R. Schwab

The protein tyrosine kinase inhibitor SU5614 inhibits FLT3 and induces growth arrest and apoptosis in AML-derived cell lines expressing a constitutively activated FLT3.

W. Hiddemann, C. Buske, K. Spiekermann, 2003, Blood.

Xenogeneic human anti-mouse T cell responses are due to the activity of the same functional T cell subsets responsible for allospecific and major histocompatibility complex-restricted responses

S. Swain, R. Dutton, J. Yamamoto, 1983, The Journal of experimental medicine.

Overexpression and constitutive activation of FLT3 induces STAT5 activation in primary acute myeloid leukemia blast cells.

W. Hiddemann, K. Spiekermann, Ksenia Bagrintseva, 2003, Clinical cancer research : an official journal of the American Association for Cancer Research.

Constitutive activation of STAT3 and STAT5 is induced by leukemic fusion proteins with protein tyrosine kinase activity and is sufficient for transformation of hematopoietic precursor cells.

W. Hiddemann, K. Spiekermann, R. Schwab, 2002, Experimental hematology.

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.