Four young pediatric cancer research fellows earn $1 million in awards
The Damon Runyon Cancer Research Foundation has named four outstanding young scientists as recipients of the prestigious Damon Runyon-Sohn Pediatric Cancer Fellowship Award, committing nearly $1 million to help address a critical shortage of funding for pediatric cancer research.
The Fellowship Award provides funding to basic scientists and clinicians who conduct research with the potential to significantly impact the prevention, diagnosis or treatment of one or more pediatric cancers. Each recipient receives a four-year award totaling $231,000. Since 2012, this award has supported twenty-two innovative pediatric cancer researchers who were selected through a highly competitive process that includes evaluation by a prestigious committee of pediatric oncologists from the leading cancer centers in the U.S.
"The program provides critically needed support for high quality young investigators working on high impact pediatric cancer research. We need their brilliant minds focused on curing childhood cancers. That is why this award is so important," says Andrew L. Kung, MD, PhD, Chair of the Damon Runyon-Sohn Pediatric Cancer Fellowship Award Committee, and Chair of the Department of Pediatrics, Memorial Sloan Kettering Cancer Center.
Because cancer occurs less frequently in children and young adults than in the adult population, pediatric cancer research does not receive significant funding from either the National Cancer Institute (only four percent of its budget) or the biopharmaceutical industry. To help fill this gap, in 2012, the Sohn Conference Foundation, dedicated to curing pediatric cancers, partnered with the Damon Runyon Cancer Research Foundation, the leading charity supporting innovative young cancer researchers, to establish the award. The Sohn Conference Foundation has committed nearly $2.7 million to the program to date. The award program continues to receive additional funding and recognition within the philanthropic community.
"Our Damon Runyon-Sohn fellows are already making great progress investigating pediatric cancer pathology ," says Evan Sohn of the Sohn Conference Foundation. "We are inspired by the emerging talent of the new 2017 Damon Runyon-Sohn fellows and believe they too will make significant contributions in outsmarting cancer."
2017 Damon Runyon-Sohn Fellows
Robert L. Bowman, PhD, with his sponsor Ross L. Levine, MD, at Memorial Sloan Kettering Cancer Center, New York, focuses on acute myeloid leukemia (AML), a blood cancer that can be characterized by successive development of genetic mutations. While some mutations are found in nearly every cell of the disease, others are found in sub-populations and are thought to arise at later stages of disease development. It remains unclear if these late mutations are necessary for leukemic progression and are actionable therapeutic targets. He aims to develop models to test the oncogenic dependency of one of the most commonly mutated genes in AML, FLT3. Further models will be developed to understand the role of mutation order in AML disease development in both children and adults.
Marissa Rashkovan, PhD, with her sponsor Adolfo A. Ferrando, MD, PhD, at Columbia University, New York, studies T-cell acute lymphoblastic leukemia (T-ALL), an aggressive hematologic malignancy that accounts for 10-15% of pediatric and 25% of adult ALL cases. While survival rates have improved with intensified treatment regimens, 25% of pediatric T-ALL cases still relapse because of refractory disease. Furthermore, the intensity of these treatment regimens has led to increased secondary effects in these children later in life. This underscores the need for the development of efficient, targeted and highly specific anti-leukemic therapies to treat T-ALL. Dr. Rashkovan studies a distinct subgroup of immature T-ALL, ETP-ALL, which phenotypically resembles early thymic progenitors (ETPs), has been associated with early relapse, and poor prognosis. There is a particularly urgent need for targeted therapies for ETP-ALL, which is notoriously difficult to treat. She will assess the metabolic vulnerabilities of ETP-ALL in order to propose new, targeted therapies which could be beneficial for the treatment of this high-risk leukemia group.
Yadira M. Soto-Feliciano, PhD, with her sponsor C. David Allis, PhD, at The Rockefeller University, New York, is examining the mechanisms underlying pediatric acute myeloid leukemia (AML), which has the lowest survival rate among all pediatric cancers. MLL gene rearrangements (MLL-r) occur in about 20% of children diagnosed with AML. This subtype of leukemia is exquisitely sensitive to inhibition of the interaction between MLL and the chromatin adaptor Menin. Dr. Soto-Feliciano is combining genetic, genomics, and mouse modeling approaches to identify factors that regulate the function of Menin in MLL-r and non-MLL-r leukemia. The identification of cellular mechanisms that mediate the response to Menin-MLL inhibitor-based therapies (already in pre-clinical studies), will inform us about the molecular mechanisms driving acute leukemia. She anticipates that the results of these experiments will provide a better understanding of gene expression programs and chromatin landscapes governing the leukemic state. In addition, this project has the potential to identify novel dependencies that can lead to development of novel drug targets for the treatment of pediatric leukemia.
Kathryn R. Taylor, PhD, with sponsor Michelle L. Monje, MD, PhD, at Stanford University, Stanford, is investigating the impact of neural activity on pediatric high-grade glioma (pHGG) invasion. The innate ability of pHGGs to diffusely infiltrate healthy brain tissue is a classical hallmark of the disease, which represents a major contributor to the devastating prognosis. Using optogenetic techniques to stimulate neuronal activity, she will directly and noninvasively test the effect of activity-dependent secreted proteins on tumor cell invasion in human cancer cells and animal models. She plans to confirm the pro-infiltrative effect of candidate proteins on pHGG and subsequently uncover the mechanisms by which they alter the molecular dynamics of the tumor cell. Her hope is to highlight a novel means by which the neural microenvironment drives glioma progression and most importantly identify a new set of therapeutic targets to limit glioma spread.
Provided by Damon Runyon Cancer Research Foundation
