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Bedeutung Ca2+-aktivierter K+-Kanäle für Tumorproliferation, Zytostatika- und Strahlenresistenz beim Mammakarzinom
Antragsteller
Professor Dr. Peter Ruth
Fachliche Zuordnung
Pharmakologie
Förderung
Förderung von 2014 bis 2019
Projektkennung
Deutsche Forschungsgemeinschaft (DFG) - Projektnummer 248631763
Erstellungsjahr
2020
Zusammenfassung der Projektergebnisse
Our findings provide important new knowledge with regards to the in vivo biological role of BKα and BKγ1 in breast cancer onset and progression supporting the notion that both BK and BKα/γ1 may be suitable pharmacological targets for breast cancer. To this end, we suggest, that given BKα’s pleiotropic functions and expected multiple adverse effects upon global channel inhibition, a targeting of epithelial and cancer-associated BKα/γ1 complexes may offer a suitable opportunity to develop tolerable treatments that may be useful in combination with antihormonal treatment.
Projektbezogene Publikationen (Auswahl)
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(2017) SK4 channels modulate Ca2+ signalling and cell cycle progression in murine breast cancer. Mol Oncol. 11, 1172-1188
Steudel FA, Mohr CJ, Stegen B, Nguyen HY, Barnert A, Steinle M, Beer-Hammer S, Koch P, Lo WY, Schroth W, Hoppe R, Brauch H, Ruth P, Huber SM, Lukowski R
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(2019) Cancer-Associated Intermediate Conductance Ca2+-Activated K⁺ Channel KCa3.1. Cancers 11, E109
Mohr CJ, Steudel FA, Gross D, Ruth P, Lo WY, Hoppe R, Schroth W, Brauch H, Huber SM, Lukowski R
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(2019) KCa3.1 Channels Confer Radioresistance to Breast Cancer Cells. Cancers 11, E1285
Mohr CJ, Gross D, Sezgin EC, Steudel FA, Ruth P, Huber SM, Lukowski R