| Budget Amount *help |
¥2,500,000 (Direct Cost: ¥2,500,000)
Fiscal Year 1997: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1996: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Research Abstract |
High rate of tumorigenesis was observed in transgenic mice carrying combined E1A and E1B gene of the adenovirus type 12 fused with the human renin promoter. All the tumors were primitive neutoectodermal tumor (PNET) of the identical histology. We investigated the mode of tumoringenesis in the transgenic mice and the precise character of the tumors. Fused gene of the human renin promoter and the combined E1A-E1B was introduced into the fertilized eggs of C57BL/6J mice for producing transgenic mice. One hundred and fifty five transgenic mice out of 394 offspring were obtained by mating of transgenic mice with inbred wild type mice. Tumors were observed and confirmed as PNET histologically by autopsy in 132,85% of transgenic mice. Among the 155 transgenic mice, abdominal distension caused by marked intestinal dilatation, mimicking Hirschsprung disease, was observed in 8 mice. Tumor became obvious from 7 weeks to 17 month of age. Tumor developed preferentially in extremities, trunk, abdomen and intrapelvic before 19 weeks of age and in head after 20 weeks. There was no obvious correlation of the sites of origin to the sympathetic chains or the adrenal gland. Immunohistochemical study revealed positive to PGP9.5 and NF but all negative to NSE,CD57, tyrosine hydroxylase, GFAP,MIC2, vimentin, desmin and myoglobin indicating very primitive neuroectodermal tumor. This transgenic mice model will hopefully elucidate the tumorigenesis of PNET.
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