2005Zhongguo weishengtaixue zazhiRequires access

HPV-16 and EBV infections associating with expression of PCNA in the carcinogenesis of cervical carcinoma

Mei Li

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Abstract

Objective To illustrate the influences of HPV-16 and EBV to proliferate cellular nuclear antigen (PCNA) and to evaluate their role in the occurrence of cervical carcinoma. Methods Formalin-fixed and paraffin-embedded tissues from 59 cases of cervical carcinoma and 20 cases of cervical non-carcinoma were used to detect protein expressions of HPV-16, EBV and PCNA by immunohistochemistry method. Results The expression rates of HPV-16, EBV and PCNA were 69.49%, 57.63% and 77.97% in the tissues from cervical carcinoma and 30%, 25% and 15% in the tissues from cervical non-carcinoma respectively. The coexisted rates of HPV-16 and EBV were 35.59% in those from cervical carcinoma, while 0% from cervical non-carcinoma. The expression rates of HPV-16, EBV and PCNA in cervical carcinoma were all higher than those in cervical non-carcinoma. The expression rates of HPV-16 and EBV were not significantly different among tissues from cervical carcinoma in different grades and phases. PCNA expression rate increased with the grades of the carcinoma, while it did not with different phases. The PCNA expression rate was higher in the tissues with HPV-16 or EBV infection than that without. The expression rate of PCNA was 100% in the tissues infected with HPV-16 and EBV simultaneously. Conclusions The infection of HPV-16 and EBV may contribute to carcinogenesis of cervical carcinoma by increasing PCNA expression. The expression of PCNA may be served as an prediction of carcinogenesis.

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Objective To illustrate the influences of HPV-16 and EBV to proliferate cellular nuclear antigen (PCNA) and to evaluate their role in the occurrence of cervical carcinoma. Methods Formalin-fixed and paraffin-embedded tissues from 59 cases of cervical carcinoma and 20 cases of cervical non-carcinoma were used to detect protein expressions of HPV-16, EBV and PCNA by immunohistochemistry method. Results The expression rates of HPV-16, EBV and PCNA were 69.49%, 57.63% and 77.97% in the tissues from cervical carcinoma and 30%, 25% and 15% in the tissues from cervical non-carcinoma respectively. The coexisted rates of HPV-16 and EBV were 35.59% in those from cervical carcinoma, while 0% from cervical non-carcinoma. The expression rates of HPV-16, EBV and PCNA in cervical carcinoma were all higher than those in cervical non-carcinoma. The expression rates of HPV-16 and EBV were not significantly different among tissues from cervical carcinoma in different grades and phases. PCNA expression rate increased with the grades of the carcinoma, while it did not with different phases. The PCNA expression rate was higher in the tissues with HPV-16 or EBV infection than that without. The expression rate of PCNA was 100% in the tissues infected with HPV-16 and EBV simultaneously. Conclusions The infection of HPV-16 and EBV may contribute to carcinogenesis of cervical carcinoma by increasing PCNA expression. The expression of PCNA may be served as an prediction of carcinogenesis.

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Available abstract

Objective To illustrate the influences of HPV-16 and EBV to proliferate cellular nuclear antigen (PCNA) and to evaluate their role in the occurrence of cervical carcinoma. Methods Formalin-fixed and paraffin-embedded tissues from 59 cases of cervical carcinoma and 20 cases of cervical non-carcinoma were used to detect protein expressions of HPV-16, EBV and PCNA by immunohistochemistry method. Results The expression rates of HPV-16, EBV and PCNA were 69.49%, 57.63% and 77.97% in the tissues from cervical carcinoma and 30%, 25% and 15% in the tissues from cervical non-carcinoma respectively. The coexisted rates of HPV-16 and EBV were 35.59% in those from cervical carcinoma, while 0% from cervical non-carcinoma. The expression rates of HPV-16, EBV and PCNA in cervical carcinoma were all higher than those in cervical non-carcinoma. The expression rates of HPV-16 and EBV were not significantly different among tissues from cervical carcinoma in different grades and phases. PCNA expression rate increased with the grades of the carcinoma, while it did not with different phases. The PCNA expression rate was higher in the tissues with HPV-16 or EBV infection than that without. The expression rate of PCNA was 100% in the tissues infected with HPV-16 and EBV simultaneously. Conclusions The infection of HPV-16 and EBV may contribute to carcinogenesis of cervical carcinoma by increasing PCNA expression. The expression of PCNA may be served as an prediction of carcinogenesis.

Key concepts: Proliferating cell nuclear antigen, Carcinogenesis, Immunohistochemistry, Cervical carcinoma, Carcinoma, Pathology, Medicine, Cancer research

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