Damon Runyon is pleased to announce that Meghan Raveis was elected to the Board of Directors in June. 

Damon Runyon Cancer Research Foundation has announced the 2021 recipients of the Damon Runyon Clinical Investigator award—six outstanding early career physician-scientists working to develop new cancer therapies under the mentorship of the nation's leading scientists and clinicians.

Researchers at Stanford University have discovered sugar-bound RNA strands protruding from the cell surface, challenging the long-held assumption that these two types of molecules are kept separate within the cell. These newfound “glycoRNAs,” identified by former Damon Runyon Fellow Ryan Flynn, MD, PhD, may serve an important role in immune signaling. A shock to biologists across disciplines, this finding has particular significance in the world of cancer research, as the development of effective immunotherapies hinges on our understanding of how the immune system is activated.

Immune checkpoint blockades are remarkably effective at exposing tumor cells to immune system attack, but only in the minority of patients with highly mutated tumors. While a high number of genetic mutations may seem like a bad thing, more mutations mean tumors produce more antigens, making them more recognizable to immune T-cells, and thus more susceptible to immunotherapy. In a groundbreaking report, Damon Runyon alumni Robert K. Bradley, PhD, and Omar Abdel-Wahab, MD, offer proof of concept that introducing errors in the short-lived RNA—rather than permanent DNA damage—still causes tumors to present antigens on their cell surface, stimulating immune response. The hope is that drugs that induce such RNA errors could be used in combination with checkpoint blockades to shrink therapy-resistant tumors.

Selection bias occurs when those chosen to participate in a study are not representative of the target population, limiting how much we can trust the study results. In order to quantify this selection bias, researchers have come up with a metric known as the diagnosis-to-treatment interval (DTI), which measures treatment urgency among trial participants. DTI, however, is not an ideal metric for selecting trial participants, as non-biological factors like access to medical care also influence the amount of time between diagnosis and treatment. Finding a biological basis for DTI would offer a more objective measure of clinical urgency, and thus be more useful in mitigating selection bias.

Note: This is an extended version of an interview published in the Spring 2021 issue of our print newsletter, Momentum.

Former Damon Runyon Clinical Investigator Li Li, MD, PhD, MPH has been appointed to the U.S. Preventive Services Task Force, a sixteen-member panel of experts that makes recommendations for screenings and other preventive healthcare measures for the entire U.S. population. He spoke with us about the role of prevention in the continuum of cancer care.

The American Society of Clinical Oncologists hosted their annual meeting this past weekend (June 4th-8th, 2021), giving oncology professionals from around the globe the chance to present cutting-edge research on new cancer therapies, ongoing clinical trials, and standards of patient care. Among the studies presented were those of several former and current Damon Runyon Clinical Investigators, whose research unites lab inquiry with clinical application.

One of the many ways tumor cells evade capture by the immune system is by presenting proteins on their surface that signal “don’t touch me” to immune T-cells. These proteins are called immune checkpoints. Therapies that block them—known as immune checkpoint blockades (ICB)—are remarkably effective, but they only work for a minority of cancer patients. In search of more widely beneficial immunotherapies, Damon Runyon Physician-Scientist Gabriel Griffin, MD, and colleagues at the Broad Institute of MIT and Harvard are investigating other mechanisms of immune system evasion to target in combination with ICB. Specifically, they have set out to find epigenetic regulators—proteins that turn genes “on” and “off”—that play a role in helping cancer cells avoid detection.

Prostate cancer (PCa), second only to skin cancer in prevalence among American men, has multiple subtypes defined by which key gene was mutated early in disease progression. Molecular analysis of PCa tumors has illuminated these subtype-defining genetic events, yet it remains unclear how these early alterations influence later genetic events and, eventually, result in different clinical outcomes. While molecular characterization often guides treatment decisions in breast and other cancers, more clarity is needed about these pathways for PCa subtyping to be clinically relevant. At Weill Cornell Medicine, Damon Runyon Clinical Investigator Chris Barbieri, MD, PhD, and colleagues are leading this charge.