Public Release: 

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

Damon Runyon Cancer Research Foundation awards $2.1 million to 9 innovative early career scientists

Damon Runyon Cancer Research Foundation

New York, NY (January 5, 2017) - The Damon Runyon Cancer Research Foundation announced that nine scientists with novel approaches to fighting cancer have been named 2017 recipients of the Damon Runyon-Rachleff Innovation Award. Three initial grants of $300,000 over two years were awarded to four early career scientists (two individuals and one collaborative team) 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). This year, continued "Stage 2" support was granted to five awardees who demonstrated 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.

New 2017 Damon Runyon-Rachleff Innovators:

Benjamin L. Martin, PhD and David Q. Matus, PhD
Stony Brook University, Stony Brook
Hallmarks of cancer progression are increases in both uncontrolled proliferation and invasive behavior, leading to the spread of tumor cells throughout the body. This collaborative project is founded upon an experimental observation made by Dr. Matus, in the model roundworm, C. elegans, that cell invasion and cell division are mutually exclusive behaviors. In other words, a cell cannot simultaneously invade and divide. This functional link between cell cycle arrest and invasive behavior has not been directly made before, although in a variety of cancers there is correlative data suggesting that tumor cells become less proliferative during invasion. Cell invasive behavior occurs during normal embryonic development, immune surveillance, and is dysregulated during metastatic cancer progression. As two cell and developmental biologists, Drs. Matus and Martin will leverage their expertise in the strengths of two model systems, C. elegans and the zebrafish, D. rerio, to identify how regulation of the cell cycle intersects with acquisition of cell invasive behavior. Together, they will examine and manipulate the cell cycle state of human cancer cells during metastasis, visualizing invasive behavior at high resolution using light sheet microscopy. Insights from their work will have profound implications in future design of therapeutics to eradicate invasive cells that may escape traditional chemotherapeutic agents that only target actively dividing cells.

Marcela V. Maus, MD, PhD
Massachusetts General Hospital, Boston
Dr. Maus has developed a way of engineering the body's own immune T cells, so that they are re-directed to fight deadly brain tumors like glioblastoma. However, in studies of patients with brain tumors, she has found that the tumor cells try to escape the engineered T cells. She will use the Innovation Award to redesign the T cells so that they block two forms of escape used by the tumors. By preventing tumor escape from immune cells, she expects that the engineered T cells will be more powerful and may become a new form of potentially curative treatment for brain tumors. Furthermore, if this system works for brain tumors, it has potential to be applied as a therapy for other forms of cancer.

Rushika M. Perera, PhD
University of California, San Francisco
Cancer cells have a unique ability to rapidly and efficiently remodel their internal composition and metabolic dependencies in order to maintain accelerated growth, metastasize and resist anti-cancer therapies. A newly identified central regulator of this increased plasticity is an internal organelle called the lysosome. Through processing and recycling of a variety of macromolecules, the lysosome serves as an important regulator of cellular remodeling and as a source of fuel for cancer cell growth. Dr. Perera proposes to develop a novel genetically engineered mouse model that enables isolation and purification of lysosomes from three stages during the life cycle of a tumor growing within a host organism - the primary tumor, the metastatic lesion, and following tumor relapse - with a particular focus on pancreatic cancer which is highly dependent on lysosomes for growth. She will investigate how changes in lysosome function at different stages of tumor progression contribute to metabolic adaptation and survival. This work has the potential to uncover new ways to target the altered metabolism intrinsic to pancreatic cancer and other malignancies.

2017 Stage 2 Damon Runyon-Rachleff Innovators:

Nicholas T. Ingolia, PhD
University of California, Berkeley
Dr. Ingolia studies a cellular process called translation, which generates protein from RNA. Important gene expression changes result from differences in the translation of mRNAs into functional proteins, rather than the abundance of these mRNAs in the cell. He has developed innovative techniques to comprehensively profile translation in cells and proposes to apply this approach to understand the gene expression differences between normal and cancerous cells. These gene expression changes will reveal distinctive features of cancer cells that explain their pathological behavior and potentially expose new vulnerabilities of these cells that could be targeted to treat cancer.

Christopher M. Jewell, PhD
University of Maryland, College Park
Dr. Jewell is uniquely trained in both immunology and materials science. He is harnessing bioengineering, immunology, and polymer design to create degradable vaccine "depots" in lymph nodes. The goal is to use these depots to control how T cells develop, promoting a cell fate specific for attacking tumors that also maintains the ability to proliferate at the extremely high rates needed to clear existing tumors and protect against regrowth. The findings from his research will support development of a new class of cancer vaccines that could clear existing tumors and prevent relapse.

Guillem Pratx, PhD
Stanford University, Stanford
Dr. Pratx, an engineer by training, is developing a novel method that would enable flow cytometry to measure single cell uptake of any non-fluorescent molecule. This challenging feat will be accomplished by exploiting the fact that molecules can be labeled by radioisotopes. This new tool could transform the ability to study normal and abnormal molecular processes in single cancer cells by allowing flow cytometry to interrogate a much wider range of biomolecules, with high throughput and high temporal resolution.

Brian H. Shirts, MD, PhD
University of Washington, Seattle
Dr. Shirts is a clinical geneticist whose goal is to empower patients who have been diagnosed with rare genetic mutations (variants of uncertain significance, or VUS) to actively participate in family tree pedigree building to understand their own genetic risk for cancer and other diseases. He has developed an online toolkit (findmyvariant.org) to help cancer patients use publicly available genealogy and networking resources to determine if their own variants travel with cancer in their extended family. This project will pioneer an efficient way for patients and their families to work with genetics laboratories to classify VUS, giving cancer patients control over their own genetic information. This innovative strategy will also create a new source for the highest quality genotype-cancer correlation data, which will benefit cancer researchers and, eventually, everyone at risk for cancer.

Elçin Ünal, PhD
University of California, Berkeley
Dr. Ünal proposes to study a natural developmental process, called gametogenesis, which reverses cellular aging. She will use this as a platform to illuminate the molecular causes of aging and to develop new strategies to counteract age-induced cellular damage. Her approach will identify the genes that play a direct role in attenuating the aging process and could facilitate the development of novel strategies to improve human health by decreasing susceptibility to cancer.

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DAMON RUNYON CANCER RESEARCH FOUNDATION

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 $320 million and funded over 3,550 young scientists. This year, it will commit approximately $17 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.

For more information visit http://www.damonrunyon.org

CONTACT

Yung S. Lie, PhD
Deputy Director and Chief Scientific Officer
Damon Runyon Cancer Research Foundation
yung.lie@damonrunyon.org
212.455.0521

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