Relations between the expression of p53, c-erbB-2, Ki-67 and HPV infection in cervical carcinomas and cervical dysplasias.
BACKGROUND
The analysis of mutual relations between HPV infection and the expression of cancer gene products and proliferative activity in cervical carcinomas and dysplasias.


METHODS
The expression of p53, c-erbB-2 oncoproteins and proliferative activity (Ki-67) was evaluated immunohistochemically in 41 cervical carcinomas and 29 dysplasias. HPV infection (type 16, 18) was assessed by in situ hybridization technique.


RESULTS
HPV-positive carcinomas were found in 68.3% of cases. HPV type 16 infection were detected in 54% and HPV 18 in 39% of carcinomas. Simultaneous appearance of both virus types was shown in 25% of carcinomas. In dysplastic lesions, HPV infection was observed in 62.1% of cases. HPV type 16 was found in 34.5% and HPV 18 in 44.8% of patients. Both virus types were found in 17.2% of dysplasias. HPV infection was more extensive in cervical carcinomas than in dysplasias. Similarly the expression of oncoproteins was more intensive and referred to a higher percentage of cells in carcinomas. No relations between p53, c-erbB-2 overexpression and HPV infection were found. Ki-67 activity was found in a higher percentage of HPV-positive than in HPV-negative, both carcinomas and dysplasias.


CONCLUSIONS
HPV infection, especially accompanied by increase of proliferative activity in dysplasias may define the cell subpopulation predisposed to malignant process development. The employment of in situ hybridization technique appears to be useful in detecting the viral infection in cytological smears even with no morphological changes in the cells.
Bar
J K
JK
Department of Clinical Immunology, Medical University, Wrocław, Poland. immuno@immuno.am.wroc.pl
Harłozińska
A
A
Sedlaczek
P
P
Kasiak
J
J
Markowska
J
J
D005260:Female; D006801:Humans; D019394:Ki-67 Antigen / Q000096:biosynthesis* / Q000235:genetics; D027383:Papillomaviridae / Q000302:isolation & purification*; D030361:Papillomavirus Infections / Q000378:metabolism* / Q000473:pathology / Q000821:virology; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000096:biosynthesis* / Q000235:genetics; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis* / Q000235:genetics; D014412:Tumor Virus Infections / Q000378:metabolism* / Q000473:pathology / Q000821:virology; D002578:Uterine Cervical Dysplasia / Q000145:classification / Q000378:metabolism* / Q000473:pathology / Q000821:virology; D002583:Uterine Cervical Neoplasms / Q000378:metabolism* / Q000473:pathology / Q000821:virology
D019394:Ki-67 Antigen; D018719:Erb-b2 Receptor Tyrosine Kinases; D016159:Tumor Suppressor Protein p53