S. Vempati

发表

Selective Inhibition of Hdac1 and Hdac2 as a Potential Therapeutic Option for B-all Short Title: B-alls Are Sensitive to an Hdac1/hdac2 Inhibitor

Tina N. Davis, S. Armstrong, J. Qi, 2022 .

Selective Inhibition of HDAC1 and HDAC2 as a Potential Therapeutic Option for B-ALL

Tina N. Davis, S. Armstrong, J. Qi, 2015, Clinical Cancer Research.

AML1–ETO meets JAK2: clinical evidence for the two hit model of leukemogenesis from a myeloproliferative syndrome progressing to acute myeloid leukemia

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

Point mutations in the juxtamembrane domain of FLT3 define a new class of activating mutations in AML.

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

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.

H3K79 methylation profiles define murine and human MLL-AF4 leukemias.

Xiaobo Xia, Andrew L Kung, Scott A Armstrong, 2008, Cancer cell.

MLL-rearranged leukemia is dependent on aberrant H3K79 methylation by DOT1L.

Lars Bullinger, Andrew L Kung, Scott A Armstrong, 2011, Cancer cell.

Arginine 595 is duplicated in patients with acute leukemias carrying internal tandem duplications of FLT3 and modulates its transforming potential.

W. Hiddemann, K. Spiekermann, S. Schnittger, 2007, Blood.

CBL Exon 8/9 Mutants Activate the FLT3 Pathway and Cluster in Core Binding Factor/11q Deletion Acute Myeloid Leukemia/Myelodysplastic Syndrome Subtypes

W. Hiddemann, S. Bohlander, C. Buske, 2009, Clinical Cancer Research.

Selective Inhibition of HDAC1 and HDAC2 as a Potential Therapeutic Option for B-ALL

Tina N. Davis, S. Armstrong, J. Qi, 2015, Clinical Cancer Research.