J
Justus Duyster
Researcher at Technische Universität München
Publications - 128
Citations - 7853
Justus Duyster is an academic researcher from Technische Universität München. The author has contributed to research in topics: Imatinib & Imatinib mesylate. The author has an hindex of 45, co-authored 102 publications receiving 7352 citations. Previous affiliations of Justus Duyster include University Medical Center Freiburg & Novartis.
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Journal ArticleDOI
One vs three years of adjuvant imatinib for operable gastrointestinal stromal tumor: a randomized trial.
Heikki Joensuu,Mikael Eriksson,Kirsten Sundby Hall,Jörg T. Hartmann,Daniel Pink,Jochen Schütte,Giuliano Ramadori,Peter Hohenberger,Justus Duyster,Salah-Eddin Al-Batran,Marcus Schlemmer,Sebastian Bauer,Eva Wardelmann,Maarit Sarlomo-Rikala,Bengt Nilsson,Harri Sihto,Odd R. Monge,Petri Bono,Raija Kallio,Aki Vehtari,M. Leinonen,Thor Alvegård,Peter Reichardt +22 more
TL;DR: Adjuvant imatinib administered for 12 months after surgery has improved recurrence-free survival (RFS) of patients with operable gastrointestinal stromal tumor (GIST) compared with placebo and overall survival of GIST patients with a high risk of Gist recurrence.
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NF-kappaB is a negative regulator of IL-1beta secretion as revealed by genetic and pharmacological inhibition of IKKbeta.
Florian R. Greten,Florian R. Greten,Melek C. Arkan,Melek C. Arkan,Julia Bollrath,Li-Chung Hsu,Jason Goode,Cornelius Miething,Serkan Ismail Göktuna,Michael Neuenhahn,Joshua Fierer,Stephan Paxian,Nico van Rooijen,Yajun Xu,Timothy D. Ocain,Bruce Jaffee,Dirk H. Busch,Justus Duyster,Roland M. Schmid,Lars Eckmann,Michael Karin +20 more
TL;DR: An unanticipated role for IKKbeta-dependent NF-kappaB signaling in the negative control of IL-1beta production is unraveled and potential complications of long-term IKK beta inhibition are highlighted.
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BCR-ABL gene mutations in relation to clinical resistance of Philadelphia-chromosome-positive leukaemia to STI571: a prospective study
TL;DR: Different mutations within the kinase domain of BCR-ABL can be responsible for refractoriness of Ph+ leukaemia to STI571, which might be a frequent mechanism of STi571 resistance in lymphoid disease.
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Sorafenib in Combination With Intensive Chemotherapy in Elderly Patients With Acute Myeloid Leukemia: Results From a Randomized, Placebo-Controlled Trial
Hubert Serve,Utz Krug,Ruth Wagner,M. Cristina Sauerland,Achim Heinecke,Uta Brunnberg,Markus Schaich,Oliver G. Ottmann,Justus Duyster,Hannes Wandt,Thomas Fischer,Aristoteles Giagounidis,Andreas Neubauer,Albrecht Reichle,Walter E. Aulitzky,Richard Noppeney,Igor Wolfgang Blau,Volker Kunzmann,Reingard Stuhlmann,Alwin Krämer,Karl-Anton Kreuzer,Christian Brandts,Björn Steffen,Christian Thiede,Carsten Müller-Tidow,Gerhard Ehninger,Wolfgang E. Berdel +26 more
TL;DR: Combination of standard induction and consolidation therapy with sorafenib in the schedule investigated in the trial is not beneficial for elderly patients with AML.
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Constitutively activated phosphatidylinositol-3 kinase (PI-3K) is involved in the defect of apoptosis in B-CLL: association with protein kinase Cδ
Ingo Ringshausen,Folker Schneller,Christian Bogner,Susanne Hipp,Justus Duyster,Christian Peschel,Thomas Decker +6 more
TL;DR: It is concluded that activated PI-3K might be important in the pathogenesis of B-CLL, and survival signals might be mediated via PKCcdelta, and inhibition of PI- 3K or PKCdelta may be an innovative approach to treat B- CLL.