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Markus Bredel

Researcher at University of Alabama at Birmingham

Publications -  107
Citations -  5735

Markus Bredel is an academic researcher from University of Alabama at Birmingham. The author has contributed to research in topics: Glioma & Cancer. The author has an hindex of 34, co-authored 94 publications receiving 5013 citations. Previous affiliations of Markus Bredel include Northwestern University & Stanford University.

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Neuronal Activity Promotes Glioma Growth through Neuroligin-3 Secretion.

TL;DR: Findings indicate the important role of active neurons in the brain tumor microenvironment and identify secreted NLGN3 as an unexpected mechanism promoting neuronal activity-regulated cancer growth.
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CHD5 Is a Tumor Suppressor at Human 1p36

TL;DR: This approach functionally identifies chromodomain helicase DNA binding domain 5 (Chd5) as a tumor suppressor that controls proliferation, apoptosis, and senescence via the p19(Arf)/p53 pathway and demonstrates that Chd5 functions as a tumors suppressor in vivo and implicate deletion of CHD5 in human cancer.
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Chemogenomics: an emerging strategy for rapid target and drug discovery

TL;DR: The hope is that chemogenomics will concurrently identify and validate therapeutic targets and detect drug candidates to rapidly and effectively generate new treatments for many human diseases.
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Functional Network Analysis Reveals Extended Gliomagenesis Pathway Maps and Three Novel MYC-Interacting Genes in Human Gliomas

TL;DR: In this article, the authors applied refined network knowledge to the analysis of key functions and pathways associated with gliomagenesis in a set of 50 human gliomas of various histogenesis, using cDNA microarrays, inferential and descriptive statistics, and dynamic mapping of gene expression data into a functional annotation database.
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Glioma Stem Cell Proliferation and Tumor Growth Are Promoted by Nitric Oxide Synthase-2

TL;DR: It is demonstrated that glioma stem cells (GSCs) produce nitric oxide via elevated Nitric oxide synthase-2 (NOS2) expression, providing insight into how GSCs are mechanistically distinct from their less tumorigenic counterparts and suggest that NOS2 inhibition may be an efficacious approach to treating this devastating disease.