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Titlebook: Systems Biology of Tumor Dormancy; Heiko Enderling,Nava Almog,Lynn Hlatky Book 2013 The Editor(s) (if applicable) and The Author(s), under

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书目名称Systems Biology of Tumor Dormancy
编辑Heiko Enderling,Nava Almog,Lynn Hlatky
视频video
概述Based on the Workshop on Systems Biology of Tumor Dormancy meeting.Qualitative and quantitative approaches to the problem of cancer.Looks at both the molecular and systems levels of cancer research.In
丛书名称Advances in Experimental Medicine and Biology
图书封面Titlebook: Systems Biology of Tumor Dormancy;  Heiko Enderling,Nava Almog,Lynn Hlatky Book 2013 The Editor(s) (if applicable) and The Author(s), under
描述This volume is based on the Workshop on Systems Biology of Tumor Dormancy meeting, held July 25th to July 28th, 2011. The first annual CCSB workshop brought together biologists, clinicians, mathematicians, and computer scientists to discuss various aspects of tumor dormancy and develop novel mathematical/computational models with the keynote speakers. Specific topics included the angiogenic switch, immune system interactions, cancer stem cells and signaling.
出版日期Book 2013
关键词Systems Biology
版次1
doihttps://doi.org/10.1007/978-1-4614-1445-2
isbn_softcover978-1-4899-9882-8
isbn_ebook978-1-4614-1445-2Series ISSN 0065-2598 Series E-ISSN 2214-8019
issn_series 0065-2598
copyrightThe Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Science+Busines
The information of publication is updating

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The Host Support Niche as a Control Point for Tumor Dormancy: Implications for Tumor Development andular interest are dynamical interactions between tumor and host cell populations that can themselves strongly impact the fate of established cancer lesions. Regardless of tumor type, all cancers face the common problem of having to breach the barrier of angiogenic competency in order to advance from
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Cancer Stem Cells and Tumor Dormancy tumors, while the bulk of the population comprises non-stem cancer cells that lack tumor initiation potential. The interactions of these two phenotypically distinct populations can provoke various nonlinear growth kinetics in the emerging tumor. An environmentally independent, intrinsic dormant sta
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Tumor Dormancy, Oncogene Addiction, Cellular Senescence, and Self-Renewal Programsenes to normal physiologic regulation can elicit dramatic reversal of the neoplastic phenotype, including reduced proliferation and increased apoptosis of tumor cells (Science 297(5578):63–64, 2002). In some cases, oncogene inactivation is associated with compete elimination of a tumor. However, in
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