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Aichler, M. ; Algül, H.* ; Behne, D.* ; Hölzlwimmer, G. ; Michalke, B. ; Quintanilla-Martinez, L. ; Schmidt, J. ; Schmid, R.M. ; Brielmeier, M.

Selenium status alters tumour differentiation but not incidence or latency of pancreatic adenocarcinomas in Ela-TGF-alpha p53+/ mice.

Carcinogenesis 28, 2002-2007 (2007)
DOI PMC
Open Access Green as soon as Postprint is submitted to ZB.
Genetic predisposition and environmental factors act in concert in the pathogenesis of multi-factorial diseases. Selenoproteins represent fundamental antioxidative systems for the maintenance of cellular redox homeostasis, which is altered in various disease processes. Optimal function of selenoproteins requires availability of sufficient amounts of the essential trace element selenium, but in many countries the nutritive selenium supply is regarded insufficient. Supplemental selenium has been shown to have cancer-protective effects in a variety of experimental settings and clinical studies. Pancreatic carcinoma has so far not been tested as an end-point in such studies. We thus investigated the influence of supplemental nutritive selenium on pancreatic carcinogenesis in selenium-deficient animals by use of a genetically defined disease model. Over a period of 800 days, all animals (n = 131) in the study developed tumours. Within this time, the mean total tumour latency was not influenced by the selenium status (471 versus 472 days). Also, the mean latency of pancreatic carcinomas (n = 83) was not influenced (464 versus 466 days). In contrast, the percentage of pancreatic tumors within all tumours was lower in the selenium-deficient group (55 versus 70%). A highly significant difference in the differentiation grade of the pancreatic tumours was evident between the two groups: selenium-deficient mice (n = 33) developed predominantly undifferentiated anaplastic carcinomas (26 anaplastic versus 7 differentiated), whereas in the selenium-supplemented group (n = 50) mainly well-differentiated carcinomas were detected (20 anaplastic versus 30 differentiated). These data point at a new role of the trace element selenium in carcinogenesis.
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Publication type Article: Journal article
Document type Scientific Article
Corresponding Author
ISSN (print) / ISBN 0143-3334
e-ISSN 1460-2180
Journal Carcinogenesis
Quellenangaben Volume: 28, Issue: 9, Pages: 2002-2007 Article Number: , Supplement: ,
Publisher Oxford University Press
Non-patent literature Publications
Reviewing status Peer reviewed
Institute(s) Institute of Ecological Chemistry (IOEC)
CF Comparative Medicine (CF-Comparative Medicine)
Institute of Pathology (PATH)