Grant Finder

LLS investigators are outstanding scientists at the forefront of leukemia, lymphoma and myeloma research at centers throughout the world. Search to see the many research projects that LLS is currently funding.

Grant: 6527-18 | Translational Research Program (TRP):

Location:Dana-Farber Cancer Institute, Boston, Massachusetts 02215

Year: 2017

Project Title: Assessment Of Epigenetic Reprogramming Of The T Cell Response To CTLA-4 Blockade In AML

Project Summary:

The prognosis for patients with relapsed or refractory acute myeloid leukemia (AML)/myelodysplastic syndrome (MDS) whose disease comes back is poor, and innovative new therapeutic approaches are urgently needed. We conducted and published results from a clinical trial for patients whose blood cancer came back after bone marrow transplantation with ipilimumab, which is an antibody drug that uses the immune system to kill cancer cells. A small number of patients, including those with relapsed AML, had durable clinical responses.

Grant: 6534-18 | Translational Research Program (TRP):

Location:Yale University, New Haven, Connecticut 06520-8327

Year: 2017

Project Title: Exploiting Mutant IDH1/2-induced BRCAness With PARP Inhibitors As A Novel AML/MDS Therapy.

Project Summary:

We have identified a novel approach to treat certain types of leukemias that harbor a mutation in key genes that are involved in cellular metabolism. We found that these mutations create an altered chemical in the cell, which blocks the ability of tumor cells to repair broken DNA. This "achilles heel" can be exploited by treating such tumors with DNA damaging agents combined with DNA repair inhibitors.

Grant: 6532-18 | Translational Research Program (TRP):

Location:The Regents of the University of California, San Francisco, San Francisco, California 94143

Year: 2017

Project Title: Inducing Effective Anti-leukemic Immunity With Novel AML Vaccines Expressing CD80/IL-15/IL-15R-alpha

Project Summary:

Patients with high-risk acute myelogenous leukemia (AML) have poor outcomes because current drug regimens fail to eradicate disease. Transplants of bone marrow or peripheral blood stem cells from matched related, or unrelated donors (allo-transplants) improve survival due to elimination of residual AML by immune cells present in donor cell populations. However, many patients are not eligible for allo-transplants, either because they lack suitable donors, or because they have pre-existing conditions making transplant too risky.

Grant: 1346-18 | Career Development Program (CDP):

Location:University of Cincinnati, Cincinnati, Ohio 45221-0222

Year: 2017

Project Title: The Oncogenic Role And Underlying Mechanism Of TET1 In Acute Myeloid Leukemia

Project Summary:

Acute myeloid leukemia (AML) is one of the most common and fatal forms of hematopoietic malignancies. Thus, it is urgent to better understand the mechanisms underlying the pathogenesis of AML, and on the basis of such understanding, to develop novel therapies with higher efficacy and minimal side effects to treat AML. The properties of cancer are often determined by the proteins that are expressed from information provided by the genes in the cell.

Grant: R6507-18 | Translational Research Program (TRP):

Location:Dana-Farber Cancer Institute, Boston, Massachusetts 02215

Year: 2017

Project Title: MYD88 And CXCR4 WHIM-like Mutations Offer A Targeted Treatment Approach For WM

Project Summary:

Ibrutinib is an active drug that is approved by the U.S. FDA and European Medicines Agency for the treatment of WM. WM patients who have a mutation in MYD88 (over 90% do) respond to ibrutinib, while those with mutations in CXCR4 show lower levels of response and delayed responses. Despite the overall high levels of response to ibrutinib among WM patients, the achievement of complete responses is lacking. We discovered as part of the LLS sponsored study that two important pathways exist by which mutated MYD88 can support growth and survival of WM cells.

Grant: 5462-18 | Career Development Program (CDP):

Location:Yale University, New Haven, Connecticut 06520-8327

Year: 2017

Project Title: A Protein Degradation Approach For The Treatment Of Acute Myeloid Leukemia

Project Summary:

Many cancers result from a genetic mutation causing an “always on” protein. Current treatments are based on the deactivation of the proteins by blocking that protein’s active site. Herein I propose an alternative approach in which proteins are permanently degraded rather than temporarily deactivated, which may prove to be a more favourable form of therapy. To do this, I will take advantage of the cell’s own natural ability to degrade its own proteins when they are in excess or no longer needed.

Grant: 1344-18 | Career Development Program (CDP):

Location:Fred Hutchinson Cancer Research Center, Seattle, Washington 98109-1024

Year: 2017

Project Title: The Biological And Therapeutic Consequences Of SF3B1 Mutations In Myelodysplastic Syndromes

Project Summary:

Myelodysplastic syndromes (MDS) are a group of blood disorders characterized by impaired differentiation of hematopoietic stem cells into functional blood cells. MDS frequently has a poor prognosis and is associated with a high risk of transformation into acute myeloid leukemia. There are few treatment options for MDS, largely because the underlying molecular changes that drove MDS were not known until recently. 

Grant: 5465-18 | Career Development Program (CDP):

Location:The Regents of the University of California, San Francisco, San Francisco, California 94143

Year: 2017

Project Title: Inhibiting The Palmitoylation/Depalmitoylation Cycle As A Selective Therapeutic Strategy In NRAS Mutant Leukemia.

Project Summary:

Acute myeloid leukemia (AML) is an aggressive blood cancer that affects children and adults. Recent advances for sequencing the DNA of leukemia cells have greatly advanced our understanding of the genetic causes of AML; however, this new knowledge has not yet resulted in better treatments. 

Grant: 3380-18 | Career Development Program (CDP):

Location:Dana-Farber Cancer Institute, Boston, Massachusetts 02215

Year: 2017

Project Title: Interrogating The Sf3b1 Mutated/Atm Deleted Mouse As A Novel Faithful Model Of Chronic Lymphocytic Leukemia

Project Summary:

Human genomic analyses have defined the complex genetic heterogeneity of chronic lymphocytic leukemia (CLL) as the most common indolent B-cell malignancy. These studies have revealed that selection of certain genetic alterations occurs throughout disease progression and correlates with therapy failure. Despite the remarkable efficacy of a number of recently introduced therapies, CLL remains incurable, and resistance to these novel drugs is challenging the clinical management of CLL patients.

Grant: 6530-18 | Translational Research Program (TRP):

Location:The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19178-1457

Year: 2017

Project Title: CBL Regulation Of Ubiquitination And Cytokine Signaling In Myeloid Malignancies

Project Summary:

CBL mutations are found in diverse myeloid malignancies, MDS (myelodysplastic syndrome), myeloproliferative neoplasm (MPN), acute myeloid leukemia (AML), and particularly MDS/MPN overlap syndrome, a disease with both MDS and MPN features. MDS/MPN overlaps are often diagnosed as juvenile myelomonocytic leukemia (JMML) or chronic myelomonocytic leukemia (CMML) in which CBL mutations have the most occurrence, ~20%.