Tobias M. Kohl

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.

W. Hiddemann, K. Spiekermann, S. Schnittger, 2005, Blood.

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.

W. Hiddemann, K. Spiekermann, S. Schnittger, 2004, Blood.

The AML1-ETO fusion gene and the FLT3 length mutation collaborate in inducing acute leukemia in mice.

W. Hiddemann, S. Bohlander, C. Buske, 2005, The Journal of clinical investigation.

1 KIT-D 816 mutations in AML 1-ETO positive AML are associated with impaired event-free and overall survival

W. Hiddemann, T. Haferlach, K. Spiekermann, 2005 .

BH3 mimetic ABT-737 neutralizes resistance to FLT3 inhibitor treatment mediated by FLT3-independent expression of BCL2 in primary AML blasts

W. Hiddemann, S. Bohlander, C. Buske, 2007, Leukemia.

Transformation by Oncogenic Mutants and Ligand-Dependent Activation of FLT3 Wild-type Requires the Tyrosine Residues 589 and 591

W. Hiddemann, C. Buske, K. Spiekermann, 2008, Clinical Cancer Research.

D324N single‐nucleotide polymorphism in the FLT3 gene is associated with higher risk of myeloid leukemias

W. Hiddemann, T. Haferlach, K. Spiekermann, 2006, Genes, chromosomes & cancer.