| Project/Area Number |
06671984
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Surgical dentistry
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| Research Institution | HOKKAIDO UNIVERSITY |
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Principal Investigator |
CHIBA Itsuo Hokkaido Univ., Sch. of Dent., Inst., 歯学部, 助手 (50250460)
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| Co-Investigator(Kenkyū-buntansha) |
SHINDOH Masanobu Hokkaido Univ, Sch. of Dent., Inst., 歯学部, 助手 (20162802)
NOTANI Ken-ichi Hokkaido Univ., Sch. of Dent., Assos. Prof., 歯学部, 助教授 (70113602)
FUJINAGA Kei Sapporo Med. Univ., Cancer Res. Inst., Dept. of Mol. Biol., Pro., 医学部, 教授 (10045338)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1995: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1994: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | p53 / Human papillomavirus / Oral squamous cell carcinoma / Prognosis / Betel chewing / Sri Lanka / P53遺伝子 / 口腔癌 / 癌遺伝子 / 腫瘍抑制遺伝子 |
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| Research Abstract |
We examined 38 primary, resected specimens of oral squamous cell carcinomas (SCCs) for detection of p53 mutations and human papillomavirus (HPV) intection. p53 Mutations were detected in nine cases (24%) using PCR-SSCP analysis. HPV DNA sequences were detected in eight cases (21%) by PCR with HPV-specific primers. Seven cases were p53 mutation-positive/HPV-negative, 6 cases were p53 mutation-negative/HPV-positive, and two intraosseus SCC cases were p53 mutation-positive/HPV-positive. Thus, 15/38 (49%) cases had inactivation of the p53 protein. Interestingly, p53 mutation-negative/HPV-negative cases had a poorer prognosis than p53 nunation positive or HPV-positive cases (p<0.01). We conclude that 1) mutation in tha p53 gene and/or HPV infection are frequent (40%) in oral SCC ; 2) inactivation of p53 function by mutation and HPV infection are important genetic events in the development of 40%- of oral SCCs ; 3) p53 mutation and HPV infection are not mutually exclusive events and 4) other oncogenes or tumor suppressor genes may be crucial in the development of oral SCC if the prognosis is poor. The same type of examinatioin was done for oral SCCs caused by betel chewing in Sri Lanka, where is one of the world's highest incidences of oral SCCs. We found that mutations in the p53 gene of oral cancers in Sri Lanka patients tended to cluster in exon 5. Infections of HPV are now under investigation.
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