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Life‐long over‐expression of ornithine decarboxylase (ODC) gene in transgenic mice does not lead to generally enhanced tumorigenesis or neuronal degeneration
Author(s) -
Alhonen Leena,
Halmekytö Maria,
Kosma VeliMatti,
Wahlfors Jarmo,
Kauppinen Risto,
Jänne Juhani
Publication year - 1995
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910630317
Subject(s) - ornithine decarboxylase , syngenic , ornithine decarboxylase antizyme , transgene , genetically modified mouse , biology , carcinogenesis , carboxy lyases , gene expression , microbiology and biotechnology , enzyme , gene , biochemistry , in vitro
Abstract Ornithine decarboxylase, the rate‐controlling enzyme of the biosynthetic pathway of the polyamines, is one of the most inducible mammalian enzymes showing many of the features common to the oncoproteins. Ornithine decarboxylase activity is likewise strongly induced in response to various neurotoxic stimuli, and the enhanced enzyme activity is believed to be causally related to neuronal damage. We have generated several transgenic mouse lines over‐expressing human ornithine decarboxylase gene. We have now subjected the animals to a long‐term survival study in order to assess whether constitutively over‐expressed ornithine decarboxylase would predispose them to enhanced tumorigenesis and neuronal degeneration. When the transgenic animals were 2 years old, their tissue ornithine decarboxylase activity was 20‐ to 50‐fold that in their syngenic littermates. Macroscopic and microscopic examination of organs revealed no differences between syngenic and transgenic animals as regards spontaneous tumor incidence or age‐related changes in brain.