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Prognostic value of cell adhesion in esophageal adenocarcinomas.

Falkenback, Dan LU ; Nilbert, Mef LU ; Öberg, Stefan LU and Johansson, J LU (2008) In Diseases of the Esophagus 21(2). p.97-102
Abstract
Increased understanding of the molecular processes associated with the dysplasia-adenocarcinoma sequence linked to Barrett's esophagus may be beneficial for early tumor detection and refined diagnosis as well as for improved prognostication. We applied immunohistochemical staining for the markers Ki-67, p53, beta-catenin and E-cadherin in order to evaluate their prognostic importance in 59 Barrett's esophagus-associated adenocarcinomas. Reduced or absent membranous E-cadherin staining was identified in 75% of the tumors and predicted poor prognosis in manova (hazard ratio [HR] 3.3, P = 0.05). The small subset of tumors with low levels (< 10%) of Ki-67 staining showed a worse prognosis (HR 3.2, P < 0.01), whereas immunostaining for... (More)
Increased understanding of the molecular processes associated with the dysplasia-adenocarcinoma sequence linked to Barrett's esophagus may be beneficial for early tumor detection and refined diagnosis as well as for improved prognostication. We applied immunohistochemical staining for the markers Ki-67, p53, beta-catenin and E-cadherin in order to evaluate their prognostic importance in 59 Barrett's esophagus-associated adenocarcinomas. Reduced or absent membranous E-cadherin staining was identified in 75% of the tumors and predicted poor prognosis in manova (hazard ratio [HR] 3.3, P = 0.05). The small subset of tumors with low levels (< 10%) of Ki-67 staining showed a worse prognosis (HR 3.2, P < 0.01), whereas immunostaining for p53 and beta-catenin showed no correlation with prognosis. Deranged cell adhesion has been demonstrated to be an early event in tumor development. The down-regulation of E-cadherin and its prognostic importance indicate that cell adhesion may be a prime area for targeted therapies in esophageal adenocarcinoma. (Less)
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author
; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Diseases of the Esophagus
volume
21
issue
2
pages
97 - 102
publisher
Oxford University Press
external identifiers
  • pmid:18269642
  • wos:000252929600001
  • scopus:39049139719
  • pmid:18269642
ISSN
1120-8694
DOI
10.1111/j.1442-2050.2007.00749.x
language
English
LU publication?
yes
id
5215dbf6-a29b-4c68-99ea-df3c6d52f76c (old id 1042038)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/18269642?dopt=Abstract
date added to LUP
2016-04-04 08:32:52
date last changed
2022-01-29 03:32:13
@article{5215dbf6-a29b-4c68-99ea-df3c6d52f76c,
  abstract     = {{Increased understanding of the molecular processes associated with the dysplasia-adenocarcinoma sequence linked to Barrett's esophagus may be beneficial for early tumor detection and refined diagnosis as well as for improved prognostication. We applied immunohistochemical staining for the markers Ki-67, p53, beta-catenin and E-cadherin in order to evaluate their prognostic importance in 59 Barrett's esophagus-associated adenocarcinomas. Reduced or absent membranous E-cadherin staining was identified in 75% of the tumors and predicted poor prognosis in manova (hazard ratio [HR] 3.3, P = 0.05). The small subset of tumors with low levels (&lt; 10%) of Ki-67 staining showed a worse prognosis (HR 3.2, P &lt; 0.01), whereas immunostaining for p53 and beta-catenin showed no correlation with prognosis. Deranged cell adhesion has been demonstrated to be an early event in tumor development. The down-regulation of E-cadherin and its prognostic importance indicate that cell adhesion may be a prime area for targeted therapies in esophageal adenocarcinoma.}},
  author       = {{Falkenback, Dan and Nilbert, Mef and Öberg, Stefan and Johansson, J}},
  issn         = {{1120-8694}},
  language     = {{eng}},
  number       = {{2}},
  pages        = {{97--102}},
  publisher    = {{Oxford University Press}},
  series       = {{Diseases of the Esophagus}},
  title        = {{Prognostic value of cell adhesion in esophageal adenocarcinomas.}},
  url          = {{http://dx.doi.org/10.1111/j.1442-2050.2007.00749.x}},
  doi          = {{10.1111/j.1442-2050.2007.00749.x}},
  volume       = {{21}},
  year         = {{2008}},
}