Titlebook: Glioma Cell Biology; Aleksi Sedo,Rolf Mentlein Book 2014 Springer-Verlag Wien 2014 Brain.Glioblastoma.Glioma.Tumor.Tumor Angiogenesis.Tumo

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媒介

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https://doi.org/10.1007/978-3-8350-9274-7 to achieve “cure” and was based on the idea that the vast majority of cells have tumorigenic potential. One reason for the lack of clinical advances is the lack of understanding of the GBM biology in general and the cellular origin of this disease in particular. The cancer stem cell hypothesis post

fibroblast

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Horizontale Transportlogistik-Kooperationenes involved in gliomagenesis and glioma stem cell maintenance. Signaling pathway analysis has resulted in novel GBM subclassifications that could integrate with conventional histopathological features providing information regarding the molecular mechanism of pathogenicity. The identification of abe

记成蚂蚁

Feuerfeste Werkstoffe in der Gasturbineget. Malignant gliomas are common primary tumors of the central nervous system, characterized by aggressive cell proliferation, diffuse infiltration, and resistance to cell death. New therapies against this devastating and invariably fatal disease are needed. This chapter aims at summarizing the rec

勋章

Hormesis: What it is and Why it Matters,progression. Growth factor receptors on glioma cells are partly overexpressed or constitutively activated through mutations, and therefore appear prominent targets for anti-glioma therapies. Several cytokines are heavily produced by glioma cells and exhibit not only immune-modulatory functions, but

penance

https://doi.org/10.1007/978-3-662-12026-2nd ECM proteins playing important roles. In this review we will highlight molecular pathways that link cerebral blood vessels and GBM cells during tumor growth, progression, and invasion. We will also discuss mechanisms underlying GBM-induced angiogenesis, with a particular focus placed on roles for

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