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Grantees

Fox Chase Cancer Center Title of Grant: Investigating the essential roles of Kelch-like family member KLHL11 in the pathogenesis of Anaplastic Large Cell Lymphoma and in normal T cells Description:          This project will seek to address the importance of a novel E3 ligase, KLHL11, in the pathogenesis of T cell lymphoma and in normal T […]

Title of Grant:       Role of co-stimulatory domains in CAR T cell dysfunction Description: Cell-based immune therapies have demonstrated impressive success in the treatment of blood cancers, however most patients treated with available cellular immunotherapies are not cured. The goal of this proposal is to identify the molecular pathways responsible for failure of these therapies and […]

Title of Grant:       Dissecting the role of the unfolded protein response in type 1 CALRmutated myelofibrosis  Description: The experiments proposed will help to answer why, among the two types of CALR mutations found in MPN patients, only one type causes myelofibrosis, the most deadly and difficult to treat disease among the three MPN types. This […]

Title of Grant:       Elucidating and targeting IDH2 mutations in T cell lymphoma  Description: Drugs that target mutant forms of the metabolic enzyme isocitrate dehydrogenase 2 (IDH2) are a promising appraoch to treat some cancers. The proposed research will uncover how mutant IDH2 causes T cell lymphoma and determine whether inhibiting mutant IDH2 offers an effective […]

Title of Grant: “Development of anti-KIT antibodies and immunotoxins as therapeutics and HSCT conditioning agents for pediatric acute myeloid leukemia (AML)” Acute myeloid leukemia (AML) is a frequent type of leukemia with harsh treatments and poor outcomes. We have pioneered several new antibody therapies targeting an important receptor found both on blood stem cells and AML, […]

“Increasing the Therapeutic Index of Chimeric Antigen Receptor T cells for T cell Lymphomas” Our goal is to bring the unquestioned power of CAR T cell therapy to bear on T cell lymphomas, a group of diseases with a poor prognosis and few treatment options. We will use the latest gene-editing tools to make an […]

“Reconstructing the differentiation dynamics and genealogy of cancer cells in individual patients with myeloproliferative neoplasms using single-cell sequencing” In a type of blood cancer called myeloproliferative neoplasm, the same genetic alteration results in drastically different forms of the disease in different patients. To understand this discrepancy, we will measure the molecular profile of individual cells […]

“Targeting the Innate Immunity-Independent Function of STING in treating AML” This proposal is to test if inhibiting a deubiquitinase named OTUD7B retards AML growth. We found that AML growth is controlled by an immunity sensor STING through activating an oncogenic kinase called mTOR. This process is facilitated by OTUD7B. Thus, inhibiting OTUD7B suppresses STING-mediated mTOR […]

“A simple dietary supplement to improve pediatric blood cancer therapy” We propose to improve the use of methotrexate – the standard pediatric leukemia drug – with a simple dietary supplement. By enhancing methotrexate’s efficacy, and better monitoring patients’ responses to the drug, we aim to reduce the therapy’s long-term side effects and offer hope to […]

“B Cell Specific DNA Damage Responses Prevent Leukemic Transformation” Pediatric acute lymphoblastic leukemia occurs as a result of genetic mutations that block normal development of immune cells and promote continued expansion of cancer cells. The goals of Dr. Bednarksi’s project is to understand how cells prevent generation of these mutations and how cells are eliminated […]

“The role of SIRT1 in the pathogenesis and treatment of T-Cell Acute Lymphoblastic Leukemia” T-Cell Acute Lymphoblastic Leukemia (T-ALL) is an aggressive blood cancer where 20-50% of patients relapse, and there are few therapeutic options at this stage. Notch1 activating mutations are the main driver in T-ALL. However, responses observed with targeted therapies against NOTCH1 […]

“Biology and Therapeutic Targeting of Mutant Calreticulin in Myeloproliferative Neoplasms” Somatic mutations in celreticulin (CALR)are frequent and disease-initiating in myeloproliferative neoplasms (MPN). Dr. Mullally’s laboratory recently elucidated the mechanism by which mutant CALR is oncogenic and induces MPN. Building on this work and guided by strong preliminary data they have generated, she will now identify […]