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Markus E. Diefenbacher

Researcher at University of Würzburg

Publications -  41
Citations -  1783

Markus E. Diefenbacher is an academic researcher from University of Würzburg. The author has contributed to research in topics: Cancer & Transcription factor. The author has an hindex of 18, co-authored 34 publications receiving 1395 citations. Previous affiliations of Markus E. Diefenbacher include Karlsruhe Institute of Technology & London Research Institute.

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The GATA2 Transcriptional Network Is Requisite for RAS Oncogene-Driven Non-Small Cell Lung Cancer

TL;DR: It is shown that RAS-pathway mutant NSCLC cells depend on the transcription factor GATA2, and discovery of the nononcogene addiction of KRAS mutant lung cancers to Gata2 presents a network of druggable pathways for therapeutic exploitation.
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RAS and RHO Families of GTPases Directly Regulate Distinct Phosphoinositide 3-Kinase Isoforms

TL;DR: It is shown that both RAS and RHO family GTPases directly regulate distinct ubiquitous PI3K isoforms and that RAC activates p110β downstream of GPCRs and in fibroblasts through Dock180/Elmo1-mediated RAC activation and subsequent interaction with p110 β.
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Requirement for Interaction of PI3-Kinase p110α with RAS in Lung Tumor Maintenance

TL;DR: The need for RAS interaction with p110α in the maintenance of mutant Kras-driven lung tumors was explored using an inducible mouse model and a tumor cell-autonomous effect was improved significantly by combination with MEK inhibition.
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The deubiquitinase USP28 controls intestinal homeostasis and promotes colorectal cancer.

TL;DR: Usp28 deficiency promoted tumor cell differentiation accompanied by decreased proliferation, which suggests that USP28 acts similarly in intestinal homeostasis and colorectal cancer models, and inhibition of the enzymatic activity ofUSP28 may be a potential target for cancer therapy.
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F-box and WD Repeat Domain-Containing 7 Regulates Intestinal Cell Lineage Commitment and Is a Haploinsufficient Tumor Suppressor

TL;DR: FbW7 regulates intestinal biology and tumorigenesis by controlling the abundance of different substrates in a dose-dependent fashion, providing a molecular explanation for the heterozygous mutations of fbw7 observed in human colorectal carcinoma.