Analysis of chromosomal aberration in pancreatic carcinoma by comparative genomic hybridization

• Main Authors: YI CHAO LIN, 林宜昭
• Other Authors: 鄭授德
• Format: Others
• Language: zh-TW
• Published: 2005
• Online Access: http://ndltd.ncl.edu.tw/handle/49141080339263080109

碩士 === 長庚大學 === 基礎醫學研究所 === 93 === The mortality of pancreatic cancer in male is the ninth leading cause of cancer death during year 2003 in Taiwan, and that in female ranks eighth. In order to develop the new diagnostic, therapeutic and preventive methods of the disease, we ought to define the progression of the tumorigenesis mechanism of the cancer. However, what we know about the genetic mechanism of the disease is not enough. Hruban et al. (2000) proposed the genetic progression model for pancreatic intraepithelial neoplasias. It involved a set of genetic variations. The complicated copy number amplification and deletion in particular regions of chromosomes were difficult to detect with usual methods. Therefore, we used comparative genomic hybridization (CGH) to define the variant regions of chromosomes in pancreatic cancers, and tried to define the tumor suppressor genes and oncogenes involved. Twenty-three cases of pancreatic cancer were collected, including 16 cases of pancreatic ductal adenocarcinoma, 4 cases of endocrine carcinoma, a case of acinar cell carcinoma, and 2 cases of mucinous adenocarcinoma. After CGH analyses to the 23 cases the copy number abnormality showed that the gain occured in 14 cases (61%) at chromosomes 13q, in 13 cases (57%) at each of 7p, 8q and 14p, in 12 cases (52%) at each of 5q, 13p, 19p and 21p, in 11 cases (48%) at each of 1q, 5p, 6p and 11p, and the loss in 6 cases (26%) at chromosome 16q and 18q, and in 5 cases (22%) at 1p. We also noticed among 16 cases of pancreatic ductal adenocarcinoma, that the copy number gain occurred in chromosomes 8q (63%), 13q, 14p (56%), 1q, 5q, 7p, 11q, 13p and 21p (50%), and loss in chromosomes 18q (31%) and 16q (25%). Also, in 3 among 4 cases of endocrine carcinoma it showed the gain at chromosome 6q. The results imply that the particular type of tumor may be related to the certain genomic aberration in the identified specific regions. Further investigation with the array CGH, which increases the resolution in detecting the particular regions of chromosomes, may facilitate the understanding of the specific genes that may be involved. It can be then analyzed in correspondence with the various stages of the tumors, and the tumorigenesis progression of pancreatic carcinoma.