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Titlebook: Genetic Instability and Tumorigenesis; Michael B. Kastan Book 1997 The Editor(s) (if applicable) and The Author(s), under exclusive licens

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發(fā)表于 2025-3-21 19:37:23 | 只看該作者 |倒序?yàn)g覽 |閱讀模式
書(shū)目名稱Genetic Instability and Tumorigenesis
編輯Michael B. Kastan
視頻videohttp://file.papertrans.cn/383/382542/382542.mp4
叢書(shū)名稱Current Topics in Microbiology and Immunology
圖書(shū)封面Titlebook: Genetic Instability and Tumorigenesis;  Michael B. Kastan Book 1997 The Editor(s) (if applicable) and The Author(s), under exclusive licens
描述M. B. KASTAN Cancer is a disease resulting from alterations of cellular genes which cause phe- notypic changes in somatic cells. Usually, when we think about genetic diseases, we think about inheriting one or two abnormal genes from our parents and these gene abnormalities confer the disease phenotype. In contrast, in the majority of cancers, no such inherited gene abnormalities can be identified (which does not mean that they do not exist) and there is no obvious family history suggesting an inherited disease. The vast majority of genes which are altered in the cancer cells are not transmitted through the germ line, but rather become abnormal in somatic cells sometime during the lifetime of the individual. Thus, the critical question which arises is "how do these genetic changes occur in somatic cells?". Epidemiologic data suggest that exposure to environmental carcinogens con- tributes to the genesis of at least 80% of all human cancers (DOLL and PETO 1981). Thus, it is natural to suspect that the genetic changes in somatic cells which con- tribute to the transformed phenotype arise from DNA damage caused by such exposures. Therefore, understanding how cells respond to DNA-damagi
出版日期Book 1997
關(guān)鍵詞DNA; DNA repair; Krebs; cancer; cell; cell cycle; cell nucleus; gene; genetics; molecular genetics; mutation; t
版次1
doihttps://doi.org/10.1007/978-3-642-60505-5
isbn_softcover978-3-642-64434-4
isbn_ebook978-3-642-60505-5Series ISSN 0070-217X Series E-ISSN 2196-9965
issn_series 0070-217X
copyrightThe Editor(s) (if applicable) and The Author(s), under exclusive license to Springer-Verlag GmbH, DE
The information of publication is updating

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0070-217X c cells which con- tribute to the transformed phenotype arise from DNA damage caused by such exposures. Therefore, understanding how cells respond to DNA-damagi978-3-642-64434-4978-3-642-60505-5Series ISSN 0070-217X Series E-ISSN 2196-9965
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Pathogenese des postthrombotischen Syndroms,w will focus on recent advances in cell cycle control and genetic instability in the budding yeast ., with emphasis on experimental topics in which loss of cell cycle progression control decreases the fidelity of chromosome transmission to daughter cells. Viable single gene mutations that perturb bo
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Genomic Instability and Its Role in Neoplasia,ade surrounding tissues, enter the vasculature, extravasate, and colonize a secondary site. Proficiency at each step is necessary for a tumor cell to become fully metastatic. Genetic alterations are the basis for this acquired variation (. 1987; . et al. 1987). The emergence of drug-resistant or rad
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https://doi.org/10.1007/978-3-531-90750-5 diseases, we think about inheriting one or two abnormal genes from our parents and these gene abnormalities confer the disease phenotype. In contrast, in the majority of cancers, no such inherited gene abnormalities can be identified (which does not mean that they do not exist) and there is no obvi
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Utho Creusen,Gordon Müller-Seitzon. New concepts make us realize the magnitude of the challenge of duplicating and distributing an accurate copy of the genome each time a cell divides. For each of the 10. somatic cell divisions that occur in a human lifetime, each copy of the genome must contain an intact sequence of some 3 billio
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