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DNA Diploidy of Gastric Cancer from the Aspects of DNA Heterogeneity and Chromosomal Numerical Aberrations


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Title: DNA Diploidy of Gastric Cancer from the Aspects of DNA Heterogeneity and Chromosomal Numerical Aberrations
Authors: Matsumoto, Yoshihiro
Issue Date: 15-Dec-1994
Citation: Acta medica Nagasakiensia. 1994, 39(4), p.137-146
Abstract: DNA heterogeneity, which is a problem we encounter during DNA ploidy analysis, was studied on the basis of analyzing numerical aberrations (that is, in the direction of gain) of chromosomes 7, 11 and 17 in 33 cases of gastric cancer, using fluorescence in situ hybridization (FISH). Emphasis was placed on clarification of the DNA aneuploidy formation process by comparing and characterizing three types of gastric tumor: homogeneously DNA diploid tumors (DD), the diploid portion of tumors showing DNA heterogeneity (DD-H) and the aneuploid portion of tumors showing DNA heterogeneity (DA-H). DNA heterogeneity and chromosomal heterogeneity increased markedly as gastric tumor advanced from `m' (mucosal) cancer to 'sm' (submucosal) cancer in early cancer. Thus, 'sm' cancer exhibited some features of advanced cancer. When DD and DD-H, both of which are DNA diploid, were compared in terms of chromosomal numerical aberrations, the number of chromosomes 11 and 17 was significantly higher in DD-H. When DD-H and DA-H were compared, the number of chromosomes 7 and 11 was significantly higer in DD-H, while the number of chromosome 17 was approximately the same in both. Based on these results of DNA ploidy analysis of gastric cancer, the numerical aberrations of chromosomes 11 and 17 strongly suggest the presence of DNA heterogeneity even in DNA diploid cases, and DNA diploid tumors with abnormal numbers of chromosomes 11 and 17 have features similar to those of DNA aneuploid tumors. When the DNA aneuploidy formation process was studied on the basis of chromosomal numerical aberrations, it appeard that the number of chromosomes 11 and 17 increases first, and that chromosomes 7 and 11 are closely involved in the change of a tumor into a DNA aneuploid tumor.
URI: http://hdl.handle.net/10069/16026
ISSN: 00016055
Type: Departmental Bulletin Paper
Text Version: publisher
Appears in Collections:Volume 39, No. 4

Citable URI : http://hdl.handle.net/10069/16026

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