| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Short Communication |
From the Department of Pathology,*
Josephine
Nefkens Institute, and the Department of
Surgery,
Erasmus University Rotterdam,
Rotterdam; the Rotterdam Esophageal Tumor Study Group, Rotterdam; and
the Laboratory of Cytochemistry and
Cytometry,
Department of Molecular Cell
Biology, Leiden University Medical Center, Leiden, The Netherlands
Analyses of cancer incidence data in the United States and Western
Europe revealed steadily rising rates over the past decades of
adenocarcinomas of the esophagus and gastric cardia. Genetic
information on gastric cardia adenocarcinoma and its preneoplasias is
sparse. We have used comparative genomic hybridization to obtain a
genome-wide overview of 20 archival gastric cardia adenocarcinomas and
10 adjacent preneoplastic lesions (4 metaplasias, 1 low-grade
dysplasia , 5 high-grade dysplasias). Multiple genetic
alterations were discriminated in all adenocarcinomas. Frequent loss
(
25% of all tumors) was detected, in decreasing order of
frequency, on 5q, 18q, 4q, 3p,
9p, 2q, 11q, 14q, 21q,
4p, 9q, 16q, 1p, and 8p. Frequent gain
(25% of all tumors) was disclosed, in decreasing order of
frequency, on 20q, 7p, 8q, 1q,
7q, 20p, 17q, 13q, Xp,
6q, 8p, 19q, 5p, 6p, and Xq.
Loss of the Y chromosome was found in 60% of male cases. High level
amplification was frequently (>10% of all tumors) detected on
7q21, 8p22, 12p11.2, 17q12-q21, and
19q13.1-q13.2. The precursor lesions showed multiple aberrations
in all high-grade dysplasias, whereas few genetic changes were
discerned in LGD and metaplasias. High level amplifications were also
found in high-grade dysplasias, ie, on 7q21,
8p22, and 17q12-q21. Moreover, the percentage of
aberrations was not significantly different for invasive carcinomas or
high-grade dysplasias. Approximately 70% of the precursor aberrations
were also present in the adjacent carcinoma. Minimal overlapping
regions in the preneoplasias included loss on 18q12-q21 and gains on
8q23 and 17q12-q21, suggesting involvement of genes residing in
these regions. In conclusion, we have (i) created a map of
genetic alterations in gastric cardia adenocarcinomas and (ii) provided
evidence for the presence of a metaplasia-dysplasia-carcinoma sequence
in this poorly understood type of cancer.
This article has been cited by other articles:
 |
|
 |
|
  J. Harper, L. Yan, R. M. Loureiro, I. Wu, J. Fang, P. A. D'Amore, and M. A. Moses Repression of Vascular Endothelial Growth Factor Expression by the Zinc Finger Transcription Factor ZNF24 Cancer Res., September 15, 2007; 67(18): 8736 - 8741. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. Granelli, M. Cattaneo, S. Ferrero, L. Bottiglieri, S. Bosari, G. Fichera, and I. Biunno SEL1L and Squamous Cell Carcinoma of the Esophagus Clin. Cancer Res., September 1, 2004; 10(17): 5857 - 5861. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M M Weiss, E J Kuipers, C Postma, A M Snijders, M Stolte, M Vieth, D Pinkel, S G M Meuwissen, D Albertson, and G A Meijer Genome wide array comparative genomic hybridisation analysis of premalignant lesions of the stomach Mol. Pathol., October 1, 2003; 56(5): 293 - 298. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. C-M. Tang, J. S. T. Sham, D. Xie, Y. Fang, K.-K. Huo, Q.-L. Wu, and X.-Y. Guan Identification of a Candidate Oncogene SEI-1 within a Minimal Amplified Region at 19q13.1 in Ovarian Cancer Cell Lines Cancer Res., December 15, 2002; 62(24): 7157 - 7161. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
