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Titlebook: Mechanisms in Carcinogenesis and Cancer Prevention; Harri U. Vainio,Eino K. Hietanen Book 2003 Springer-Verlag Berlin Heidelberg 2003 angi

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發(fā)表于 2025-3-21 20:05:39 | 只看該作者 |倒序瀏覽 |閱讀模式
書目名稱Mechanisms in Carcinogenesis and Cancer Prevention
編輯Harri U. Vainio,Eino K. Hietanen
視頻videohttp://file.papertrans.cn/629/628690/628690.mp4
概述Includes supplementary material:
叢書名稱Handbook of Experimental Pharmacology
圖書封面Titlebook: Mechanisms in Carcinogenesis and Cancer Prevention;  Harri U. Vainio,Eino K. Hietanen Book 2003 Springer-Verlag Berlin Heidelberg 2003 angi
描述A large proportion of cancers is preventable. External factors, discovered by epidemiological studies during the last 50 years, account for a majority of all cancer deaths. However,?still rather little is?known, about how environmental and genetic factors interact, how they may regulate gene activation etc. And?it is a long way from the discovery of a basic regulatory mechanism to practical patient treatment. This volume describes the?present state of the art in carcinogenesis, possibilities for cancer prevention, and gives genetic background in cancer development. Attention is given to the host-environment interaction, considering how this interaction may lead to cancer formation and how it can be utilised in cancer prevention. The molecular basis for cancer development and the molecular basis for prevention are described.
出版日期Book 2003
關鍵詞angiogenesis; apoptosis; cancer genomics; cancer prevention; carcinogenesis; lead; xenobiotics
版次1
doihttps://doi.org/10.1007/978-3-662-08602-5
isbn_softcover978-3-642-07859-0
isbn_ebook978-3-662-08602-5Series ISSN 0171-2004 Series E-ISSN 1865-0325
issn_series 0171-2004
copyrightSpringer-Verlag Berlin Heidelberg 2003
The information of publication is updating

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Genetic and Environmental Factors in Carcinogenesis,even when cultured or when injected in immunologically tolerant experimental animals (. and . 2000; . and . 1998). Yet, the views about the environmental (somatic) and inherited origin of the genetic alterations in human cancer have been debated and any reasonable agreement can be reached only when
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Signalling Pathways as Targets in Cancer Prevention,cell growth, or undergo apoptosis. Transformed cells either fail to respond or receive inappropriate signals which favor proliferation and avoidance of apoptosis. Thus, it is no coincidence that many oncogenes and tumor suppressor genes are components of signalling pathways. Despite the great variet
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Deficient DNA Mismatch Repair in Carcinogenesis,isincorporation during DNA synthesis. The genes coding for MMR proteins are highly conserved throughout evolution. The human proteins that correspond to the bacterial MutS proteins and participate in MMR include MSH2, MSH3, and MSH6, whereas the human MutL proteins include MLH1, PMS1, PMS2, and MLH3
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Epigenetic Changes, Altered DNA Methylation and Cancer,specialized chromatin structures are capable of stably modulating gene expression over many cell generations. Thus, an epigenetic mutation can have the same effect like a classical, genetic mutation, i.e., loss- or gain-of-function of any given gene. Sensitive methods for the detection of epigenetic
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