In situ hybridization for the detection of telomerase RNA in the progression from Barrett's esophagus to esophageal adenocarcinoma

Carmela P. Morales, Edward L. Lee, Jerry W. Shay

Research output: Contribution to journalArticle

105 Citations (Scopus)

Abstract

BACKGROUND. The rate of incidence of esophageal adenocarcinoma has surpassed that of all other malignancies in the U.S. Esophageal adenocarcinoma arises from Barrett's esophagus through the multistep accumulation of genetic mutations in metaplastic cells, accompanied by histologic changes from metaplasia to low grade and high grade dysplasia and finally to carcinoma. Although telomerase activity has been demonstrated in 85-90% of human cancers, to the authors' knowledge there are no reports regarding esophageal adenocarcinoma. The objective of this study was to determine whether telomerase RNA is increased in esophageal adenocarcinoma and at what point in the histologic progression such an increase occurs. METHODS. Formalin-fixed, paraffin-embedded esophageal biopsies from patients with Barrett's esophagus and surgical resection specimens of esophageal adenocarcinoma containing varying stages of neoplastic progression were obtained. Adjacent sections from each specimen were evaluated by routine histology and in situ hybridization for the RNA component of human telomerase. RESULTS. The authors found that 100% of esophageal adenocarcinomas and high grade dysplasias were strongly positive for telomerase RNA. Basal crypt cells of Barrett's metaplasia demonstrated weak to moderate telomerase RNA in 70% of cases, whereas 90% of low grade dysplasias had moderate levels of telomerase RNA. CONCLUSIONS. The results of this study showed that 1) Barrett's epithelium may contain a population of immortalized cells, 2) a marked increase in the level of telomerase RNA accompanies the transition from low grade to high grade dysplasia, and 3) high levels of telomerase RNA accompany the development of esophageal adenocarcinoma in the vast majority of cases.

Original languageEnglish (US)
Pages (from-to)652-659
Number of pages8
JournalCancer
Volume83
Issue number4
DOIs
StatePublished - Aug 15 1998

Fingerprint

Barrett Esophagus
In Situ Hybridization
Adenocarcinoma
Telomerase
Metaplasia
telomerase RNA
Paraffin
Formaldehyde
Neoplasms
Histology
Carcinoma
Biopsy
Incidence
Population

Keywords

  • Barrett's esophagus
  • Esophageal adenocarcinoma
  • In situ hybridization
  • Telomerase RNA

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

Cite this

In situ hybridization for the detection of telomerase RNA in the progression from Barrett's esophagus to esophageal adenocarcinoma. / Morales, Carmela P.; Lee, Edward L.; Shay, Jerry W.

In: Cancer, Vol. 83, No. 4, 15.08.1998, p. 652-659.

Research output: Contribution to journalArticle

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abstract = "BACKGROUND. The rate of incidence of esophageal adenocarcinoma has surpassed that of all other malignancies in the U.S. Esophageal adenocarcinoma arises from Barrett's esophagus through the multistep accumulation of genetic mutations in metaplastic cells, accompanied by histologic changes from metaplasia to low grade and high grade dysplasia and finally to carcinoma. Although telomerase activity has been demonstrated in 85-90{\%} of human cancers, to the authors' knowledge there are no reports regarding esophageal adenocarcinoma. The objective of this study was to determine whether telomerase RNA is increased in esophageal adenocarcinoma and at what point in the histologic progression such an increase occurs. METHODS. Formalin-fixed, paraffin-embedded esophageal biopsies from patients with Barrett's esophagus and surgical resection specimens of esophageal adenocarcinoma containing varying stages of neoplastic progression were obtained. Adjacent sections from each specimen were evaluated by routine histology and in situ hybridization for the RNA component of human telomerase. RESULTS. The authors found that 100{\%} of esophageal adenocarcinomas and high grade dysplasias were strongly positive for telomerase RNA. Basal crypt cells of Barrett's metaplasia demonstrated weak to moderate telomerase RNA in 70{\%} of cases, whereas 90{\%} of low grade dysplasias had moderate levels of telomerase RNA. CONCLUSIONS. The results of this study showed that 1) Barrett's epithelium may contain a population of immortalized cells, 2) a marked increase in the level of telomerase RNA accompanies the transition from low grade to high grade dysplasia, and 3) high levels of telomerase RNA accompany the development of esophageal adenocarcinoma in the vast majority of cases.",
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N2 - BACKGROUND. The rate of incidence of esophageal adenocarcinoma has surpassed that of all other malignancies in the U.S. Esophageal adenocarcinoma arises from Barrett's esophagus through the multistep accumulation of genetic mutations in metaplastic cells, accompanied by histologic changes from metaplasia to low grade and high grade dysplasia and finally to carcinoma. Although telomerase activity has been demonstrated in 85-90% of human cancers, to the authors' knowledge there are no reports regarding esophageal adenocarcinoma. The objective of this study was to determine whether telomerase RNA is increased in esophageal adenocarcinoma and at what point in the histologic progression such an increase occurs. METHODS. Formalin-fixed, paraffin-embedded esophageal biopsies from patients with Barrett's esophagus and surgical resection specimens of esophageal adenocarcinoma containing varying stages of neoplastic progression were obtained. Adjacent sections from each specimen were evaluated by routine histology and in situ hybridization for the RNA component of human telomerase. RESULTS. The authors found that 100% of esophageal adenocarcinomas and high grade dysplasias were strongly positive for telomerase RNA. Basal crypt cells of Barrett's metaplasia demonstrated weak to moderate telomerase RNA in 70% of cases, whereas 90% of low grade dysplasias had moderate levels of telomerase RNA. CONCLUSIONS. The results of this study showed that 1) Barrett's epithelium may contain a population of immortalized cells, 2) a marked increase in the level of telomerase RNA accompanies the transition from low grade to high grade dysplasia, and 3) high levels of telomerase RNA accompany the development of esophageal adenocarcinoma in the vast majority of cases.

AB - BACKGROUND. The rate of incidence of esophageal adenocarcinoma has surpassed that of all other malignancies in the U.S. Esophageal adenocarcinoma arises from Barrett's esophagus through the multistep accumulation of genetic mutations in metaplastic cells, accompanied by histologic changes from metaplasia to low grade and high grade dysplasia and finally to carcinoma. Although telomerase activity has been demonstrated in 85-90% of human cancers, to the authors' knowledge there are no reports regarding esophageal adenocarcinoma. The objective of this study was to determine whether telomerase RNA is increased in esophageal adenocarcinoma and at what point in the histologic progression such an increase occurs. METHODS. Formalin-fixed, paraffin-embedded esophageal biopsies from patients with Barrett's esophagus and surgical resection specimens of esophageal adenocarcinoma containing varying stages of neoplastic progression were obtained. Adjacent sections from each specimen were evaluated by routine histology and in situ hybridization for the RNA component of human telomerase. RESULTS. The authors found that 100% of esophageal adenocarcinomas and high grade dysplasias were strongly positive for telomerase RNA. Basal crypt cells of Barrett's metaplasia demonstrated weak to moderate telomerase RNA in 70% of cases, whereas 90% of low grade dysplasias had moderate levels of telomerase RNA. CONCLUSIONS. The results of this study showed that 1) Barrett's epithelium may contain a population of immortalized cells, 2) a marked increase in the level of telomerase RNA accompanies the transition from low grade to high grade dysplasia, and 3) high levels of telomerase RNA accompany the development of esophageal adenocarcinoma in the vast majority of cases.

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