Original Article Alpha-Methylacyl-CoA Racemase Expression Is Upregulated in Gastric Adenocarcinoma: A Study of 249 Cases
Camtu D. Truong, Wei Li, Wei Feng, Philip Cagle, T. Khoury, S. Alrawi, K Xie, J Yao and Dongfeng Tan
Department of Pathology, The University of Texas M. D. Anderson Cancer Center, Houston, TX, USA, The University of Texas Health Science Center at Houston, Houston, TX, USA, The Methodist Hospital, Houston, TX, USA, Roswell Park Cancer Institute, Buffalo, NY, USA and University of Florida Health Science Center, Jacksonville, FL, USA
Received 12 March 2008; Accepted with revision 29 March 2008; Available online 10 April 2008
Abstract: Alpha-methylacyl-CoA racemase (AMACR [P504S]) is a mitochondrial and peroxisomal enzyme involved in beta-oxidation of dietary branched-chain fatty acids and their derivatives. Recent studies showed that AMACR is expressed in several neoplasms, including prostate and colon cancer. However, AMACR expression in gastric neoplasms has yet to be thoroughly investigated. Because AMACR overexpression in human solid tumors is a potential target for cancer treatment, we aimed to evaluate the expression of AMACR in a large cohort of patients with gastric adenocarcinoma. The study evaluated 249 primary gastric adenocarcinomas by immunohistochemistry. Nonneoplastic gastric tissue samples from various sites (antrum, body, fundus, and pylorus) were also examined. The immunopositivity of each sample was graded on a scale from 0 to 3 (0, no expression; 1, weak expression, 2, intermediate expression; 3, strong expression). We observed AMACR expression in 141 tumor cases: 44, 47, and 50 cases had weak, intermediate, and strong expression, respectively. Both intestinal and signet ring cell adenocarcinoma cases had overexpression of AMACR, however intestinal adenocarcinoma had significantly higher expression than did signet ring cell adenocarcinoma (p<0.05). Nonneoplastic gastric mucosa did not show AMACR expression. The results of our study demonstrate that AMACR expression is upregulated in gastric cancer, and suggest that further prospective studies to explore the potential role of AMACR as a therapeutic target for gastric cancer are warranted. (IJCEP803008).
Address all correspondence to: Dongfeng Tan, MD, Department of Pathology and Laboratory Medicine, Unit 85, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX 77030, USA. Tel: (713) 745-4977, Fax: (713) 745-1105, Email: firstname.lastname@example.org