Increased expression of alpha-1-antitrypsin, glutathione S-transferase π and vascular endothelial growth factor in human pancreatic adenocarcinoma

This study was designed to investigate abnormalities in gene expression in ductal adenocarcinoma of the pancreas using cDNA arrays. Gene expression in pancreatic ductal adenocarcinoma was compared with normal pancreatic tissue controls. Specimens from 5 patients with pancreatic adenocarcinoma were t...

Full description

Saved in:
Bibliographic Details
Published inThe American journal of surgery Vol. 184; no. 6; pp. 642 - 647
Main Authors Trachte, Aaron L, Suthers, Sara E, Lerner, Megan R, Hanas, Jay S, Jupe, Eldon R, Sienko, Anna E, Adesina, Adekunle M, Lightfoot, Stan A, Brackett, Daniel J, Postier, Russell G
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 01.12.2002
Elsevier Limited
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:This study was designed to investigate abnormalities in gene expression in ductal adenocarcinoma of the pancreas using cDNA arrays. Gene expression in pancreatic ductal adenocarcinoma was compared with normal pancreatic tissue controls. Specimens from 5 patients with pancreatic adenocarcinoma were taken fresh at operation and analyzed using commercially prepared cDNA arrays evaluating approximately 2,000 genes. Immunohistochemical staining was used to confirm protein expression of selected genes. Alpha-1-antitrypsin (A1AT) and glutathione S-transferase π (GSTP) were significantly up-regulated in all 5 tumors. Vascular endothelial growth factor (VEGF) was up-regulated in 4 of the 5 patients. Immunohistochemical staining verified the overexpression of each of these genes. A1AT, GSTP, and VEGF are overexpressed in human pancreatic adenocarcinoma specimens taken fresh at operation. To our knowledge, this is the first study of human pancreatic ductal adenocarcinoma demonstrating the up-regulation of these genes using gene expression arrays.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0002-9610
1879-1883
DOI:10.1016/S0002-9610(02)01105-4