New York, NY (January 7, 2013) The Damon Runyon Cancer Research Foundation announced that seven scientists with novel approaches to fighting cancer have been named 2013 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.
Funding Daring Research
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. At the final stage of selection, candidates are screened by an in-person interview with committee members. Only those scientists with a strong vision and passion for curing cancer are selected to receive the prestigious award.
This program is possible through the generous support of Andy and Debbie Rachleff, the Island Outreach Foundation and Nadia's Gift Foundation.
2013 Damon Runyon-Rachleff Innovators:
Michael Z. Lin, MD, PhD
Stanford University, California
Currently available cancer treatments, such as chemotherapeutics, targeted inhibitors or immunotherapies, are not capable of fully eradicating cancers and are limited by toxicities and side effects.
Dr. Lin aims to take a new approach to cancer treatment by engineering a virus that will infect and replicate specifically in cancer cells, triggering their destruction. This strategy aims not to suppress oncogenic signaling, but to use it as a trigger for a smart biological therapy. If he succeeds, progress will be made toward developing a much-needed "magic bullet" against cancer.
Christine Mayr, MD, PhD [Island Outreach Foundation Innovator]
Memorial Sloan-Kettering Cancer Center, New York
Cancer is thought to arise through a series of genetic mutations in the DNA sequence. Depending on the location of these errors and the genes that are affected, these mutations lead to the many different features that characterize cancer cells such as uncontrolled proliferation, escape from cell death and metastasis.
Dr. Mayr proposes the existence of a new type of anomaly that can lead to cancer: non-genetic aberrations induced by modifications of RNAs, which have so far been excluded from large-scale cancer genomics efforts. She has developed a new method to identify this type of aberration in different cancers and will investigate its frequency and functional consequences for tumor growth. Her studies will help to broaden the understanding of cancers and may also help in the design of new therapeutics.
Nicholas E. Navin, PhD [Nadia's Gift Foundation Innovator]
M.D. Anderson Cancer Center, Texas
Tumors evolve from single cells. As they expand to form the tumor mass, the cells diverge and form distinct subpopulations with different genetic mutations. This salient characteristic is called "intratumor heterogeneity" and confounds basic research and clinical diagnostics. The challenge is that standard genomic tools require a large amount of input material and thus are limited to measuring an average signal from a complex population of cells.
Dr. Navin proposes the development of an innovative single-cell sequencing tool that can detect genomic mutations in single cancer cells, allowing heterogeneity in tumors to be delineated. He will apply this technique to study how single breast cancer cells disseminate from the primary tumor into the circulatory system and seed metastatic tumors. In addition, this method will have a myriad of clinical applications, which have prognostic value in predicting invasion, metastasis, survival and response to chemotherapy. Translating these methods into the clinic is likely to have a profound effect on reducing morbidity in breast cancer and other cancer types.
Trudy G. Oliver, PhD
University of Utah Huntsman Cancer Institute, Utah
Many cancers initially respond to therapy. However, cancers often acquire resistance and stop responding to further treatment. Small cell lung cancer (SCLC) is an example of a cancer that is highly sensitive to initial treatment, but quickly acquires a vicious resistance resulting in a five-year patient survival rate of less than 4%. In order to combat drug resistance and improve the quality of life for patients with SCLC, it is important to understand the key genetic changes and cellular pathways that drive resistance.
Dr. Oliver will use the most innovative next-generation sequencing technologies to comprehensively identify critical genetic changes associated with resistance. These findings will be essential for understanding how lung cancer, and potentially other types of cancer, evades chemotherapy. In addition, this work will identify novel pathways that could be targeted to re-establish drug sensitivity and thereby provide new treatment options for patients with drug-resistant disease.
Bradley L. Pentelute, PhD
Massachusetts Institute of Technology, Massachusetts
Antibodies have proven to be powerful tools in cancer research, facilitating the elucidation of disease mechanisms and generating novel and effective anti-cancer therapeutics. However, antibody biotechnology is limited by one major factor: the inability of antibodies to effectively cross the cell membrane to reach the inside of the cell, or cytosol. A new strategy is clearly necessaryone based on facile and reliable delivery of active antibody-like molecules into various cell types.
Dr. Pentelute plans to construct a new, targeted delivery platform capable of introducing stable molecules that mimic antibodies (deemed "intrabodies"). He will use this proposed delivery platform to strike the intracellular cancer target Bcr-Abl for treatment of chronic myeloid leukemia. He also aims to target the cancer-promoting complex p53/MDM2 in cancer cells. Through these innovative studies, he aims to advance the frontier by delivering a diverse array of antibody-like molecules into cells for cancer therapy.
Agnel Sfeir, PhD
New York University School of Medicine/Skirball Institute, New York
Each cell contains organelles called mitochondria, which are the powerhouses of cells, producing energy in the form of ATP. Mitochondria contain their own separate DNA, which codes for key energy-producing enzymes. Maintaining the integrity of the mitochondrial genome is necessary for optimal cellular function and for protection against diseases. Alterations in mitochondrial DNA are associated with and can promote metastasis of many tumors, such as lung, breast and prostate. Such aberrations range from single base substitutions to large-scale deletions that remove segments of the mitochondrial genome. The mechanism by which these aberrations influence disease progression remains unclear.
Dr. Sfeir aims to uncover the underlying basis for accumulation of these highly dangerous deletions in mitochondrial DNA and the mechanism by which they shape tumor behavior. This work will help identify novel strategies to preserve mitochondrial function and thwart tumor progression.
Sarah (Sadie) M. Wignall, PhD
Northwestern University, Illinois
Cancer cells exhibit uncontrolled growth and proliferation, leading to the formation of malignant tumors. Therefore, many current cancer therapies are aimed at trying to block cell multiplication, with the goal of killing cancerous cells and halting tumor growth. However, many of these treatments also affect the growth and division of non-cancerous cells in the body, leading to severe side effects.
Dr. Wignall will investigate a pathway required for the division of cancerous, but not normal cells. This pathway regulates a physical structure in the cell called the centrosome. By learning more about this pathway, she hopes to ultimately contribute to designing therapies that will specifically attack cancer cells, leading to better treatment options for cancer patients.
|Contact: Yung S. Lie, Ph.D.|
Damon Runyon Cancer Research Foundation