Area of research
Hematology · Biotechnology
Research interest
Research interests include Acute Myeloid Leukemia Research, Cancer Research and Treatments, Virus-based gene therapy research, and CAR-T cell therapy research.
Intra-Leukemic Interferon Signaling Suppresses Expansion and Mediates Chemoresistance in Human AML
Inhibition of DOCK1 prevents the clonal expansion of high-risk TP53-mutant clonal hematopoiesis induced by genotoxic stressors.
DNMT3A R882H Is Not Required for Disease Maintenance in Primary Human AML but Is Associated with Increased Leukemia Stem Cell Frequency
Dysregulated Lipid Synthesis by Oncogenic IDH1 Mutation Is a Targetable Synthetic Lethal Vulnerability
Toll‐like receptor 7/8‐matured RNA‐transduced dendritic cells as post‐remission therapy in acute myeloid leukaemia: results of a phase I trial
Response assessment in acute myeloid leukemia by flow cytometry supersedes cytomorphology at time of aplasia, amends cases without molecular residual disease marker and serves as an independent prognostic marker at time of aplasia and post-induction
Coexpression profile of leukemic stem cell markers for combinatorial targeted therapy in AML
Persistence of pre-leukemic clones during first remission and risk of relapse in acute myeloid leukemia
Minimal Residual Disease (MRD) Detection By Flow Cytometry Complements Molecular MRD Assessment in AML
Diagnosis of <scp>CLL</scp> revisited: increased specificity by a modified five‐marker scoring system including <scp>CD</scp>200
Persistence of pre-leukemic clones during first remission and risk of relapse in acute myeloid leukemia
Induction of Antigen-Specific T-Cell Responses through Dendritic Cell Vaccination in AML: Results of a Phase I/II Trial and Ex Vivo Enhancement By Checkpoint Blockade
Steroids Abrogate BiTE® Antibody Construct-Mediated Cytotoxicity in Primary AML Cells
Blockade of the PD-1/PD-L1 axis augments lysis of AML cells by the CD33/CD3 BiTE antibody construct AMG 330: reversing a T-cell-induced immune escape mechanism
CD33 target validation and sustained depletion of AML blasts in long-term cultures by the bispecific T-cell–engaging antibody AMG 330
Acetylsalicylic Acid Reduces the Severity of Dextran Sodium Sulfate-Induced Colitis and Increases the Formation of Anti-Inflammatory Lipid Mediators