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Titlebook: Chemical Carcinogenesis 2; Modulating Factors Amedeo Columbano,Francesco Feo,Paolo Pani Book 1991 Springer Science+Business Media New York

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书目名称Chemical Carcinogenesis 2
副标题Modulating Factors
编辑Amedeo Columbano,Francesco Feo,Paolo Pani
视频video
图书封面Titlebook: Chemical Carcinogenesis 2; Modulating Factors Amedeo Columbano,Francesco Feo,Paolo Pani Book 1991 Springer Science+Business Media New York
描述"chemical carcinogenesis" is the general title of the series of international meetings which are held, biannually, in sardinia (Italy) since 1981. Despite the generality of the title, the main effort of the scientific Committee has been to pursue a coherent line around one of the most distinguishing features of carcinogenesis: the "multifasic" development of the process. Given that many chemical compounds are known to cause "experimental cancer", many questions still remain unresolved or are given too simplistic answers. The very first question concerning the interaction between the chemical carcinogen and the molecular target in the cell is a debatable one despite the overwhelming literature in this field. It is certain that chemical carcinogens are toxic to cells and cause DNA damage: however it is still an open question as to how to relate these changes to the different stages of carcinogenesis including initiation. We have not to forget that 1/3 to 2/3 of the average life time of a given species elapses between the experimental administration of the carcinogen and the appearance of "cancer". The experimental manipulation of carcinogenesis through the use of "adequate biological
出版日期Book 1991
关键词DNA; apoptosis; breast cancer; cancer; carcinogenesis; cell; cell death; hormones; liver; prevention; tumor
版次1
doihttps://doi.org/10.1007/978-1-4615-3694-9
isbn_softcover978-1-4613-6642-3
isbn_ebook978-1-4615-3694-9
copyrightSpringer Science+Business Media New York 1991
The information of publication is updating

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Control of Hepatocyte Growth by Positive and Negative Growth Regulators and Mitogenic Triggers: Implof carcinogenic regimens. They constituite the most frequently occurring tumors in whole animal carcinogenesis bioassay. Liver tissue and its biochemistry have been extensively analyzed and a large data bank exists as a background for further studies. Several initiation — promotion protocols for liv
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Cell Cycle Dependent Regulation of Poly(ADP-Ribose) Polymerase Gene Expressionman T lymphocytes proliferation, 2) rat liver regeneration following partial hepatectomy, and 3) hyperplasia induced by the mitogen lead nitrate. In each case, a consistent increase in the level of poly(ADP-ribose) polymerase mRNA occurs before the start of DNA synthesis. A maximal level of the tran
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Gene Activation and Deactivation during Multistage Hepatocarcinogenesis in the Ratreful studies of carcinogenesis in defined systems take place. In at least five different species of animals, multistage carcinogenic processes have been demonstrated in more than 15 different tissues.. In addition, there is significant epidemiologic evidence that more than a half dozen human cancer
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Biochemical and Molecular Perturbations Induced in Preneoplastic Tissue by a S-Adenosyl-L-Methioninetrope-deficient diet causes cancer or enhances liver carcinogenesis induced by various carcinogens.. Liver S-adenosyl-L-methionine (SAM) deficiency has also been demonstrated in rats fed a diet containing adequate amounts of lipotropes and subjected to a promoting treatment with phenobarbital (PB)..
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Alterations of Cell Surface Receptors and Expression of Cellular Oncogenes in the Liver of Rats Fed agents widely used in the industry as plasticizers such as phthalate esters.. When administered to experimental animals, HPPs induce marked hepatocellular hypertrophy and hyperplasia, hepatic peroxisome proliferation and an increase in the activity of several peroxisome associated enzymes..
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Transformation of Human Epithelial Cells by Recombinant Human Papillomavirus DNA Associated with Ceres are divided into five groups: papillomaviruses, herpes viruses, hepatitis B family, polyoma viruses, and adenoviruses (Table 1). The first three are associated with human neoplasia on the basis of epidemiological and molecular data. The other two, polyoma virus and adenovirus, induce . transforma
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