Christine Dierks
University of Freiburg
41 Papers
180 Citations
Christine Dierks is an academic researcher from University of Freiburg. The author has contributed to research in topics: Chronic lymphocytic leukemia & Syk. The author has an hindex of 14, co-authored 41 publications. Previous affiliations of Christine Dierks include University Medical Center Freiburg.
Chat about Author
Papers
Oncogenic JAK2 V617F causes PD-L1 expression, mediating immune escape in myeloproliferative neoplasms
Alessandro Prestipino,Alica J. Emhardt,Konrad Aumann,David O’Sullivan,Sivahari P. Gorantla,Sandra Duquesne,Wolfgang Melchinger,Lukas Braun,Slavica Vuckovic,Slavica Vuckovic,Melanie Boerries,Melanie Boerries,Hauke Busch,Hauke Busch,Sebastian Halbach,Sandra Pennisi,Teresa Poggio,Petya Apostolova,Pia Veratti,Pia Veratti,Michael Hettich,Gabriele Niedermann,Mark Bartholomä,Khalid Shoumariyeh,Jonas S. Jutzi,Julius Wehrle,Christine Dierks,Heiko Becker,Annette Schmitt-Graeff,Marie Follo,Dietmar Pfeifer,Jan Rohr,Sebastian Fuchs,Stephan Ehl,Frederike A. Hartl,Susana Minguet,Cornelius Miething,Cornelius Miething,Florian H. Heidel,Nicolaus Kröger,Ioanna Triviai,Tilman Brummer,Jürgen Finke,Anna Lena Illert,Eliana Ruggiero,Chiara Bonini,Justus Duyster,Justus Duyster,Heike L. Pahl,Steven W. Lane,Steven W. Lane,Steven W. Lane,Geoffrey R. Hill,Geoffrey R. Hill,Geoffrey R. Hill,Bruce R. Blazar,Nikolas von Bubnoff,Nikolas von Bubnoff,Erika L. Pearce,Robert Zeiser +59 more
TL;DR: In MPN, constitutive JAK2/STAT3/STAT5 activation, mainly in monocytes, megakaryocytes, and platelets, caused PD-L1–mediated immune escape by reducing T cell activation, metabolic activity, and cell cycle progression, which paving the way for immunomodulatory approaches relying on PD-1 inhibition.
199
Spleen tyrosine kinase inhibition prevents chemokine- and integrin-mediated stromal protective effects in chronic lymphocytic leukemia
Maike Buchner,Constance Baer,Gabriele Prinz,Christine Dierks,Meike Burger,Thorsten Zenz,Stephan Stilgenbauer,Hassan Jumaa,Hendrik Veelken,Katja Zirlik +9 more
TL;DR: SYK blockade in CLL is a promising therapeutic principle not only for its inhibition of the BCR signaling pathway, but also by inhibiting protective stroma signals in a manner entirely independent of B CR signaling.
189
DNA Damage Signaling Instructs Polyploid Macrophage Fate in Granulomas
Laura Herrtwich,Indrajit Nanda,Konstantinos Evangelou,Teodora Nikolova,Veronika Horn,Sagar,Daniel Erny,Jonathan Stefanowski,Leif Rogell,Leif Rogell,Claudius Klein,Kourosh Gharun,Marie Follo,Maximilian Seidl,Bernhard Kremer,Nikolas Münke,Julia Senges,Manfred Fliegauf,Tom Aschman,Dietmar Pfeifer,Sandrine Sarrazin,Michael H. Sieweke,Dirk Wagner,Christine Dierks,Thomas Haaf,Thomas Ness,Mario M. Zaiss,Reinhard E. Voll,Sachin D. Deshmukh,Marco Prinz,Torsten Goldmann,Christoph Hölscher,Anja E. Hauser,Andrés J. López-Contreras,Dominic Grün,Vassilis G. Gorgoulis,Andreas Diefenbach,Philipp Henneke,Antigoni Triantafyllopoulou +38 more
TL;DR: It is proposed that, in the presence of persistent inflammatory stimuli, pathways previously linked to oncogene-initiated carcinogenesis instruct a long-lived granuloma-resident macrophage differentiation program that regulates granulomatous tissue remodeling.
113
PIM Kinases Are Essential for Chronic Lymphocytic Leukemia Cell Survival (PIM2/3) and CXCR4-Mediated Microenvironmental Interactions (PIM1)
Sarah Decker,Johannes Finter,Aaron James Forde,Sandra Kissel,Juerg Schwaller,Thomas Sebastian Mack,Anabel Kuhn,Nathanael S. Gray,Marie Follo,Hassan Jumaa,Meike Burger,Katja Zirlik,Dietmar Pfeifer,Chandrasekhar V. Miduturu,Hermann Eibel,Hendrik Veelken,Christine Dierks +16 more
TL;DR: The results show that PIM kinase inhibitors are an effective therapeutic option for CLL, not only by impairing PIM2/3-mediated CLL cell survival, but also by blocking the PIM1/CXCR4-mediated interaction of CLL cells with their protective microenvironment.
70
CXCR4-SERINE339 regulates cellular adhesion, retention and mobilization, and is a marker for poor prognosis in acute myeloid leukemia.
TL;DR: It is reported that phosphorylation of CXCR4-S339 in bone marrow (BM) biopsies correlated with poor prognosis in a cohort of AML patients and could serve as a novel prognostic marker in human AML.
37