Titlebook: Signal Transduction in Cancer Metastasis; Wen-Sheng Wu,Chi-Tan Hu Book 2010 Springer Science+Business Media B.V. 2010 Activation.Cancer me

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Alessio Giubellino,Praveen R. Aranyanalysis of other physical properties.The goal of the volume is to establish a complete andreliable compilation of critically reviewed experimentaldata, excluding purely theoretical works.The large amount of publications, more than 40.000 since1913, requires a subdivision of the data in severalsubvo

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Overview of Signal Transduction in Tumor Metastasis,rigger transendothelial passage. Moreover, various chemokine receptor/ligand pairs such as CCR4/CXCL12 can act to achieve organ preference in metastatic colonization. Distinct signaling pathways may also be responsible for determining the destination of tumor cells. The final change faced by the met

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Microenvironment Triggers EMT, Migration and Invasion of Primary Tumor via Multiple Signal Pathwaysic factors such as HGF, TGFβ and that elicited by integrin-ECM engagement are delineated. In the future, more effective cancer therapy can be developed by targeting the critical signal molecules responsible for the initiation stage of tumor metastasis.

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The ERK1/2 MAP Kinase Signaling Pathway in Tumor Progression and Metastasis,nce suggest that the ERK1/2 signaling pathway also contributes to the increased motility, invasiveness and dissemination of tumor cells. In this chapter, we review the role of ERK1/2 MAP kinase signaling in the pathogenesis of tumor metastasis.

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The Role of ROS Signaling in Tumor Progression,d by ROS are MAPK and PAK. MAPKs cascades were established to be a major signal pathway for driving tumor cell metastasis, which are mediated by PKC, TGF-beta/Smad and integrin-mediated signaling. PAK is an effector of Rac-mediated cytoskeletal remodeling that is responsible for cell migration and a

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Signal Cross Talks for Sustained MAPK Activation and Cell Migration Mediated by Reactive Oxygen Spe, PKC itself may phosphorylate integrin or paxillin-associated focal adhesion proteins to induce generation of ROS which may reactivate PKC. In the future, ROS will be validated as the promising therapeutic targets for prevention of tumor metastasis.

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