R. Grundler

发表

Sensitivity toward tyrosine kinase inhibitors varies between different activating mutations of the FLT3 receptor.

C. Miething, C. Peschel, J. Duyster, 2003, Blood.

Sensitivity toward sorafenib and sunitinib varies between different activating and drug-resistant FLT3-ITD mutations.

C. Peschel, J. Duyster, R. Grundler, 2007, Experimental hematology.

FLT3-ITD and tyrosine kinase domain mutants induce 2 distinct phenotypes in a murine bone marrow transplantation model.

C. Miething, C. Peschel, J. Duyster, 2005, Blood.

The Bcr-Abl mutations T315I and Y253H do not confer a growth advantage in the absence of imatinib

F. Lordick, C. Miething, C. Peschel, 2006, Leukemia.

Phosphorylation of tyrosine 393 in the kinase domain of Bcr-Abl influences the sensitivity towards imatinib in vivo

R. Bai, C. Miething, C. Peschel, 2003, Leukemia.

SRC is a signaling mediator in FLT3-ITD- but not in FLT3-TKD-positive AML.

S. Bohlander, K. Götze, K. Spiekermann, 2012, Blood.

Identification of a novel type of ITD mutations located in nonjuxtamembrane domains of the FLT3 tyrosine kinase receptor.

T. Haferlach, S. Schnittger, J. Duyster, 2009, Blood.

The oncogenic fusion protein nucleophosmin–anaplastic lymphoma kinase (NPM–ALK) induces two distinct malignant phenotypes in a murine retroviral transplantation model

S. Morris, C. Miething, C. Peschel, 2003, Oncogene.

Bis(1H‐indol‐2‐yl)methanones are effective inhibitors of FLT3‐ITD tyrosine kinase and partially overcome resistance to PKC412A in vitro

M. Naumann, J. Duyster, F. Heidel, 2009, British journal of haematology.

Flt3-dependent transformation by inactivating c-Cbl mutations in AML.

Chunaram Choudhary, S. Koschmieder, Mirko H. H. Schmidt, 2007, Blood.

ADAM17 regulates epidermal growth factor receptor expression through the activation of Notch1 in non-small cell lung cancer.

T. Schuster, K. Specht, C. Peschel, 2010, Cancer research.

Retroviral insertional mutagenesis identifies RUNX genes involved in chronic myeloid leukemia disease persistence under imatinib treatment

Josef Hoepfl, Michael R Speicher, M. Speicher, 2007, Proceedings of the National Academy of Sciences.

NF-κB/STAT5/miR-155 network targets PU.1 in FLT3-ITD-driven acute myeloid leukemia

D. Tenen, G. Behre, D. Niederwieser, 2014, Leukemia.

E3 ligase-defective Cbl mutants lead to a generalized mastocytosis and myeloproliferative disease.

J. Duyster, L. Tickenbrock, G. Köhler, 2009, Blood.

GP130 activation induces myeloma and collaborates with MYC.

L. Bullinger, K. Götze, F. Bassermann, 2014, The Journal of clinical investigation.

Dissection of PIM serine/threonine kinases in FLT3-ITD–induced leukemogenesis reveals PIM1 as regulator of CXCL12–CXCR4-mediated homing and migration

Stefan Knapp, Andrea Biondi, Antonello Villa, 2009, The Journal of experimental medicine.

Effects of imatinib on bone marrow engraftment in syngeneic mice

C. Miething, C. Peschel, J. Duyster, 2002, Leukemia.

Lineage-specific STAT5 target gene activation in hematopoietic progenitor cells predicts the FLT3+-mediated leukemic phenotype

L. Hennighausen, M. Rudelius, J. Duyster, 2016, Leukemia.

Running Title: Role of Cbl mutations in myeloid transformation

Chunaram Choudhary, S. Koschmieder, J. Duyster, 2013 .

Oncogenic JAK2V617F requires an intact SH2-like domain for constitutive activation and induction of a myeloproliferative disease in mice.

C. Peschel, J. Duyster, M. Kremer, 2010, Blood.

Combination of c-SRC and FLT3 Inhibitors Has An Additive Inhibitory Effect on FLT3 ITD but Not on FLT3 TKD Positive Cells

K. Götze, C. Peschel, J. Duyster, 2010 .

E3 ligase-defective Cbl mutants lead to a generalized mastocytosis and myeloproliferative disease.

J. Duyster, L. Tickenbrock, G. Köhler, 2009, Blood.

ADAM17 regulates epidermal growth factor receptor expression through the activation of Notch1 in non-small cell lung cancer.

T. Schuster, K. Specht, C. Peschel, 2010, Cancer research.

NPM-ALK Induces Tumour Development in a Murine Model of Anaplastic Large Cell Lymphoma (ALCL) Independently of Bcl-3 Expression.

C. Peschel, J. Duyster, F. Fend, 2007 .