| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1995: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1994: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Research Abstract |
It is clear that there are two kinds of tumorgenesis of uterine endometrial carcinoma ; i.e., one type of the carcinoma is accompanied with endometrial hyperplastic lesions, and the another is estrogen-independent without hyperplastic lesions occurring after a menopausal period. The cytogenetic studies of precancerous lesions are required to clarify these tumorgenesis.
We have done the interphase cytogenetic studies of the endometrial hyperplastic lesions and carcinoma using fluorescence in situ hybridization (FISH) with chromosome-specific probes. Paraffin sections of endometrial hyperplastic lesions and carcinoma, more than 20 micorometer in thickness, were hybridized with centromeric probes of chromosomes 1,6,7,16,17 and 18. The sections were observed by a confocal laser scanning micoroscope (CLSM) and the serial opticalsections were obtained. Then, three dimensional images were reconstructed by an image anasysis divice.
Loss of copy numbers of chromosomes 16,17 and 18 were observed in hyperplastic lesions and carcinoma tissues. The data explains that some types of hyperplastic lesions might change into carcinoma. Gain of chromosome 1 was observed in carcinoma tissues and it was suggested that chromosome 1 may contribute the tumorgenesis. However, there was no evidence of gain of the chromosome in hyperplastic lesions. Hence, polysomy of chromosome 1 is not the primary change of tumorgenesis of endometrial carcinoma.
Cytogenetic studies using thick sections and CLSM may be considerably helpful to clarify the tumorgenesis of endometrial carcinoma.
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