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Clinical significance of detecting elevated serum DcR3/TR6/M68 in malignant tumor patients
Author(s) -
Wu Yulian,
Han Bing,
Sheng Hongwei,
Lin Min,
Moore Paul A.,
Zhang Jun,
Wu Jiangping
Publication year - 2003
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.11138
Subject(s) - medicine , cirrhosis , malignancy , hepatocellular carcinoma , pathology
TR6/DcR3/M68 is a soluble receptor that belongs to the TNF receptor family. It is expressed in malignant cells of several tumor types and has been postulated to help tumor cells to gain survival advantage by inhibiting apoptosis and by interfering with immune surveillance. In our study, we assessed for the first time serum TR6 in tumor patients to explore its diagnostic and prognostic value. We examined serum TR6 levels with ELISA in 146 tumor patients, 19 patients with acute infection, 5 patients with liver cirrhosis and 29 healthy individuals. TR6 expression in tumor mass was studied with immunohistochemistry. TR6 gene copy number in tumor tissues was evaluated by real time PCR. Ninety‐seven point nine percent (47 of 48 cases) of healthy individuals and patients with acute infection were serum TR6‐negative. In contrast, 56.2% (82 of 146 cases) of the tumor patients were serum TR6‐positive. Almost all serum TR6‐positive individuals (98.8%, 82 out of 83 cases) had malignancy, excluding the cases of liver cirrhosis. In gastric carcinomas, serum TR6 levels were closely correlated with tumor differentiation status and TNM classification. Tumor mass was the source of serum TR6 because its levels decreased drastically after curative tumor resection. TR6 gene amplification occurred in about half of liver carcinomas, but not in gastric or pancreatic carcinomas, indicating plural mechanisms of TR6 upregulation. Our study demonstrated that serum TR6 should be considered as a novel parameter for the diagnosis, treatment and prognosis of malignancies. © 2003 Wiley‐Liss, Inc.