People

Murakami Lab

Chase Weizer, BS

Research Technician, 2022-Present

Chase Weizer is a research technician who seeks to identify developmental determinants of relapse in B-cell acute lymphoblastic leukemia (B-ALL) in order to effectively target minimal residual disease and promote long-term disease-free survival in patients. He earned his Bachelor of Science from Dickinson College. Currently, he investigates the efficacy of novel investigational agents in early phase clinical trials for both newly diagnosed and relapsed/refractory B-ALL patients, the capturing of epigenetic states of B-ALL cells marked by particular cell surface and intracellular markers and to better associate their abundance with different differentiation states and lineage restrictions, and targeting E-selectin biology to modulate the drug-tolerant persister state in B-ALL. Outside of the lab, he likes visiting breweries, tennis, and cooking. He can be contacted at Chase_Weizer@dfci.harvard.edu.

InTAC-seq

InTAC-seq is a method of capturing epigenetic states of cells marked by particular transcription factors to better associate these factors with differentiation and lineage restriction in B-ALL. We aim to perform InTAC-seq to link transcription factor abundance to chromatin changes in primary human B-ALL patient specimens. Using InTAC-seq, we aim to profile chromatin accessibility landscapes associated using a combination of extracellular, cell surface markers and intracellular, transcriptional factors in patient-derived peripheral blood and bone marrow mononuclear cells to better characterize and identify B-ALL progenitors.

Targeting E-selectin biology to modulate the drug-tolerant persister state in B-ALL

Targeting E-selectin receptor/ligand interactions is one methodology of inhibiting the ability of B-ALL progenitor cells to localize in the bone marrow microenvironment and thus avoid/adapt to treatment. We aim to generate sialofucosylation profiles of canonical and non-canonical E-selectin ligands in primary human B-ALL patient specimens spanning different molecular subtypes to correlate these profiles with engraftment efficiency as a functional surrogate for bone marrow homing and leukemia-initiating capacity. Targeting E-selectin receptor/ligand interactions with standard therapy in combination with glycomimetic therapy, we aim to evaluate the impact in vivo glycomimetic antagonism on abrogating leukemogenesis and reducing minimal residual disease burden.