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Telomerase activity in esophageal carcinoma
Author(s) -
Takubo Kaiyo,
Nakamura KenIchi,
Izumiyama Naotaka,
Mafune KenIchi,
Tanaka Yoichi,
Miyashita Masao,
Sasajima Koji,
Kato Motonobu,
Oshimura Mitsuo
Publication year - 1997
Publication title -
journal of surgical oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.201
H-Index - 111
eISSN - 1096-9098
pISSN - 0022-4790
DOI - 10.1002/(sici)1096-9098(199710)66:2<88::aid-jso3>3.0.co;2-h
Subject(s) - telomerase , telomere , ribonucleoprotein , carcinoma , medicine , pathology , cancer research , microbiology and biotechnology , biology , dna , rna , genetics , gene
Background and Objectives Telomerase is a ribonucleoprotein that synthesizes telomeric DNA. Immortalized and carcinoma cells show no loss of telomere length during cell division. Telomerase activity has been demonstrated in carcinomas of various organs, but not in nonneoplastic tissues. In patients with esophageal carcinoma, no data have been reported concerning the relationship between telomerase activity and clinicopathological findings. Materials and Methods Esophageal carcinomas from 31 patients and normal esophageal mucosae from 92 patients were examined. Telomeric Repeat Amplification Protocol assay to detect telomerase activity and Southern blot analysis to examine telomere length were performed. Results Of the 31 carcinomas, 27 (87%) had detectable telomerase activity. Twenty‐one (23%) of the 92 normal esophageal mucosae from autopsied patients also had detectable telomerase activity. There was no difference between stage and outcome and absence or presence of telomerase activity. No difference in terminal restriction fragment (TRF) length was observed between carcinomas with and without telomerase activity. Conclusion Telomerase activity was demonstrated in a considerable number of normal esophageal mucosae. This suggests the possibility of a high frequency of false positivity if the presence of telomerase activity alone is used as a tumor‐specific marker. J. Surg. Oncol. 1997;66:88–92. © 1997 Wiley‐Liss, Inc.