help button home button Am J Pathol Epitomics, Inc.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Rumpel, C. A.
Right arrow Articles by Moskaluk, C. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Rumpel, C. A.
Right arrow Articles by Moskaluk, C. A.
(American Journal of Pathology. 1999;154:1329-1334.)
© 1999 American Society for Investigative Pathology


Short Communication

Mapping of Genetic Deletions on the Long Arm of Chromosome 4 in Human Esophageal Adenocarcinomas

Craig A. Rumpel*, Steven M. Powell{dagger} and Christopher A. Moskaluk*

From the Departments of Pathology,*
Biochemistry and Molecular Genetics,{ddagger}
and Medicine,{dagger}
University of Virginia Health Sciences Center, Charlottesville, Virginia

Loss of the long arm of chromosome 4 has been identified previously as a common occurrence in adenocarcinomas of the esophagus and gastroesophageal junction by relatively low resolution genetic surveys. To better define the extent of 4q deletion in these neoplasms we isolated DNA from 29 primary carcinomas using microdissection, and used DNA obtained from xenografts of 14 carcinomas grown in immunodeficient mice in an assay of loss of heterozygosity of 25 polymorphic microsatellite markers distributed along the chromosomal arm. Two carcinomas exhibited widespread microsatellite instability and were excluded from deletion mapping. In the remaining 41 carcinomas, loss of heterozygosity was detected in 33 (80%). Twenty-three cancers showed complete or extensive reduction to homozygosity along the length of the long arm. Ten cancers had smaller discrete areas of loss and were principally useful in discerning three non-overlapping areas of consensus genetic deletion. Area 1 centered on marker D4S1534 at 4q21.1–22, area 2 centered on marker D4S620 at 4q32–33, and area 3 centered on marker D4S426 at 4q35. No known tumor suppressor genes map to these loci, but the frequent deletion of these areas in gastroesophageal carcinomas and in other carcinomas suggests that undiscovered tumor suppressor genes may reside here.





This article has been cited by other articles:


Home page
Cancer Res.Home page
D. J. Nancarrow, H. Y. Handoko, B. M. Smithers, D. C. Gotley, P. A. Drew, D. I. Watson, A. D. Clouston, N. K. Hayward, D. C. Whiteman, and for the Australian Cancer Study and the Study of D
Genome-Wide Copy Number Analysis in Esophageal Adenocarcinoma Using High-Density Single-Nucleotide Polymorphism Arrays
Cancer Res., June 1, 2008; 68(11): 4163 - 4172.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Pathol.Home page
H. van Dekken, J. C. Alers, P. H. J. Riegman, C. Rosenberg, H. W. Tilanus, and K. Vissers
Molecular Cytogenetic Evaluation of Gastric Cardia Adenocarcinoma and Precursor Lesions
Am. J. Pathol., June 1, 2001; 158(6): 1961 - 1967.
[Abstract] [Full Text] [PDF]


Home page
Cancer Res.Home page
P. H. J. Riegman, K. J. Vissers, J. C. Alers, E. Geelen, W. C. J. Hop, H. W. Tilanus, and H. van Dekken
Genomic Alterations in Malignant Transformation of Barrett's Esophagus
Cancer Res., April 1, 2001; 61(7): 3164 - 3170.
[Abstract] [Full Text]


Home page
Am. J. Pathol.Home page
A. K. Walch, H. F. Zitzelsberger, J. Bruch, G. Keller, D. Angermeier, M. M. Aubele, J. Mueller, H. Stein, H. Braselmann, J. R. Siewert, et al.
Chromosomal Imbalances in Barrett’s Adenocarcinoma and the Metaplasia-Dysplasia-Carcinoma Sequence
Am. J. Pathol., February 1, 2000; 156(2): 555 - 566.
[Abstract] [Full Text] [PDF]


Home page
Proc. Natl. Acad. Sci. USAHome page
M. Chow and H. Rubin
Coculturing diverse clonal populations prevents the early-stage neoplastic progression that occurs in the separate clones
PNAS, January 4, 2000; 97(1): 174 - 178.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1999 by the American Society for Investigative Pathology.