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Journal Articles

ABT-737 Neutralizes Resistance to FLT3 Inhibitor Treatment Mediated by Overexpression of BCL2 in Primary AML Blasts.

Tobias M. Kohl, PhD, Christine Hellinger, Wolfgang Hiddemann, MD, PhD, Stefan K. Bohlander, MD, Karsten Spiekermann, MD

Blood (2006) 108 (11): 524.

https://doi.org/10.1182/blood.V108.11.524.524

Published: 2006

Journal Articles

KIT -D816 mutations in AML1-ETO -positive AML are associated with impaired event-free and overall survival

Susanne Schnittger, Tobias M. Kohl, Torsten Haferlach, Wolfgang Kern, Wolfgang Hiddemann, Karsten Spiekermann, Claudia Schoch

Blood (2006) 107 (5): 1791–1799.

https://doi.org/10.1182/blood-2005-04-1466

Published: 2006

Journal Articles

The AML1-ETO Fusion Gene and the FLT3 Length Mutation Collaborate in Inducing Acute Leukemia in a Murine Bone Marrow Transplantation Model.

Christina Schessl, Vijay P.S. Rawat, Monica Cusan, Aniruddha Deshpande, Tobias M. Kohl, Patricia M. Rosten, Karsten Spiekermann, R.Keith Humphries, Susanne Schnittger, Wolfgang Kern, Wolfgang Hiddemann, Leticia Quintanilla-Martinez, Stefan K. Bohlander, Michaela Feuring-Buske, Christian Buske

Blood (2005) 106 (11): 100.

https://doi.org/10.1182/blood.V106.11.100.100

Published: 2005

Journal Articles

KIT exon 8 mutations associated with core-binding factor (CBF)–acute myeloid leukemia (AML) cause hyperactivation of the receptor in response to stem cell factor

Tobias M. Kohl, Susanne Schnittger, Joachim W. Ellwart, Wolfgang Hiddemann, Karsten Spiekermann

Blood (2005) 105 (8): 3319–3321.

https://doi.org/10.1182/blood-2004-06-2068

Published: 2005

Journal Articles

KIT Exon 8 Mutations Associated with Core Binding Factor (CBF) - Acute Myeloid Leukemia (AML) Cause Hypersensitivity of KIT to Its Natural Ligand Stem Cell Factor.

Tobias M. Kohl, Susanne Schnittger, PhD, Wolfgang Hiddemann, MD, Karsten Spiekermann, MD

Blood (2004) 104 (11): 92.

https://doi.org/10.1182/blood.V104.11.92.92

Published: 2004

Journal Articles

The FLT3-D324N Variant Is a Functionally Silent Polymorphism in the FLT3 Gene and May Be Associated with a Higher Risk for AML.

Susanne Schnittger, PhD, Tobias M. Kohl, Nina Leopold, Claudia Schoch, MD, Wolfgang Kern, MD, Peter Lohse, PhD, Wolfgang Hiddemann, MD, Torsten Haferlach, MD, Karsten Spiekermann, MD

Blood (2004) 104 (11): 3373.

https://doi.org/10.1182/blood.V104.11.3373.3373

Published: 2004

Journal Articles

Mutations in the tyrosine kinase domain of FLT3 define a new molecular mechanism of acquired drug resistance to PTK inhibitors in FLT3-ITD–transformed hematopoietic cells

Ksenia Bagrintseva, Ruth Schwab, Tobias M. Kohl, Susanne Schnittger, Sabine Eichenlaub, Joachim W. Ellwart, Wolfgang Hiddemann, Karsten Spiekermann

Blood (2004) 103 (6): 2266–2275.

https://doi.org/10.1182/blood-2003-05-1653

Published: 2004

NARROW

ABT-737 Neutralizes Resistance to FLT3 Inhibitor Treatment Mediated by Overexpression of BCL2 in Primary AML Blasts.

KIT -D816 mutations in AML1-ETO -positive AML are associated with impaired event-free and overall survival

The AML1-ETO Fusion Gene and the FLT3 Length Mutation Collaborate in Inducing Acute Leukemia in a Murine Bone Marrow Transplantation Model.

KIT exon 8 mutations associated with core-binding factor (CBF)–acute myeloid leukemia (AML) cause hyperactivation of the receptor in response to stem cell factor

KIT Exon 8 Mutations Associated with Core Binding Factor (CBF) - Acute Myeloid Leukemia (AML) Cause Hypersensitivity of KIT to Its Natural Ligand Stem Cell Factor.

The FLT3-D324N Variant Is a Functionally Silent Polymorphism in the FLT3 Gene and May Be Associated with a Higher Risk for AML.

Mutations in the tyrosine kinase domain of FLT3 define a new molecular mechanism of acquired drug resistance to PTK inhibitors in FLT3-ITD–transformed hematopoietic cells

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ASH Publications

American Society of Hematology

ABT-737 Neutralizes Resistance to FLT3 Inhibitor Treatment Mediated by Overexpression of BCL2 in Primary AML Blasts.

KIT -D816 mutations in AML1-ETO -positive AML are associated with impaired event-free and overall survival

The AML1-ETO Fusion Gene and the FLT3 Length Mutation Collaborate in Inducing Acute Leukemia in a Murine Bone Marrow Transplantation Model.

KIT exon 8 mutations associated with core-binding factor (CBF)–acute myeloid leukemia (AML) cause hyperactivation of the receptor in response to stem cell factor

KIT Exon 8 Mutations Associated with Core Binding Factor (CBF) - Acute Myeloid Leukemia (AML) Cause Hypersensitivity of KIT to Its Natural Ligand Stem Cell Factor.

The FLT3-D324N Variant Is a Functionally Silent Polymorphism in the FLT3 Gene and May Be Associated with a Higher Risk for AML.

Mutations in the tyrosine kinase domain of FLT3 define a new molecular mechanism of acquired drug resistance to PTK inhibitors in FLT3-ITD–transformed hematopoietic cells

Email alerts

ASH Publications

American Society of Hematology

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