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January 13, 2016

Damon Runyon-Rachleff Innovation Awards granted for pioneering ideas in cancer research

New York, NY (January 13, 2016) – The Damon Runyon Cancer Research Foundation announced that seven scientists with novel approaches to fighting cancer have been named 2016 recipients of the Damon Runyon-Rachleff Innovation Award. The grant of $300,000 over two years is awarded each year to early career scientists whose projects have the potential to significantly impact the prevention, diagnosis and treatment of cancer. Each awardee will have the opportunity for up to two additional years of funding (up to four years total for $600,000). Continued support for years three and four will be granted to those awardees who demonstrate significant progress on their proposed research during the first two years of the award.

The Damon Runyon-Rachleff Innovation Award funds cancer research by exceptionally creative thinkers with “high-risk/high-reward” ideas who lack sufficient preliminary data to obtain traditional funding. The awardees are selected through a highly competitive and rigorous process by a scientific committee comprised of leading cancer researchers who are innovators themselves. Only those scientists with a clear vision and passion for curing cancer are selected to receive the prestigious award. 

This program was established thanks to the generosity of Andy and Debbie Rachleff.

2016 Damon Runyon-Rachleff Innovators:

Christin E. Burd, PhD

Ohio State University, Columbus

The RAS oncogene is mutated in 20% of all human cancers. Different types of mutations occur that promote cancer initiation and progression, yet we do not yet understand the specificity of how each mutation affects RAS’ ability to promote cancer. Unfortunately, despite decades of scientific effort, there are no effective therapies to directly target RAS mutant cancers. Dr. Burd proposes novel, mutation-specific studies of RAS in a variety of tumor types, starting with melanoma, thyroid cancer, and acute myeloid leukemia (AML). The reason why each cancer type appears to “prefer” one RAS mutant over another is unknown; however, she postulates that the subtle differences between mutants are critical for tumor formation. Her research will lead to new understanding of RAS mechanism and function, resulting in better design of novel therapeutics to target RAS for treatment of cancer.   

Jason M. Crawford, PhD

Yale University, New Haven

Humans and the microbes in and on our bodies (“microbiota”) continuously interact in ways that influence health and disease—ways that we do not yet fully understand. Dr. Crawford, a chemical biologist, focuses on defining the bacterial contributions to colorectal cancer. DNA-damaging toxins (genotoxins) produced by bacteria in the human gut serve as cancer risk factors. He has developed an innovative genomics platform called M-PAIR, which he will use to identify novel cancer risk factors produced by the bacteria in the human gut. His findings will provide a foundation for development of anticancer compounds for cancer prevention and treatment.

Piero D. Dalerba, MD

Columbia University, New York

Dr. Dalerba proposes to use next-generation single cell genomics to analyze cancer stem cells, poorly characterized cells that are able to seed malignant tumors. He has created a model of colorectal cancer that enables the study of genetic and phenotypic properties of cancer stem cells. This research will advance understanding of the biological identity and clinical significance of these cells in colorectal cancer initiation, progression, and relapse. He aims to determine how to therapeutically target these cancer stem cells with existing drugs and/or novel compounds.

Scott J. Dixon, PhD

Stanford University, Stanford

To sustain rapid growth, cancer cells change and increase their metabolism, taking up and utilizing large amounts of glucose. One product of metabolism in all cells is methylglyoxal (MG), which is toxic if it accumulates in the cell; therefore, cells have a mechanism to detoxify MG. Dr. Dixon seeks to understand the chemical and biological mechanisms by which MG confers toxicity. He is developing new small molecule inhibitors that will enhance the accumulation of these toxic metabolites in cancer cells, to promote cancer cell-selective death. This work has the potential to uncover a novel means of harnessing the abnormal metabolism of cancer cells and could apply to all cancer types. 

Philip A. Romero, PhD

University of California, Los Angeles

Dr. Romero is a biomedical engineer whose expertise is in the area of microfluidics. He proposes to develop new technology that can be used to detect circulating tumor cells (CTCs) in the bloodstream. CTCs are cells that have detached from a solid primary tumor and entered into the bloodstream; they can go on to colonize distant sites and form metastases. Detecting CTCs is an enormous challenge, as the cells are present at an ultra-low abundance (one out of billions of blood cells). His approach is to develop a highly specific system, a “DNA-based logic circuit,” to detect and profile CTCs, which could ultimately be applied for cancer diagnosis, prognosis indication, and measurement of a patient’s response to treatment.

Peter J. Turnbaugh, PhD

University of California, San Francisco

Variations in drug efficacy and toxicity between patients are a major limitation to the long-term treatment of cancer. Even if the initial treatment is successful, cancers can return due to the emergence of cancer drug resistance. Dr. Turnbaugh seeks to determine how the gut microbiome (bacteria residing in the human body) contributes to drug efficacy and resistance. He will combine microbiology and pharmacology approaches to identify new microbiome-based biomarkers for monitoring and predicting acquired drug resistance. The findings will also have broad implications for development of more effective treatment regimens for patients with colorectal as well as other cancers.

Roberto Zoncu, PhD

University of California, Berkeley

Cancer cell metabolism differs from that of healthy cells because cancer cells have extreme requirements for energy. An organelle inside the cell called the lysosome has recently been defined as a “metabolic signaling center,” which senses cellular nutrient levels and communicates them to a growth regulator protein called mTORC1. Dr. Zoncu proposes to synthesize novel molecules that can specifically disable the lysosomal-mTORC1 signaling pathway as a new means of starving cancer cells and thus blocking tumor growth. He will investigate how this pathway controls the function of the lysosome and another organelle, the mitochondria, in mediating the resilience of cancer cells to challenges such as starvation, hypoxia and chemotherapeutic drugs. This research may impact all cancer types, but particularly pancreatic and lung cancers, which appear to be uniquely sensitive to levels of mTORC1.




To accelerate breakthroughs, the Damon Runyon Cancer Research Foundation provides today’s best young scientists with funding to pursue innovative research. The Foundation has gained worldwide prominence in cancer research by identifying outstanding researchers and physician-scientists. Twelve scientists supported by the Foundation have received the Nobel Prize, and others are heads of cancer centers and leaders of renowned research programs. Each of its award programs is extremely competitive, with less than 10% of applications funded. Since its founding in 1946, the Foundation has invested over over $300 million and funded over 3,500 young scientists. This year, it will commit approximately $15 million in new awards to brilliant young investigators.

100% of all donations to the Foundation are used to support scientific research. Its administrative and fundraising costs are paid from its Damon Runyon Broadway Tickets Service and endowment.

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Yung S. Lie, PhD

Deputy Director and Chief Scientific Officer

Damon Runyon Cancer Research Foundation