| Research Abstract |
(1) DNA Copy Number Changes in Primary Gastric Carcinomas by Comparative Genomic Hybridization.
We examined 33 primary gastric carcinomas using comparative genomic hybridization to detect changes in DNA copy number and chromosomal location of these changes.
Ninety-four percent (31/33) showed one or more DNA copy number changes, such as increases at 2p23-p25 (observed 21% of the total cases), 3q26.3-q27 (24%), 7p15 (24%), 9p22-pter (18%), and 13q22-q34 (21%), and decreases at 1p34.2-p36.2 (18%) and Y (52%).
Histological examination indicated that increases at 3q26.1-q26.3 and 7p15, and decreases at 1p36.1-p36.2 and Y were commonly observed in both differentiated and undifferentiated types. Increases at 3q27,6q23-q25, and 7cen-p14, and decreases at 1p34.2-p35 and 17p12 were predominantly observed in differentiated type, and increases at 2p23-pter, 9p22-pter, and 13q31-qter, and decrease at 6p21.3 were predominantly observed in undifferentiated type.
In addition, clinical staging of tumors sh
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owed that increases at 2p23-p25,7p14-p21,7q31-q32, and 9p22-pter, and decrease at Y were observed from early stage tumors, whereas, increases at 9q32-q33 and 15q26 were observed only in late stage tumors.
Many of the abnormalities detected in this study were not previously reported in gastric carcinomas. Our comparative genomic hybridization results indicate the presence of genetic alterations that may play some important role in the development and progression of gastric carcinomas.
(2) DNA Copy Number Changes in Adrenocortical tumors by Comparative Genomic Hybridization.
We examined 37 adrenocortical tumors using comparative genomic hybridization to screen for chromosomal regions with DNA copy number changes.
The common changes observed in 25 adrenocortical adenomas and 12 adenocarcinomas were DNA copy number increases at 1cen-q22,3cen-p12,3cen-q12,4cen-p12,4cen-q12,5cen-p12,5cen-q12,6cen-p12,8cen-p11.2,8cen-q12,10cen-p11.2,10cen-q21 (including the site of ret), and 11cen-p11.2, and decreases at Yp and Ycen-q11.2. In contrast, DNA copy number increases at 5q13-q33,7cen-q32 (including the site of erb-B and c-met), 10q22,11cen-q12,12cen-p12,18cen-p11.2,20p, 20cen-q11.2, Xcen-p11.2, Xp11.4-p21, and Xq25-q26, and decreases at 1p34.2-pter and 20q12-qter were predominantly observed in adenocarcinomas. On the other hand, DNA copy number increases at 1cen-p13,13cen-q13,15cen-q13,16cen-p11.2, and 16cen-q12.2 were predominantly observed in adenomas. Thus, regions predominantly observed in adenocarcinomas may contain genes associated with the transformation from benign to malignant behavior in adrenocortical tumors, and regions predominantly observed in adenomas may be relevant to the tumorigenesis of benign character.
In addition, comparison of the differences among aldosterone-producing, cortisol-producing, and non-functioning tumors showed that increases at 1cen-q22,5cen-p12,10cen-p11.2,10cen-q21 (including the site of ret), and 16cen-q12.2, and decreases at Yp and Ycen-q11.2 were commonly observed in all three types, whereas an increase at 5q13-q31.1,7q22,12p12, and 16cen-p11.2, and a decrease at 1p36.1 were observed predominantly in the aldosterone-producing type, increases at 1cen-p13,6cen-p12,7cen-q11.2,10q22,13cen-q13, and 20cen-q11.2, and a decrease at 20q12-qter were observed predominantly in the cortisol-producing type, and increases at 3q13.1-q13.3,7q31-q32,11cen-q12,12cen-p11.2,20cen-p11.2, Xcen-p11.2, Xp11.4-p21, and Xq25-q26, and a decrease at Xq25-qter were observed predominantly in the non-functioning type. These differences may be relevant to the excessive hormone-producing properties of the tumors.
Many of the abnormalities detected in this study have not previously been reported in adrenocortical tumors. Our comparative genomic hybridization results indicate that genetic alterations may play an important role in the cell growth and progression of adrenocortical tumors. Less
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