The Damon Runyon Cancer Research Foundation announced that five scientists with novel approaches to fighting cancer have been named 2011 recipients of the Damon Runyon-Rachleff Innovation Award. The grant of $450,000 over three years is awarded each year to early career scientists whose projects have the potential to significantly impact the prevention, diagnosis and treatment of cancer.
The 2011 Damon Runyon-Rachleff Innovators are:
Alexei A. Aravin, PhD
California Institute of Technology, Pasadena, California
About one half of the human genome is occupied by sequences of DNA called transposable elements that can move within the genome, damaging normal genes and causing mutations or chromosomal rearrangements. Often referred to as "junk DNA," several lines of research highlight the importance of transposable elements in cancer development.
Dr. Aravin's goal is to comprehensively investigate the role that transposable elements play in cancer. He will study how transposable elements mobilize, their effect on gene regulation, and how they contribute to cancer initiation and growth. His research will provide a better understanding of tumorigenesis and may form the basis for new diagnostic and therapeutic strategies for cancer.
James E. Bradner, MD
Dana-Farber Cancer Institute, Boston, Massachusetts
The ability to undergo cell division is encoded in the genomes of all human cells. This process requires a symphony of growth genes to be turned on, and then silenced when cell division is no longer needed. The activation of the growth program in healthy cells is conducted by a small number of master regulatory genes called transcription factors. In contrast, abnormal unrestricted cell growth is encoded in the genomes of all cancer cells. This uncontrolled growth is attributable to acquired mutations in the genome, which result in hyperactivity of the master regulators. Many people in the field of cancer research regard these master regulators as the most desirable targets for drug discovery. Unfortunately, developing drugs against these proteins has proven to be technically difficult.
Dr. Bradner is using new chemical approaches to develop small molecule drugs directed at the master regulators of cancer cell growth. The primary focus of his efforts is a master regulator called Myc. Abnormal activation of Myc is one of the most common events in all human cancers. By targeting Myc in cancer cells, he hopes to discover new, prototype drugs that can be used as more effective targeted anti-cancer agents.
Joshua E. Elias, PhD
Stanford University School of Medicine, Stanford, California
A great deal of cancer research focuses on investigating the methods by which tumors cope with damage to their DNA. Less is known about the ways cancer cells deal with damage to any of the thousands of proteins necessary for cell survival. Cancerous cells often occupy environments that subject them to numerous stresses, including oxygen and nutrient depletion, which can lead to protein damage or misfolding. To survive and proliferate in these conditions, cancer cells use specific protective mechanisms to destroy or restore damaged proteins; in contrast, normal cells would die in such surroundings.
Cancer cells may, for example, activate degradation pathways to do away with dysfunctional proteins. Dr. Elias proposes that cancer cells may also promote long-term survival by dividing asymmetrically, thus producing one daughter cell free of damaged proteins. To test these ideas, he will measure the lifetimes of damaged proteins, model the processes cancer cells use to dispose of proteins, and investigate the ways by which these methods contribute to tumor formation. By understanding the mechanisms cancer cells depend on to escape death and promote growth, he hopes to discover new treatments and diagnostics, as well as ways to better target existing therapeutics to individual patients' cancers.
Benjamin P. Tu, PhD
UT Southwestern Medical Center, Dallas, Texas
Despite decades of research, how cell growth and proliferation are coordinated with the metabolism in a cell has remained a critical unresolved question. Understanding these specific mechanisms would address the long-standing question of how cells assess their metabolic and nutritional state to decide when to proliferate.
Dr. Tu has discovered a key mechanism by which carbon sources, such as glucose, signal cells to grow and divide; these studies were conducted in the model organism, baker's yeast. His goal is to investigate these mechanisms in mammalian cells and determine whether such mechanisms can be exploited to selectively kill rapidly proliferating cancer cells. He also aims to explore whether novel, unconventional metabolic strategies might be highly effective for the treatment of a variety of cancers.
Matthew G. Vander Heiden, MD, PhD
Massachusetts Institute of Technology, Cambridge, Massachusetts
Nutrient metabolism in cancer cells is different from that in most normal cells. This metabolic difference has not yet been exploited for therapy.
Dr. Vander Heiden aims to rigorously define how altered cell metabolism contributes to cancer cell proliferation; he seeks to elucidate exactly how nutrients are used by cancer cells. This approach will lead to a better understanding of how specific metabolic pathways are used to help cancer cells grow, and holds the key to targeting metabolism for better cancer treatments.
|Contact: Yung S. Lie, Ph.D.|
Damon Runyon Cancer Research Foundation