Search Results - "Korovkina, Darya"

Two mouse models reveal an actionable PARP1 dependence in aggressive chronic lymphocytic leukemia by Knittel, Gero, Rehkämper, Tim, Korovkina, Darya, Liedgens, Paul, Fritz, Christian, Torgovnick, Alessandro, Al-Baldawi, Yussor, Al-Maarri, Mona, Cun, Yupeng, Fedorchenko, Oleg, Riabinska, Arina, Beleggia, Filippo, Nguyen, Phuong-Hien, Wunderlich, F. Thomas, Ortmann, Monika, Montesinos-Rongen, Manuel, Tausch, Eugen, Stilgenbauer, Stephan, P. Frenzel, Lukas, Herling, Marco, Herling, Carmen, Bahlo, Jasmin, Hallek, Michael, Peifer, Martin, Buettner, Reinhard, Persigehl, Thorsten, Reinhardt, H. Christian

“…Chronic lymphocytic leukemia (CLL) remains an incurable disease. Two recurrent cytogenetic aberrations, namely del(17p), affecting TP53 , and del(11q),…”
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Rewired NFκB signaling as a potentially actionable feature of activated B-cell-like diffuse large B-cell lymphoma by Knittel, Gero, Liedgens, Paul, Korovkina, Darya, Pallasch, Christian P., Reinhardt, Hans Christian

“…Diffuse large B‐cell lymphoma (DLBCL) is the most common type of aggressive lymphoma in the Western world and remains a clinical challenge. Two types of DLBCL…”
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B-cell–specific conditional expression of Myd88p.L252P leads to the development of diffuse large B-cell lymphoma in mice by Knittel, Gero, Liedgens, Paul, Korovkina, Darya, Seeger, Jens M., Al-Baldawi, Yussor, Al-Maarri, Mona, Fritz, Christian, Vlantis, Katerina, Bezhanova, Svetlana, Scheel, Andreas H., Wolz, Olaf-Oliver, Reimann, Maurice, Möller, Peter, López, Cristina, Schlesner, Matthias, Lohneis, Philipp, Weber, Alexander N.R., Trümper, Lorenz, Staudt, Louis M., Ortmann, Monika, Pasparakis, Manolis, Siebert, Reiner, Schmitt, Clemens A., Klatt, Andreas R., Wunderlich, F.Thomas, Schäfer, Stephan C., Persigehl, Thorsten, Montesinos-Rongen, Manuel, Odenthal, Margarete, Büttner, Reinhard, Frenzel, Lukas P., Kashkar, Hamid, Reinhardt, H.Christian

“…The adaptor protein MYD88 is critical for relaying activation of Toll-like receptor signaling to NF-κB activation. MYD88 mutations, particularly the p.L265P…”
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