PMID- 15068673
OWN - NLM
STAT- MEDLINE
DCOM- 20041029
LR  - 20181130
IS  - 1522-8002 (Print)
IS  - 1476-5586 (Electronic)
IS  - 1476-5586 (Linking)
VI  - 6
IP  - 1
DP  - 2004 Jan-Feb
TI  - Zoning of mucosal phenotype, dysplasia, and telomerase activity measured by 
      telomerase repeat assay protocol in Barrett's esophagus.
PG  - 85-92
AB  - Glandular dysplasia in Barrett's esophagus may regress spontaneously but can also 
      progress to cancer. The human telomerase RNA template and the human telomerase 
      reverse transcriptase enzyme which do not, of themselves, correlate strongly with 
      telomerase activity, are too often overexpressed in Barrett's dysplasia to 
      predict individual cancer risk. This study relates telomerase activity, mucosal 
      phenotype, and dysplasia in Barrett's esophagus. Biopsies (n = 256) from squamous 
      esophagus, columnar-lined esophagus every 2 cm, esophago-gastric junction, 
      gastric body, and antrum from 32 patients with long-segment Barrett's esophagus 
      were evaluated by telomerase repeat assay protocol (TRAP). Three biopsies for 
      histology (n = 794) were simultaneously taken at each anatomical level. These and 
      all prior and subsequent biopsies (n = 1917) were reviewed for mucosal phenotypes 
      and dysplasia severity. Intestinal-type Barrett's mucosa was present at all 
      levels in Barrett's esophagus. At least one Barrett's biopsy was TRAP(+) in 22 of 
      32 patients. TRAP positivity of intestinal-type Barrett's mucosa increased 
      distally, possibly as a consequence of mucosal exposure to acid or bile reflux. 
      Native gastric mucosa was rarely TRAP(+) (1/31 corpus, 2/32 antrum), whereas 
      native squamous mucosa usually was TRAP(+) (31/32). Dysplasia almost always 
      involved intestinal-type Barrett's mucosa (85/87; P <.00001), without evidence of 
      proximal-distal zoning. TRAP could be positive without dysplasia and negative in 
      extensive, even high-grade, dysplasia. TRAP activity merits evaluation as a 
      candidate biomarker for increased risk of persistent dysplasia and cancer 
      progression in Barrett's esophagus.
FAU - Going, James J
AU  - Going JJ
AD  - Department of Pathology, University of Glasgow, Glasgow, Scotland, UK. 
      going@udcf.gla.ac.uk
FAU - Fletcher-Monaghan, Aileen J
AU  - Fletcher-Monaghan AJ
FAU - Neilson, Lisa
AU  - Neilson L
FAU - Wisman, Bea A
AU  - Wisman BA
FAU - van der Zee, Ate
AU  - van der Zee A
FAU - Stuart, Robert C
AU  - Stuart RC
FAU - Keith, W Nicol
AU  - Keith WN
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Neoplasia
JT  - Neoplasia (New York, N.Y.)
JID - 100886622
RN  - 0 (Biomarkers, Tumor)
RN  - EC 2.7.7.49 (Telomerase)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Barrett Esophagus/*metabolism/*pathology
MH  - Biomarkers, Tumor/*analysis
MH  - Biopsy
MH  - Cell Transformation, Neoplastic/metabolism
MH  - Esophagogastric Junction/metabolism/pathology
MH  - Female
MH  - Gastric Mucosa/metabolism
MH  - Humans
MH  - Intestinal Mucosa/*metabolism/*pathology
MH  - Male
MH  - Middle Aged
MH  - Phenotype
MH  - Precancerous Conditions/metabolism/pathology
MH  - Stomach/pathology
MH  - Telomerase/*metabolism
PMC - PMC1508632
EDAT- 2004/04/08 05:00
MHDA- 2004/10/30 09:00
PMCR- 2004/01/01
CRDT- 2004/04/08 05:00
PHST- 2004/04/08 05:00 [pubmed]
PHST- 2004/10/30 09:00 [medline]
PHST- 2004/04/08 05:00 [entrez]
PHST- 2004/01/01 00:00 [pmc-release]
AID - 03361 [pii]
PST - ppublish
SO  - Neoplasia. 2004 Jan-Feb;6(1):85-92.