Area of research
Molecular Biology · Pathology and Forensic Medicine
Research interest
Research interests include Lymphoma Diagnosis and Treatment, Epigenetics and DNA Methylation, Cancer-related gene regulation, and Cancer Genomics and Diagnostics.
Evaluating the analytical validity of circulating tumor DNA sequencing assays for precision oncology
TET2 Deficiency Causes Germinal Center Hyperplasia, Impairs Plasma Cell Differentiation, and Promotes B-cell Lymphomagenesis
Histone demethylase LSD1 is required for germinal center formation and BCL6-driven lymphomagenesis
AICDA drives epigenetic heterogeneity and accelerates germinal center-derived lymphomagenesis
<i>CREBBP</i> Inactivation Promotes the Development of HDAC3-Dependent Lymphomas
EZH2 and BCL6 Cooperate to Assemble CBX8-BCOR Complex to Repress Bivalent Promoters, Mediate Germinal Center Formation and Lymphomagenesis
Rationally designed BCL6 inhibitors target activated B cell diffuse large B cell lymphoma
miR-181a negatively regulates NF-κB signaling and affects activated B-cell–like diffuse large B-cell lymphoma pathogenesis
The histone lysine methyltransferase KMT2D sustains a gene expression program that represses B cell lymphoma development
TET1 is a tumor suppressor of hematopoietic malignancy
Epigenomic evolution in diffuse large B-cell lymphomas
DNA Methylation Dynamics of Germinal Center B Cells Are Mediated by AID
IL10 receptor is a novel therapeutic target in DLBCLs
CTCF Haploinsufficiency Destabilizes DNA Methylation and Predisposes to Cancer
Variability in DNA methylation defines novel epigenetic subgroups of DLBCL associated with different clinical outcomes
EZH2 Is Required for Germinal Center Formation and Somatic EZH2 Mutations Promote Lymphoid Transformation
Mechanism-Based Epigenetic Chemosensitization Therapy of Diffuse Large B-Cell Lymphoma
Aberration in DNA Methylation in B-Cell Lymphomas Has a Complex Origin and Increases with Disease Severity
Downregulation of FOXP1 is required during germinal center B-cell function
MALT1 Small Molecule Inhibitors Specifically Suppress ABC-DLBCL In Vitro and In Vivo