Damon Runyon News

By Michael W. Drazer, MD, Damon Runyon Physician-Scientist at The University of Chicago

Physician-scientists are uniquely positioned to identify the next generation of scientific breakthroughs and then efficiently translate these discoveries into clinically effective, life-changing therapies for people with cancer. This unique set of opportunities, however, is accompanied by a distinct set of obstacles that confront early career physician-scientists in the scientific and clinical realms. These challenges include financial debt from years of professional training, a lack of protected time for the development of scientifically sound, ambitious research programs, low salaries during years of extended training, and an increasingly unstable and unpredictable funding environment for biomedical research at the national level.

David M. Livingston, MD (Damon Runyon Board Member), of Dana-Farber Cancer Institute, Boston, has been named the 20th recipient of the Pezcoller Foundation-AACR International Award for Cancer Research. Dr. Livingston is honored for his fundamental contributions to the field of basic cancer research. His work has been pivotal to the understanding of retinoblastoma pathway of cell cycle control as well as the transcriptional co-activation function of the key regulatory proteins, p300 and CBP.

At the junction of growth and starvation stands a signaling protein called mechanistic Target of Rapamycin Complex 1 (mTORC1). Inside the cell, mTORC1 regulates metabolism, growth, protein and organelle recycling (autophagy), proliferation, and survival. When something goes wrong in the pathway, various diseases such as cancer, obesity, and type 2 diabetes, can develop. An outstanding challenge is to understand how mTORC1 becomes activated in response to a wide variety of stimuli including nutrients, growth factors, and stressors, in normal and cancer states.

By Yi Yin, PhD, Damon Runyon Fellow, University of Washington

The Damon Runyon Cancer Research Foundation recently asked some of our current award recipients how cancer will be prevented, diagnosed, and/or treated differently in the future. What can a future cancer patient, say 10-20 years from now, expect to experience? Their responses were fascinating, and over the next few months we will share their visions for the future on this blog.

I think cancer will be prevented, diagnosed and/or treated very differently within the next 10-20 years.

Anjana Rao, PhD (Damon Runyon Fellow ’79), and James Scott-Browne, PhD (Damon Runyon Fellow ’11-’13), at the La Jolla Institute for Allergy and Immunology, La Jolla, and colleagues, are focusing on a key issue of how tumor-fighting T cells can lose their effectiveness or become “exhausted.”  The researchers identified two proteins, NFAT and Nr4a, that can bind to the DNA of T cells and shut down their tumor-fighting activity.  Next steps will be to determine if these processes can be interfered with or reversed in order to re-motivate immune cells to eradicate a pati

The Damon Runyon Cancer Research Foundation recently asked some of our current award recipients how cancer will be prevented, diagnosed, and/or treated differently in the future. What can a future cancer patient, say 10-20 years from now, expect to experience? Their responses were fascinating, and over the next few months we will share their visions for the future on this blog.

By Amanda Balboni, PhD, Damon Runyon Sohn Fellow at the Dana-Farber Cancer Institute

In the next 10-20 years, I anticipate that tumor genetic testing will become standard practice as sequencing technology becomes faster and more cost effective. This will revolutionize the way cancer is treated clinically and make personalized cancer medicine a reality. 

Don X. Nguyen, PhD (Damon Runyon Fellow ’05-’08), of Yale Cancer Center, New Haven, and colleagues, reported new findings that explain the propensity of latent lung adenocarcinoma (LUAD) to relapse. They showed that differential expression of extracellular matrix (ECM) molecules and their interacting proteins contributes to risk of relapse in distinct LUAD subtypes. One protein called hyaluronan receptor HMMR, when overexpressed, was associated with inflammation and poor prognosis.

By Megan Insco, MD, PhD, Damon Runyon Fellow at Boston Children's Hospital

When I was in 7th grade, my mother was diagnosed with breast cancer.  I was devastated and directionless.  When she passed away two years later, my broad set of interests resolved around a singular focus.  I would channel my passion for discovery and my need to see my work manifest productively in the world, into a career discovering and delivering life-enhancing therapies for cancer patients. 

Christine Iok In Chio, PhD (Damon Runyon Shirley Stein Fellow ’13-’17), in the laboratory of her sponsor David Tuveson, MD, PhD, and colleagues at Cold Spring Harbor Laboratory, Cold Spring Harbor, created a new 3D model of pancreatic cancer, which allowed them to identify two distinct stroma cell populations called cancer-associated fibroblasts  (CAF’s), that work together with cancer cells to protect and help the tumor grow.

Today we realize that cancer is not a single disease, but something unique to each individual. Even within a single tumor there is complexity and diversity unrecognized just a decade ago.

Employing this knowledge, along with emerging technological advances, will lead to fundamental changes in the patient population. To this end, more sensitive and specific diagnostics will greatly reduce the number of late-stage cancer diagnoses. This early detection, along with an increasing breadth of cancer therapeutics, will revolutionize the way we assess clinical outcomes.