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Titlebook: Apoptosis, Senescence and Cancer; David A. Gewirtz,Shawn E. Holt,Steven Grant Book 2007Latest edition Humana Press 2007 Tumor.apoptosis.le

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期刊全称Apoptosis, Senescence and Cancer
影响因子2023David A. Gewirtz,Shawn E. Holt,Steven Grant
视频video
发行地址In-depth discussions of different modes of cell death.Introductory chapters provide detailed overviews of topics
学科分类Cancer Drug Discovery and Development
图书封面Titlebook: Apoptosis, Senescence and Cancer;  David A. Gewirtz,Shawn E. Holt,Steven Grant Book 2007Latest edition Humana Press 2007 Tumor.apoptosis.le
影响因子.Apoptosis, Senescence and Cancer provides insight into established practices and research into apoptosis and senescence by thoroughly examining novel and emerging techniques and research in the fields of cell death pathways, senescence growth arrest, drugs and resistance, DNA damage response, and other topics which still hold mysteries for researchers. ..The volume is divided into six easy to follow sections. The first is Apoptosis and Alternative Modes of Cell Death, followed by chapters on Telomeres and Telomerase, Senescence, Genomic Instability and Tumorigenesis. The third part covers DNA Damage Response, Signaling Pathways and Tumorigenesis, while the fourth delves into Resistance and Sensitization. The book concludes with Established Cancer Therapies and a section which looks toward the future with Recent and Developing Cancer Therapies...In total, this volume provides basic scientists and clinicians with a deeper and more complete understanding of the cellular responses of malignancies which may determine the effectiveness of treatment, both in the initial stages of the disease as well as in disease recurrence..
Pindex Book 2007Latest edition
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The Role of Telomeres in Genomic Instabilitymaintained by the enzyme telomerase. Telomeres are maintained in the germ line but shorten with age in most somatic cells due to the lack of sufficient telomerase. This telomere shortening serves as a signal for replicative cell senescence, which protects against the unlimited cell division required
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Resistance/Signaling Pathwayseramide, whereas others have been noted to be dependent on mitochondria-derived reactive oxygen/nitrogen species and the activation of growth factor receptor tyrosine kinases. The precise roles of growth factor receptors and signal transduction pathways in cellular responses following exposure to no
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