KURODA Akira Univ.Tokyo, Director, 医学部・附属病院, 講師 (70010270)
山形 誠一 東京大学, 医学部・附属病院, 助手
WADA Yoshiyuki Univ.Tokyo, Assistant, 医学部・附属病院, 助手 (70107647)
KIMURA Wataru Univ.Tokyo, Assistant, 医学部・附属病院, 助手 (00169947)
YAMAGATA Seiichi Univ.Tokyo, Assistant
|Budget Amount *help
¥1,900,000 (Direct Cost : ¥1,900,000)
Fiscal Year 1994 : ¥300,000 (Direct Cost : ¥300,000)
Fiscal Year 1993 : ¥1,600,000 (Direct Cost : ¥1,600,000)
Nuclear DNA content of 131pancreatic duct epithelial lesions, including 10 normal ducts, 30 intraductal proliferations with mibel atypia (group I-II), 30 with moderate atypia (group III), 24 with severe atypia (group IV), 14 of carcinoma in situ (groupV), and 23 invasive carcinomas, was analyzed using microspectrophoto metry. DNA histograms. were cl asified into diploid, polyploid and aneuploid patterns.
All of normal duct epithelia showed diploidy. Polyploid patterns a observed in 3 (10%) lesions of groups I-II,17 (56.7%) of group III 14 (58.4%) of group IV,7 (50%) of group V,and 6 (26.1%) of in vasive carcinomas, and aneuploid patterns were observed in 0%, 10%, 33.3 50% and 73.9%, respectively. This distribution of ploidy patterns re vealed a gradual shift to the main ploidy from diploid to polyploid followed by aneuploid in proportion to the increase of the degree of epithelial atypia.
The frequencies of polyploid cells in each lesiong were determined. Their averages were 0.2% in group I-II,1.9% in group III,3.4% in group IV,4.4% group V,and 6.7% in invasive carcinoma. The S・G_2M phase fractions were Significantly higher in proliferative epithelia than in normal. The results of the study suggest that duct epithelial proliferations of the pancreas have "go instability" leading to a serial clonel evolution and play a significant role in the progressions of pancreatic duct cell carcinoma.