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Grantees

The role of inflammation during STAG-2 mutant MDS and AML initiation and progression Although we know that cohesin mutations cause myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML), we currently cannot target these mutations in a specific manner. My project will identify unique vulnerabilities in cohesin-mutant MDS and AML with the goal to develop less […]

Modulating UBA 1 to treat Myelodysplastic Syndrome Myelodysplastic syndrome (MDS) is a common blood cancer which is caused by genetic mutations. Our lab has identified a new genetic driver of MDS, UBA1, and here we propose to study why these mutations cause disease and how to reverse these defects to help patients.

The Epigenetic Mechanism of Vitamin C in Tumor Suppression Low vitamin C (VC) intake is linked to increased lymphoma risk. However, how VC prevents cancers is unclear. We hypothesize that VC protects our epigenome, which affects how our DNA is read, and helps turn on cancer-suppressing genes. We will identify the proteins that partner with […]

Targeting SLAMF7 using Chimeric Antigen Receptor T-cell Therapy and HMGA1 in Myelofibrosis We propose a novel approach to treating myelofibrosis, a fatal blood cancer, using chimeric antigen receptor (CAR) T-cells. We will study the effects of inhibiting fibrosis-inducing cells with CAR T-cells in mouse models with and without HMGA1 insufficiency. Data from this study will […]

Dissecting MYC Influence on mRNA Processing and  Protein Translation During Acute Myeloid Leukemia Initiation Therapeutic options for patients with Acute Myeloid Leukemia (AML) remain limited, and relapse is common. No studies have addressed the cellular and molecular consequences of MYC overexpression and mutations in AML. Through in-vitro and in-vivo experiments in genetically engineered mouse models, […]

Investigating the role of oncogenic dependency in NPM1-mutant  AML The NPM1 gene is mutated in 20-35% of acute myeloid leukemias (AML). However, it is unclear how mutant NPM1 drives leukemia development and whether the imparted cellular changes are reversible. This proposal aims to define the cellular consequences of mutant NPM1 and whether loss/inhibition of NPM1 […]

Project Title: Therapeutic use of HDL to enhance the anti-leukemia effects of allo-HCT while preventing GvHD Project Description: Clinical goal of bone marrow transplantation (BMT) is to enhance anti-leukemia effects of BMT while preventing its major side effect, graft-versus-host disease (GvHD). We have identified gene products that are modulated by HDL, the good cholesterol, as […]

Project Title: Developing genomic biomarkers for multiple myeloma and T-cell immunotherapy from cell-free DNA Project Description: Multiple myeloma (MM) is the second most common blood cancer. While new treatments have emerged for MM in the last decade, tests to diagnose MM have not changed. We will develop ‘liquid biopsies’ to diagnose, detect, and study MM, […]

Project Title: Overcoming CAR T Resistance in Acute Myeloid Leukemia by Using Systemic Vaccination Project Description: This project aims to investigate the mechanisms by which a novel cancer vaccine enhances tumor rejection caused by genetically modified immune cells against acute myeloid leukemia. Genetically engineered immune cells have not yet shown great promise against this specific […]

Project Title: Recipient specific CAR-T cells for AML relapse after allogeneic hematopoietic stem cell transplantation Project Description: Bone marrow transplants are the best treatment for some leukemia patients, but there are few good treatments for leukemia that relapses after transplant. In this project, we exploit genetic differences between patients and their donors to make immune […]

Project Title: Chemical genetic dissection of oncoenhancers in multiple myeloma Project Description: Multiple myeloma is caused by faulty activation of growth genes. Our research aims to develop new therapeutics that target the factors driving this malfunctioning expression. The support of Gabrielle’s Angel Foundation will enable us to develop tools to study the myeloma epigenome and […]

Project Title: A multiomic dissection of clonal evolution in MDS Project Description: Our research will serve to identify patterns of “clonal evolution”, wherein multiple distinct populations of similar cells, called subclones, gain or lose prominence as they react to the treatment given. This project will allow us to leukemia cell “family trees” in a patient […]