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KMID : 0358419960390040715
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Korean Journal of Obstetrics and Gynecology
1996 Volume.39 No. 4 p.715 ~ p.727
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Human Papillomavirus Infection and p53 Tumor Suppressor Gene Mutation in Primary Cervical Carcinoma
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김진우
조율희/김봉윤/김재훈/김은중/한구택/남궁성은
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Abstract
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Tumor specimens obtained from 136 patients with primary carcinoma of the uterine cervix were analysed for presence of human papillomavirus (HPV) sequences and for mutation of p53 tumor suppressor gene.
HPV detection was done using polymerase chain reaction(PCR) amplification with HPV E6 region type specific primers as well as L1 consensus primers. Mutations of the p53 gene were examined by single-strand conformation polymorphism(SSCP) analysis
of
PCR
products.
@ES The results were as follows:
@EN 1. PCR showed that 130 of 136(96%) tumors contained oncogenic HPV 16 or 18 sequence. Three(2%) lacked HPV DNA. Of the 127 tumor specimens cell carcinomas analyzed, only 14(11%) showed HPV 18, in contrast to 122 of 127 (96%) having HPV
16(including
13 tumors coinfected with HPV 16 and 18). Of the 9 cases of adenocarcinomas, HPV 16 and HPV 18 were identified in five cases(56%) each (including 3 tumors coinfected with HPV 16 and 18). These results suggest that HPV 16 is predominant type in
cervical
squamous cell carcinomas (P<0.05) and HPV 18 is isgnificantly associated with cervical adenocarcinomas (P<0.05) and HPV 18 is significantly associated with cervical adenocarcinomas (P<0.05). There was no relationship between HPV positivity and
tumor
stage. Histologic grading was reviewed with respect to HPV infection. The more dedifferentiated the primary tumor, the more frequent HPV 16 infection (P<0.05) and the more differentiated, the more frequent HPV 18 infection (P<0.05). HPV 16 was
idenified
in all tumors of large cell keratinizing type (29 of 29) and small cell type of squamous carcinomas (3 fo 3).
2. Two of 136(1.5%) tumors demonstrated a SSCP band shift in exons 4 to 9 of the gene, including 1 in exon 4 and 1 in the region encompassing exons 5 and 6. These abnormal DNA fragments have been further characterized by direct DNA sequencing.
One(positive for HPV 18) had a nonsense mutation of codon 101 in exon 4 from AAA to TAA transversion. Another(positive for L1 consensus primer set0 showed a point mutation involving codon 179 in exon 5 changing CAT to GGT transition and causing
substitution of arginine for histidine in the protein. This results showed that p53 mutations occurred in combination with HPV infection. The three specimens negative for HPV did not contain p53 gene mutations.
3. Our datga show that muation of p53 is infrequent in primary cervical carcinoma and there is no inverse correlation between HPV infection and p53 gene mutation. Other mechanisms independent of p53 inactivation may also be involved in
tumorgenesis of
the uterine cervix.
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KEYWORD
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