Research we fund

In October 2026, TAP made a strategic investment in AvenCell Therapeutics to support the clinical development of investigational, allogeneic, or “off-the-shelf,” CAR-T cell therapy for people with relapsed or refractory blood cancers. 

AvenCell Therapeutics is a clinical-stage biotechnology company developing next-generation allogeneic CAR-T cell therapies for blood cancers. The company’s technology combines healthy donor-derived, gene-edited T cells with a switchable targeting system designed to give physicians greater control over CAR-T activity. Unlike traditional CAR-T therapies that are manufactured individually from a patient's own cells, AvenCell's approach is designed to provide an off-the-shelf therapy that can be available when patients need treatment.

TAP support will help advance the Phase 1b expansion of AVC-201 and generate additional evidence about its safety, durability of response, blood-count recovery, and potential role for patients with AML.

AvenCell is also developing AVC-203, an investigational allogeneic CAR-T therapy targeting CD19 and CD20 for patients with B-cell malignancies, including B-cell lymphomas (NCT07284433). AVC-203 is earlier in clinical development and provides an opportunity to evaluate AvenCell's allogeneic CAR-T platform across another group of blood cancers.

In October 2026, TAP made a strategic investment in AvenCell Therapeutics to support the clinical development of investigational, allogeneic, or “off-the-shelf,” CAR-T cell therapy for people with relapsed or refractory blood cancers. 

AvenCell Therapeutics is a clinical-stage biotechnology company developing next-generation allogeneic CAR-T cell therapies for blood cancers. The company’s technology combines healthy donor-derived, gene-edited T cells with a switchable targeting system designed to give physicians greater control over CAR-T activity. Unlike traditional CAR-T therapies that are manufactured individually from a patient's own cells, AvenCell's approach is designed to provide an off-the-shelf therapy that can be available when patients need treatment.

TAP support will help advance the Phase 1b expansion of AVC-201 and generate additional evidence about its safety, durability of response, blood-count recovery, and potential role for patients with AML.

AVC-201 is AvenCell's lead program and is being developed for relapsed or refractory AML. The therapy targets CD123, a protein found on many AML cells, using a separately administered targeting module that connects the CAR-T cells to the cancer cells. This switchable approach allows treatment activity to be controlled by adjusting or stopping the targeting module, an important feature because CD123 can also be found on healthy blood-forming cells. Early clinical findings have shown encouraging activity in heavily pretreated patients, and the program is advancing into Phase 1b expansion. AVC-201 is being evaluated in the Phase 1/1b RevSTAR-123 clinical trial (NCT05949125).

Acute myeloid leukemia (AML) is the leading cause of leukemia-related deaths despite intensive chemotherapy and stem cell transplantation. New approaches are urgently needed to improve survival. My research focuses on optimizing chimeric antigen receptor (CAR) T cells that target CLEC2A, a newly identified AML-specific target. I aim to expand the therapeutic potential of CLEC2A CAR T cells to safely and effectively treat AML and explore how prior treatments influence CAR T cell response.

Our proposal aims to expand upon a novel, successful strategy to treat chronic myelomonocytic leukemia. It involves use of a novel oral medication (can be taken as a pill) called onvansertib to selectively kill cancer cells and spare normal ones. The goal is to add an arm to study combination of this effective medication with decitabine which is already an approved medication for this cancer.

This five-year study will implement, evaluate, and scale a multilevel intervention to improve clinical trial enrollment among adolescents and young adults and older adults with blood cancers. The intervention combines real-time electronic health record (EHR)-based identification of potentially eligible patients with coordinated provider support, patient-centered trial matching, and navigation through Blood Cancer United’s Clinical Trial Support Center. It will be tested in a three-arm randomized trial at Columbia University Irving Medical Center and adapted for community oncology affiliates, generating real-world evidence to support broader dissemination.

Acute myeloid leukemia (AML) is subject to macrophage-mediated immune clearance, although the mechanisms remain poorly understood. Using genome-wide CRISPRi screens in AML cells co-cultured with macrophages, we identified new regulators of susceptibility to phagocytosis, including a therapeutically targetable link to RHOA signaling. I will dissect the underlying mechanisms and test combinatorial RHOA and PI3Kγ inhibition to nominate novel treatment strategies that overcome AML immune evasion.

MYST family acetyltransferases KAT6A and KAT7 are targetable dependencies in MLLr and NPM1-mutant AML. However, it is unclear how they regulate gene expression and if they have distinct or partially redundant roles. We will deploy systems where endogenous KAT6A or KAT7 can be rapidly degraded, to understand how these proteins regulate chromatin and transcription. By elucidating how KAT6A/KAT7 sustain oncogenic programs, we hope to define how best to use KAT6 and KAT7 inhibitors for AML therapy.

In this study, I will co-opt macrophage quality assurance mechanisms for hematopoietic stem cells (HSCs) to develop a new macrophage-based therapy for AML. I found SFK inhibition increases ‘eat me’ signal Calreticulin (CALR) on leukemic stem cells (LSCs) surface without harming normal HSCs. In this project, I will employ phosphoproteomics and murine models to identify SFK-dependent regulators of CALR and conduct SFK-/- studies in zebrafish to investigate CALR regulation and AML immune clearance.

Myelodysplastic syndromes (MDS) are blood cancers caused by gene mutations that have few treatment options. We are focused on understanding how mutations cause MDS to develop and make the disease worse. We use whole genome sequencing (WGS) of blood cells at serial timepoints to track mutations in patients who are at high risk for developing MDS or already have MDS. By better understanding the genetic changes that cause MDS, we hope to find ways to help prevent it from developing and progressing.

This project explores methionine metabolism as a therapeutic target in acute myeloid leukemia (AML). Methionine addiction is a hallmark of many malignancies. In AML, enzymes and transporters related to methionine metabolism are specifically upregulated in poor-risk and treatment-refractory disease. By characterizing this metabolic dependency, this work aims to establish a mechanistic foundation for exploiting methionine metabolism as a novel treatment strategy in AML.