Four Young Scientists Receive Damon Runyon–Sohn Pediatric Cancer Research Fellowship Awards


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The Damon Runyon Cancer Research Foundation has named four outstanding young scientists as recipients of the prestigious Damon ­Runyon–Sohn Pediatric Cancer Research 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 4-year award totaling $248,000. Since 2012, this award has supported 18 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 United States.

2016 Damon Runyon–Sohn Fellows

Challice L. Bonifant, MD, PhD, with her sponsor Pavan Reddy, MD, at the University of Michigan, is studying how best to direct the immune system to combat acute myeloid leukemia (AML). By specifically directing T immune cells to AML, she hopes to make therapy stronger and more effective while also reducing toxicity. She is exploring the activity of T cells targeting multiple AML-specific antigens that do not affect normal cells. 

Michael A. Koldobskiy, MD, PhD, with his sponsor Andrew P. Feinberg, MD, at Johns Hopkins University, studies the ways that cancer cells rely on “epigenetic” modifications. Variability of epigenetic marks allows cancer cells flexibility in turning genes “on” and “off” and may account for resistance to treatment. By dissecting the mechanisms of epigenetic modification in pediatric acute lymphoblastic leukemia (ALL), the most common cancer in children, he aims to identify new targets for treatment.

Tamara P. Miller, MD, with her sponsor Richard Aplenc, MD, PhD, at the Children’s Hospital of Philadelphia, focuses on improving how the side effects of leukemia treatment are reported. Currently, toxicities of cancer treatment for patients enrolled on clinical trials are identified through manual review of the medical record, but prior work has shown that this method of identification leads to underreporting of side effects. She aims to develop a new method that uses electronic medical record data to identify and report toxicities during treatment for leukemia. Her goals are to show that this new method is more accurate than the current system used in clinical trials and to apply this method to describe the true rates of toxicities of leukemia therapy.

Cara A. Rabik, MD, PhD, with her sponsor Patrick A. Brown, MD, at Johns Hopkins University, is examining how mutations in the WT1 gene result in methylation changes in AML. WT1 recruits the machinery necessary for demethylation to its target genes, ultimately regulating gene expression. When WT1 is mutated, these genes remain methylated and inactive, preventing normal hematopoiesis. She is identifying WT1 target genes and mapping their methylation landscape both in leukemic and normal settings. She will also test drugs designed to cause demethylation to evaluate whether these drugs can treat the leukemia caused by mutations in WT1. ■

Challice L. Bonifant, MD, PhD

Challice L. Bonifant, MD, PhD

Pavan Reddy, MD

Pavan Reddy, MD

Michael A. Koldobskiy, MD, PhD

Michael A. Koldobskiy, MD, PhD

Andrew P. Feinberg, MD

Andrew P. Feinberg, MD

Tamara P. Miller, <br />MD

Tamara P. Miller,
MD

Richard Aplenc, MD, PhD

Richard Aplenc, MD, PhD

Cara A. Rabik, MD, PhD

Cara A. Rabik, MD, PhD

Patrick A. Brown, MD

Patrick A. Brown, MD

 



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