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Titlebook: Nongenotoxic Carcinogenesis; Andrew Cockburn,Lewis Smith Conference proceedings 1994 Springer-Verlag Berlin Heidelberg 1994 DNA.Hormone.br

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發(fā)表于 2025-3-25 03:29:00 | 只看該作者
978-3-662-03024-0Springer-Verlag Berlin Heidelberg 1994
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發(fā)表于 2025-3-25 09:26:55 | 只看該作者
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發(fā)表于 2025-3-25 15:17:52 | 只看該作者
Nongenotoxic Mechanisms in Thyroid Carcinogenesis,Nongenotoxic mechanisms of thyroid carcinogenesis are of general application and also of potential importance to regulatory toxicology. To understand the way in which administration of xenobiotics can lead to thyroid tumours through a nongenotoxic mechanism it is necessary first to consider the pathophysiology of the thyroid gland.
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發(fā)表于 2025-3-25 19:49:05 | 只看該作者
Ernst Schering Foundation Symposium Proceedingshttp://image.papertrans.cn/n/image/667274.jpg
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https://doi.org/10.1007/978-3-662-03022-6DNA; Hormone; breast cancer; cancer; carcinogenesis; cell; hormones; kidney; liver; liver tumor; prevention; to
26#
發(fā)表于 2025-3-26 03:46:02 | 只看該作者
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發(fā)表于 2025-3-26 04:31:28 | 只看該作者
Conference proceedings 1994sis, underlining the complexity of the topic. The clarity of the view that all carcinogens act by mutating DNA, origin- ally advocated by Bruce Ames nearly 20 years ago, has been clouded by the increasing numbers of compounds which are not genotoxic but which nevertheless can cause cancer. There is
28#
發(fā)表于 2025-3-26 11:43:25 | 只看該作者
,α2μ-Globulin Mediated Male Rat Kidney Carcinogenesis,ans. Research from several laboratories has elucidated the mechanism responsible for this remarkable sex- and species-specific disease. This understanding of mechanisms led the EPA (1991) to conclude that renal tumors mediated through α. should not be used in human risk assessment.
29#
發(fā)表于 2025-3-26 15:18:52 | 只看該作者
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發(fā)表于 2025-3-26 20:20:48 | 只看該作者
The Interaction of Genes and Hormones in Murine Hepatocarcinogenesis,nt of more common malignancies because of the low effective penetrance of such genes and the large variation in environmental factors that influence cancer development in humans. Animal models provide a powerful approach to the identification and characterization of such risk-modifier genes.
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