Expression of Telomerase Catalytic Component, Telomerase Reverse Transcriptase, in Human Gastric Carcinomas
Telomerase activity is believed to be crucial for cellular immortality, which is considered to participate in the development of a majority of human cancers. Human telomerase reverse transcriptase (TERT) has recently been identified as a catalytic subunit of telomerase. We examined the expression of...
Saved in:
Published in | Cancer science Vol. 89; no. 11; pp. 1099 - 1103 |
---|---|
Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Oxford, UK
Blackwell Publishing Ltd
01.11.1998
Japanese Cancer Association John Wiley & Sons, Inc |
Subjects | |
Online Access | Get full text |
Cover
Loading…
Summary: | Telomerase activity is believed to be crucial for cellular immortality, which is considered to participate in the development of a majority of human cancers. Human telomerase reverse transcriptase (TERT) has recently been identified as a catalytic subunit of telomerase. We examined the expression of TERT and other telomerase components such as human telomerase RNA component (hTR, encoded by TERC) and human telomerase‐associated protein (TEP1) by reverse transcription‐polymerase chain reaction in human gastric carcinomas and non‐neoplastic mucosa, in addition to measuring the telomerase activity. Of 20 gastric carcinomas examined, 18 (90%) and 18 (90%) showed increased expression of TERT and higher telomerase activity in comparison with corresponding non‐neoplastic mucosa, respectively. Increased expression of hTR/TERC was also observed in 15 (75%) of the gastric carcinomas. Immunohistochemically, strong expression of TERT protein was detected in the nuclei of the tumor cells of all carcinoma tissues, while the expression of TERT in non‐neoplastic mucosal cells as well as stromal elements (except lymphocytes) was weak or negative. These findings suggest that increased TERT expression associated with telomerase activity may serve as a novel marker for the diagnosis of stomach cancer. |
---|---|
Bibliography: | These authors contributed equally to this work. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0910-5050 1347-9032 1349-7006 1876-4673 |
DOI: | 10.1111/j.1349-7006.1998.tb00502.x |