Research We Fund

In-frame mutations affecting the basic leucine zipper (bZIP) domain of C/EBPα characterize a distinct subset of acute myeloid leukemia with relatively favorable prognosis, though five-year overall survival remains roughly 60%. Using new mouse models, this project will identify targets of endogenous bZIP–mutated C/EBPα. We will test whether modulating mutant-specific targets alters disease course in mouse models and in patient-derived xenografts, thereby nominating new approaches to therapy.

EZB lymphomas, driven by BCL2 translocations and EZH2 mutations, induce macrophages to adopt a supportive role, essential for maintaining the malignant phenotype. This reprogramming suppresses phagocytosis and promotes pro-tumor activation, mediated by immune synapse signaling and cytokine release. Our study aims to identify molecular pathways involved in this macrophage reprogramming and explore restoring anti-tumor functions as a therapeutic approach.

Improving survival for patients with diffuse large B-cell lymphoma requires tailoring treatment to lymphoma genetic heterogeneity, addressing minimal residual disease (MRD), and bringing safer, effective therapies for frail patients who cannot tolerate aggressive regimens. I address these challenges with genomic subtype targeted treatment, bispecific antibody to eliminate MRD, and novel treatment for frail patients. My goal is to improve outcomes by bringing biomarkers to standard of care.

I focus on developing bispecific antibodies (BsAb) for the treatment of B-cell non-Hodgkin lymphoma (B-NHL). We are testing chemo-free epcoritamab or mosunetuzumab combinations in follicular lymphoma, incorporating glofitamab or epcoritamab in the treatment of aggressive lymphomas, studying resistance mechanisms in patient samples from our trials, analyzing our experience to increase BsAb safety. Our goal is to leverage BsAb to improve upon current standards and shift B-NHL treatment paradigms.