1. in situ hybridization에 의한 인유두종바이러스 16/18형의 감염율은 66%(48/73)이고 PCR-Southe- rn blot 방법에 의한 인유두종 바이러스의 감염율은 74%(32/43)이었다. 2. p53 과발현율은 전체 73례중 22례에서 양성으로 나타나 30%였다. 3. HPV infection과 p53 과발현사이에 역상관관 계가 있다. 4. 인유두종 바이러스의 감염이나 p53 과발현은 자궁경부암의 예후인자인 연령, 종양의 크기, 종양의 침윤정도, 세포의 유형, 분화도, 임파절 전이 등과는 유의성이 있는 관계를 보이지 않았다. 5. 73례에서 HPV 감염과 p53 과발현 유무에 따 른 누적생존율의 비교에서는 유의한 차이를 보이지 않았다. 6. p53 유전자 변이는 43례중 8례에서 나타났으며 인유두종 바이러스의 유형과는 상관관계를 보이지 않았다. 7. 자궁경부암의 발생에 있어서 고위험군 인유두 종 바이러스와 p53 유전자 변이가 중요한 역할을 하 지만 이들 두 가지의 요인은 각각 단독으로 자궁경 부암의 발생을 유도할 수 있으며 또한 한 가지 요인 이 있다고해서 다른 요인이 존재하지 않을 필요는 없고 오히려 두가지 요인이 함께 공존할 수도 있다.

Oncogenic human papillomavirus(HPV) infection has been implicated in the pathogenesis of cervical carcinoma. The HPV E6 and E7 oncoproteins are thought to play a crucial role in this process by their interactions with the p53 protein and the retinoblastoma suceptibility gene products respectively. The E6 protein binds to and stimulates the degradation of the p53 protein and mutations involving evolutionary conserved regions of the p53 gene also can alter p53 fu-nction, so both HPV E6 protein and p53 mutation may play a role in the carcinogenesis of cer-vical carcinoma. The purposes of this study are to examine the role of p53 gene in relation to the presence of HPV DNA in primary cervical carcinoma and to assess the prognostic value of the p53 gene and HPV infection in surgically treated cervical carcinoma. Formalin fixed, paraffin embeded blocks of 73 cervical carcinomas were evaluated for the status of oncogenic HPV infection by in situ hybridization, and the p53 overexpression by immunohistochemical staining. 43 cases out of 73 cervical carcinomas were evaluated for the HPV type by polymerase chain reaction (PCR)-Southern blot analysis, and the presence of mutations involving exon 4-10 of the p53 gene was examined by polymerase chain reaction-single stranded conformation polymorphism (PCR-SSCP), and then, confirmed by direct DNA sequencing. 48 cases of 73 cervical carcinomas showed oncogenic HPV DNA by in situ hybridization and 22 cases showed p53 overexpression by immuno-histochemical staining. There was inverse correlationship between HPV infection and p53 overexpression(p=0.03). HPV infection and p53 overexpression were not significantly correlated with clinicopathological parameters such as age, FIGO stage, histologic type, tumor size, lymph node metastasis, depth of invasion, and tumor differentiation. 32 cases of 43 cervical carcinomas showed oncogenic HPV DNA by PCR-Southern blot analysis. 30 cases(69.8%) of 43 cervical carcinomas showed HPV 16 DNA and 9 cases(20.9%) showed HPV 18 DNA and 11 cases(25.6%) showed no HPV 16/18 DNA. 8 cases of 43 cervical carcinomas showed p53 gene mutation in PCR-SSCP analysis. 7 cases of 8 mutations showed positive p53 overexpression and another 1 case showed negative p53 overexpression. 4 cases of 8 mutations had no HPV 16/18 infection and another 4 cases had HPV 16 and/or 18 infection. There was no significant correlation between p53 mutation and HPV infection. In 8 cases showing mutation, 4 cases showed point mutation, 3 cases sho- wed frame shift mutation, and another 1 case showed deletion from codon 125 to 132. p53 mutations were located at exon 4, 5, 6, 7, and 8, highly conserved region. Oncogenic HPV DNA can be identified in most cervical carcinomas, and mutations involving highly conserved regions of p53 gene, although infrequent in cervical cancer, occur preferentially in tumors without HPV infection but indenpendently. Although HPV infection and p53 overexpression shows no prognostic values in our study, further investigation is required for clarifyng its prognostic value in gynecologic malignancies.