Michaela Bissinger
University Hospital Heidelberg
15 Papers
23 Citations
Michaela Bissinger is an academic researcher from University Hospital Heidelberg. The author has contributed to research in topics: Tumor necrosis factor alpha & Carcinogenesis. The author has an hindex of 11, co-authored 15 publications. Previous affiliations of Michaela Bissinger include Heidelberg University.
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Papers
Induction of Chromosome Instability by Activation of Yes-Associated Protein and Forkhead Box M1 in Liver Cancer
S Weiler,Federico Pinna,Thomas Wolf,Teresa Lutz,Aman Geldiyev,Carsten Sticht,M Knaub,Stefan Thomann,Michaela Bissinger,S Wan,S Rössler,D Becker,Norbert Gretz,Hauke Lang,Frank Bergmann,Vladimir Ustiyan,Tatiana V. Kalin,Stephan Singer,Ju Seog Lee,Jens U. Marquardt,Peter Schirmacher,Vladimir V. Kalinichenko,Kai Breuhahn +22 more
TL;DR: By analyzing cell lines, genetically modified mice, and HCC tissues, it is found that YAP cooperates with FOXM1 to contribute to chromosome instability and agents that disrupt this pathway might be developed as treatments for liver cancer.
140
Autocrine insulin‐like growth factor‐II stimulation of tumor cell migration is a progression step in human hepatocarcinogenesis
Tanja Nussbaum,Jana Samarin,Volker Ehemann,Michaela Bissinger,Eduard Ryschich,Akmal Khamidjanov,Xiaolei Yu,Norbert Gretz,Peter Schirmacher,Kai Breuhahn +9 more
TL;DR: Activation of IGF‐II/IGF‐IR signaling is likely a progression switch selected by function that promotes tumor cell dissemination and aggressive tumor behavior.
108
Overexpression of far upstream element binding proteins: A mechanism regulating proliferation and migration in liver cancer cells
Mona Malz,Achim Weber,Stephan Singer,Vera Riehmer,Michaela Bissinger,Marc Oliver Riener,Thomas Longerich,Christopher Soll,Arndt Vogel,Peter Angel,Peter Schirmacher,Kai Breuhahn +11 more
TL;DR: Analyzing nuclear and cytoplasmic areas of HCC cells revealed that reduced FBP‐1 levels affected cell morphology and were associated with a less malignant phenotype, indicating a new potential target structure for HCC treatment.
98
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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Nuclear accumulation of seven in absentia homologue-2 supports motility and proliferation of liver cancer cells
Mona Malz,Antje Aulmann,Jana Samarin,Michaela Bissinger,Thomas Longerich,Sabrina Schmitt,Peter Schirmacher,Kai Breuhahn +7 more
TL;DR: Data show that SIAH‐2—as described for SIAh‐1—accumulates in nuclei of HCC cells where it supports tumor growth and tumor cell dissemination, and represents a promising therapeutic strategy for HCC.
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