| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1995: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1994: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Research Abstract |
Genetic alterations including activation of K-ras oncogene and inactivation of APC (adenomatous polyposis coli), p53, and DCC (deleted in colon cancer) tumor suppressor genes are sequentially accumulated during colorectal adenoma-carcinoma sequence. Investigators have postulated that differentiated adenocarcinomas of the stomach and colorectel carcinomas may share similar genetic pathway and that differentiated adenocarcinomas of the stomach also may develop from pre-existing adenomas, however, few reports focused on the molecular mechanism of gastric adenoma-carcinoma sequence. In the present research, we have found that the sequential accumulation of ganetic alterations charcteristic of the colorectal adenoma-carcinoma sequence mentioned above did not occur between gastric adenoma and adenocarcinoma, although p53 gene mutations and DCC-LOH (loss of heterozygosity) were highly prevalent in gastric carcinomas. In addition, an allelotype study have revealed that several specific chromosomes were frequently deleted in carcinomas even in their early stages, but not in adenomas. RER (replication error) also was a frequent event in carcinomas, but not in adenomas. From these results, we have concluded that the majority of differentiated adenocarcinomas of the stomach may develop through a de novo pathway.
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