| Project/Area Number |
06671991
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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 | Chiba University |
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Principal Investigator |
NARUKAWA Yoshiaki Chiba University, School of Medicine, assistant, 医学部, 助手 (30260475)
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| Co-Investigator(Kenkyū-buntansha) |
SATO Kenichi Chiba University, School of Medicine, Professor, 医学部, 教授 (40009139)
TAKAHARA Masaaki Chiba University, School of Medicine, Lectarer, 医学部, 講師 (90143297)
TANAWA Hideki Chiba University, School of Medicine, Associated Professor, 医学部, 助教授 (50236775)
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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 |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1995: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1994: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | Oral SCC / point mutation / Precancerous lesion / Loss of heterozyosity (LOH) / 点突然売買 / 癌抑制遺伝子 / APC遺伝子 / LOH |
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| Research Abstract |
Recent studics have suggcsted that abnormalities in the adenomatous polyposis coli gene (APC gene) are associated with the development not only familial adenomatous polyposis coli (FAP) but also of cancers in digestive organs. In order to elucidate whether abnormalities of the APC gene could contribute to the development of oral squamous-cell carcinoma (SCC), gcnomic DNAs from tumors and normal tissues of 24 unrelated Japanese patients were examined by using PCR-SSCP (polymerase chain reaction single-strand conformation polymorphism) and sequence analyzes. Five novel nucleotide substitutions of the APC gene in tumor tissues were identified in 3 patients with oral SCC (12.5%), resulting in 3 amino-acidreplacements or a truncation of the APC gene product. We also examined 24 tumor and 24 normal tissue samples for loss of heterozygosity (LOH) at exon 11 of the APC gene by PCR-LOH assay. In this analysis, 45.8% of samples were informative and LOH was detected in 72.2% of informative cases. The frequency of LOH in oral SCC was similar to that previously reported in esophageal SCC.These results sugest that abnormalities in the APC gene are associated with the development of human oral SCC.
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