There is a negative correlation between FHIT and p53 expression. The rate of HPV16/18 infection in the depleted expression of FHIT group was significantly higher than that in FIHT normal expression group (P < 0.01).


CONCLUSIONS
(1) The FHIT-depletion is related with cervical carcinogenesis. It may be used as a marker to serve mass screening of CIN-high risk subjects and diagnostic indicator for early cervical carcinoma. (2) Depleted expression of FHIT is frequently associated with p53 over-expression in CIN and CC subjects, but there is no direct correlation between them. (3) HPV16/18 infection may probably be the common cause leading to altered FHIT and p53 expression.
Zhang
Wen-Miao
WM
The First Affiliated Hospital of Wenzhou Medical College, Wenzhou 325000, China. zhwm63@hotmail.com
Shuai
Ci-Xia
CX
Zheng
Fei-Yun
FY
Huang
Yin-Ping
YP
Wang
Qun-Ji
QJ
Zhu-Hua
He
Qiu-Xiang
QX
D017766:Acid Anhydride Hydrolases / Q000378:metabolism*; D002294:Carcinoma, Squamous Cell / Q000378:metabolism / Q000821:virology; D005260:Female; D052162:Human papillomavirus 16 / Q000235:genetics; D052161:Human papillomavirus 18 / Q000235:genetics; D006801:Humans; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D009363:Neoplasm Proteins / Q000378:metabolism*; D030361:Papillomavirus Infections / Q000378:metabolism* / Q000821:virology; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism*; D002583:Uterine Cervical Neoplasms / Q000378:metabolism* / Q000821:virology; D002578:Uterine Cervical Dysplasia / Q000378:metabolism* / Q000821:virology; D000099170:Bis(5'-adenosyl)triphosphatase
D017766:Acid Anhydride Hydrolases; D009363:Neoplasm Proteins; D016159:Tumor Suppressor Protein p53; D000099170:Bis(5'-adenosyl)triphosphatase