A Brauckhoff
University Hospital Heidelberg
5 Papers
11 Citations
A Brauckhoff is an academic researcher from University Hospital Heidelberg. The author has contributed to research in topics: Ubiquitin ligase & Transcription factor. The author has an hindex of 4, co-authored 5 publications. Previous affiliations of A Brauckhoff include Heidelberg University.
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Papers
Prognostic Value of Tumor Necrosis Factor–Related Apoptosis-Inducing Ligand (TRAIL) and TRAIL Receptors in Renal Cell Cancer
Stephan Macher-Goeppinger,Sebastian Aulmann,Katrin E. Tagscherer,Nina Wagener,Axel Haferkamp,Roland Penzel,A Brauckhoff,Markus Hohenfellner,Jaromir Sykora,Henning Walczak,Bin Tean Teh,Frank Autschbach,Esther Herpel,Esther Herpel,Peter Schirmacher,Wilfried Roth +15 more
TL;DR: High TRAil-R2, high TRAIL, and low TRAIL-R4 expression levels are associated with a worse disease-specific survival in patients with RCCs, suggesting that the assessment of TRAIL/TRAIL- R expression offers valuable prognostic information that could be used to select patients for adjuvant therapy studies.
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Nuclear expression of the ubiquitin ligase seven in absentia homolog (SIAH)-1 induces proliferation and migration of liver cancer cells
A Brauckhoff,Mona Malz,Darjus F. Tschaharganeh,Nisar P. Malek,Achim Weber,Marc-Oliver Riener,Christopher Soll,Jana Samarin,Michaela Bissinger,Jan Schmidt,Thomas Longerich,Volker Ehemann,Peter Schirmacher,Kai Breuhahn +13 more
TL;DR: Interference with SIAH-1 activity represents a promising approach to suppress HCC growth and supports different pro-tumorigenic cellular processes associated with tumor growth and tumor cell dissemination in human hepatocarcinogenesis.
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•Journal Article
[Reduced expression of the E3-ubiquitin ligase seven in absentia homologue (SIAH)-1 in human hepatocellular carcinoma].
TL;DR: It is concluded that distinct SIAH-1 levels mediate pro-tumorigenic effects in HCC cells and that further SIAh-1 inhibition may represent a new therapeutic strategy in the treatment of human hepatocellular carcinoma.
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Protumorigenic overexpression of stathmin/Op18 by gain-of-function mutation in p53 in human hepatocarcinogenesis.
Stephan Singer,Volker Ehemann,A Brauckhoff,Martina Keith,Sebastian Vreden,Peter Schirmacher,Kai Breuhahn +6 more
TL;DR: It is demonstrated that overexpression of stathmin is an early protumorigenic event in human hepatocarcinogenesis, and its up‐regulation can be mediated by gain‐of‐function mutations in p53.