Journal Article

Selenium status alters tumour differentiation but not incidence or latency of pancreatic adenocarcinomas in <i>Ela</i>-TGF-α p53<sup>+/−</sup> mice

Michaela Aichler, Hana Algül, Dietrich Behne, Gabriele Hölzlwimmer, Bernhard Michalke, Leticia Quintanilla-Martinez, Jörg Schmidt, Roland M. Schmid and Markus Brielmeier

in Carcinogenesis

Volume 28, issue 9, pages 2002-2007
Published in print September 2007 | ISSN: 0143-3334
Published online July 2007 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/bgm165
Selenium status alters tumour differentiation but not incidence or latency of pancreatic adenocarcinomas in Ela-TGF-α p53+/− mice

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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.

Journal Article.  3863 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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