Gastric Cancer
Copyright ©The Author(s) 2002. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Aug 15, 2002; 8(4): 586-590
Published online Aug 15, 2002. doi: 10.3748/wjg.v8.i4.586
The expression of hTERT mRNA and cellular immunity in gastric cancer and precancerosis
Xi-Xian Yao, Lei Yin, Zhong-Cheng Sun
Xi-Xian Yao, Lei Yin, Department of Digestive Medicine, the 2nd Hospital of Hebei Medical University, Shijiazhuang 050000, Hebei Province, China
Zhong-Cheng Sun, The Traditional Chinese Medical College of Hebei Medical University, Shijiazhuang 050081, Hebei Province, China
Author contributions: All authors contributed equally to the work.
Supported by Science and Technology Fund, Governmental Department of Health, Hebei Province, No.2K007
Correspondence to: Professor Xi-Xian Yao, Department of Digestive Medicine, the 2nd Hospital of Hebei Medical University, Shijiazhuang 050000, Hebei Province, China. yaoxixian@263.net
Telephone: +86-311-7046901 Ext.8631, 8632
Received: June 3, 2001
Revised: December 4, 2001
Accepted: December 8, 2001
Published online: August 15, 2002
Abstract

AIM: To observe the expression of Human telomerase reverse transcriptase (hTERT) in gastric carcinomas and precancerosis lesions, to evaluate the immune state of such patients, and to then study the clinical significance of hTERT and immune state for the diagnosis, treatment and prognosis of gastric cancer.

METHODS: In situ hybridization was used to detect the expression of hTERT mRNA in 116 endoscopic of gastric mucosa. Analyzed tissue samples were as follows: 30 cases of chronic superficial gastritis (CSG), 44 of precancerosis lesions (including 27 of chronic atrophic gastritis, 8 of adenomatous polyp and 9 of gastric ulcer) and 42 of gastric cancer (GC). In addition, the T lymphocyte subsets (CD3+, CD4+, CD8+, CD4+/CD8+) and natural killer cells (NK) in peripheral blood were determined by flow cytometric analysis (FCM) in 30 cases of CSG, 27 of precancerosis (chronic atrophic gastritis, CAG), and 42 of GC. The data were compared with those of normal control (NC).

RESULTS: The detected positive rate of hTERT varied as follows: 86% (36/42) in GC, 36% (16/44) in precancerosis lesions and 0% (0/30) in CSG. The expression of hTERT mRNA was not associated with patient gender, tumor location, macroscopic type, lymph node metastasis, or degree of differentiation. It was found that the CD3+, CD4+ of the CSG group were lower than that of NC (P < 0.05). Meanwhile, the T lymphocyte subsets (CD3+, CD4+, CD4+/CD8+ ratio) and NK cells of CAG were remarkably lower than that of NC and CSG groups (P < 0.05-0.01). Values of T cells and NK cells of the GC group were significantly abnormal when compared with the CAG group (P < 0.05-0.01). Furthermore, with tumor progression, the function of T cells was weakened gradually.

CONCLUSION: The expression of telomerase may be a crucial step in gastric carcinogenesis and increased hTERT mRNA may serve as a novel marker for diagnosis of GC. The immune state of patients with GC and precancerosis was somewhat depressed, which indicates the importance of cellular immunological assays in cancer patients.

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