V
Viktoria von Manstein
Publications - 4
Citations - 354
Viktoria von Manstein is an academic researcher. The author has contributed to research in topics: Cell signaling & Tumor microenvironment. The author has an hindex of 4, co-authored 4 publications receiving 284 citations.
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Jak Stat signaling and cancer: Opportunities, benefits and side effects of targeted inhibition.
TL;DR: The direct and mediated mechanisms of Jak stat signaling in and on tumors cells, the interactions with other signaling pathways and transcription factors and the targeting of the functionally crucial secondary modifications of Stat molecules suggest novel approaches to the future development of Jak Stat based cancer therapeutics.
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Resistance of Cancer Cells to Targeted Therapies Through the Activation of Compensating Signaling Loops
Viktoria von Manstein,Chul Min Yang,Diane Richter,Natalia Delis,Vida Vafaizadeh,Bernd Groner +5 more
TL;DR: The treatment of HNSCC with a specific inhibitor of c-Src initially resulted in reduced Stat3 and Stat5 activation and subsequently an arrest of cell proliferation and increased apoptosis, indicating that the inhibition of a single tyrosine kinase might not be sufficient to induce lasting therapeutic effects in cancer patients.
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Tumor cell resistance against targeted therapeutics: the density of cultured glioma tumor cells enhances Stat3 activity and offers protection against the tyrosine kinase inhibitor canertinib
TL;DR: Tumor cell resistance to drug treatment severely limits the therapeutic success of treatment and the number of patients treated with these drugs is limited.
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Expression of the miR‐302/367 cluster in glioblastoma cells suppresses tumorigenic gene expression patterns and abolishes transformation related phenotypes
Chul Min Yang,Tomohiro Chiba,Boris Brill,Natalia Delis,Viktoria von Manstein,Vida Vafaizadeh,Thomas Oellerich,Bernd Groner +7 more
TL;DR: The epigenetic reprogramming potential of the miR‐302/367 cluster is used to “de‐program” tumor cells, that is, hift their gene expression pattern towards an alternative program associated with more benign cellular phenotypes and can potentially become a new approach for cancer therapy.