Microarray-based identification of differentially expressed growth- and metastasis-associated genes in pancreatic cancer

Pancreatic ductal adenocarcinoma (PDAC) has an extremely poor prognosis. To improve diagnosis and treatment, key mechanisms of deregulated molecular functions have to be identified. Using microarray analysis, the expression patterns of 5600 human genes were assessed in PDAC by comparison with the no...

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Bibliographic Details
Published in:Cellular and molecular life sciences : CMLS 2003-06, Vol.60 (6), p.1180-1199
Main Authors: Friess, H, Ding, J, Kleeff, J, Fenkell, L, Rosinski, J A, Guweidhi, A, Reidhaar-Olson, J F, Korc, M, Hammer, J, Büchler, M W
Format: Article
Language:English
Subjects:
Adenocarcinoma - genetics
Adenocarcinoma - pathology
Adenocarcinoma - secondary
Adult
Aged
Aged, 80 and over
Deoxyribonucleic acid
DNA
Female
Gene expression
Gene Expression Profiling
Humans
Male
Metastasis
Middle Aged
Molecular biology
Oligonucleotide Array Sequence Analysis
Pancreatic cancer
Pancreatic Neoplasms - genetics
Pancreatic Neoplasms - pathology
Pancreatitis - genetics
RNA, Messenger - genetics
RNA, Messenger - metabolism
Transforming Growth Factor beta - genetics
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Summary:Pancreatic ductal adenocarcinoma (PDAC) has an extremely poor prognosis. To improve diagnosis and treatment, key mechanisms of deregulated molecular functions have to be identified. Using microarray analysis, the expression patterns of 5600 human genes were assessed in PDAC by comparison with the normal pancreas and chronic pancreatitis (CP). The expression of 467 of 5600 genes was increased in PDAC in comparison to the normal pancreas, and the expression of 120 of these genes was not increased in CP. In addition, 341 of 5600 genes were expressed at decreased levels in PDAC tissues, of which 96 were decreased in comparison to both normal and CP tissues. Thus, a total of 808 of 5600 human genes were differentially expressed in pancreatic cancer. The identification of a large panel of altered genes in PDAC will stimulate additional studies that will lead to improved understanding of the molecular mechanisms underlying pancreatic malignant growth.
ISSN:1420-682X
1420-9071
DOI:10.1007/s00018-003-3036-5