Clinical Research
Copyright ©The Author(s) 2004. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jun 1, 2004; 10(11): 1643-1646
Published online Jun 1, 2004. doi: 10.3748/wjg.v10.i11.1643
Tumor type M2 pyruvate kinase expression in gastric cancer, colorectal cancer and controls
Bo Zhang, Jian-Ying Chen, Dao-Da Chen, Guo-Bin Wang, Ping Shen
Bo Zhang, Jian-Ying Chen, Dao-Da Chen, Guo-Bin Wang, Department of General Surgery, Affiliated Xiehe Hospital of Huazhong University of Science and Technology, Wuhan 430022, Hubei Province, China Ping Shen, Department of Biology, Wuhan University, Wuhan 430074, Hubei Province, China
Author contributions: All authors contributed equally to the work.
Correspondence to: Bo Zhang, Department of General Surgery, Affiliated Xiehe Hospital of Huazhong University of Science and Technology, Wuhan 430022, Hubei Province, China. wavestor@whu.edu.cn
Telephone: +86-27-87648533
Received: September 18, 2003
Revised: October 4, 2003
Accepted: October 7, 2003
Published online: June 1, 2004
Abstract

AIM: Tumor formation is generally linked to an expansion of glycolytic phosphometabolite pools and aerobic glycolytic flux rates. To achieve this, tumor cells generally overexpress a special glycolytic isoenzyme, termed pyruvate kinase type M2. The present study was designed to evaluate the use of a new tumor marker, tumor M2-PK, in discriminating gastrointestinal cancer patients from healthy controls, and to compare with the reference tumor markers CEA and CA72-4.

METHODS: The concentration of tumor M2-PK in body fluids could be quantitatively determined by a commercially available enzyme-linked immunosorbent assay (ELISA) -kit (ScheBo® Tech, Giessen, Germany). By using this kit, the tumor M2-PK concentration was measured in EDTA-plasma of 108 patients. For the healthy blood donors a cut-off value of 15 U/mL was evaluated, which corresponded to 90% specificity. Overall 108 patients were included in this study, 54 patients had a histological confirmed gastric cancer, 54 patients colorectal cancer, and 20 healthy volunteers served as controls.

RESULTS: The cut-off value to discriminate patients from controls was established at 15 U/mL for tumor M2-PK. The mean tumor M2-PK concentration of gastric cancer was 26.937 U/mL. According to the TNM stage system, the mean tumor M2-PK concentration of stage I was 16.324 U/mL, of stage II 15.290 U/mL, of stage III 30.289 U/mL, of stage IV 127.31 U/mL, of non-metastasis 12.854 U/mL and of metastasis 35.711 U/mL. The mean Tumor M2-PK concentration of colorectal cancer was 30.588 U/mL. According to the Dukes stage system, the mean tumor M2-PK concentration of Dukes A was 16.638 U/mL, of Dukes B 22.070 U/mL, and of Dukes C 48.024 U/mL, of non-metastasis 19.501 U/mL, of metastasis 49.437 U/mL. The mean tumor M2-PK concentration allowed a significant discrimination of colorectal cancers (30.588 U/mL) from controls (10.965 U/mL) (P < 0.01), and gastric cancer (26.937 U/mL) from controls (10.965 U/mL) (P < 0.05). The overall sensitivity of tumor M2-PK for colorectal cancer was 68.52%, while that of CEA was 43.12%. In gastric cancer, tumor M2-PK showed a high sensitivity of 50.47%, while CA72-4 showed a sensitivity of 35.37%.

CONCLUSION: Tumor M2-PK has a higher sensitivity than markers CEA and CA72-4, and is a valuable tumor marker for the detection of gastrointestinal cancer.

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