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Titlebook: Cell Adhesion and Cytoskeletal Molecules in Metastasis; Anne E. Cress,Raymond B. Nagle Book 2006 Springer Science+Business Media B.V. 2006

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發(fā)表于 2025-3-21 19:22:17 | 只看該作者 |倒序瀏覽 |閱讀模式
書目名稱Cell Adhesion and Cytoskeletal Molecules in Metastasis
編輯Anne E. Cress,Raymond B. Nagle
視頻videohttp://file.papertrans.cn/223/222731/222731.mp4
概述Compiled information on cell adhesion molecules in human cancer tissue specimens.Explains how cell adhesion influences DNA damage responses.Explains how cell adhesion influences chemotherapeutic drug
叢書名稱Cancer Metastasis - Biology and Treatment
圖書封面Titlebook: Cell Adhesion and Cytoskeletal Molecules in Metastasis; Anne E. Cress,Raymond B. Nagle Book 2006 Springer Science+Business Media B.V. 2006
描述.In this volume, the expression of specific adhesion molecules within human cancer tissues are highlighted. The expression signatures from published DNA microarray and immunohistochemistry studies are detailed. The concept that the alteration of specific adhesion molecules influence the cancer migration ability and cancer damage responses is detailed in this volume; both features are essential for the survival of an invading tumor cell. Defining the minimal adhesion receptors preserved on cancer cells during tumor progression will define the metastatic adhesion signature. Understanding the metastatic adhesion signature will reveal vulnerabilities that could be exploited for the prevention and/or eradication of the invading cancer cell..
出版日期Book 2006
關(guān)鍵詞Migration; Regulation; adhesion structures; cancer; damage response; epithelium; extracellular matrix; tiss
版次1
doihttps://doi.org/10.1007/978-1-4020-5129-6
isbn_softcover978-90-481-7290-0
isbn_ebook978-1-4020-5129-6Series ISSN 1568-2102 Series E-ISSN 2215-1648
issn_series 1568-2102
copyrightSpringer Science+Business Media B.V. 2006
The information of publication is updating

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On the Biological Origin of Design in Naturetely silenced in cancer is discussed. Understanding the molecular features of the epigenetic switch is likely to provide a therapeutic opportunity to induce transcriptional reprogramming and prevent devastating disease processes such as epithelial cancer metastasis.
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