One way to determine how successfully a patient’s cancer treatment has eradicated the disease is to check the bloodstream for free-floating DNA originating from tumor cells, also known as circulating tumor DNA (ctDNA). The detection of ctDNA can serve as a powerful prognostic tool, allowing clinicians to assess the effectiveness of treatment and predict the likelihood of disease recurrence.

For Vassiliki Karantza, MD, PhD, the past seven years have been a whirlwind. Since starting her first job in the pharmaceutical industry in 2014, the former Damon Runyon Clinical Investigator has overseen the development of a new drug for breast cancer from early clinical trials to approval by the Food and Drug Administration. As of March 2021, the drug, pembrolizumab (Keytruda), is FDA-approved for the treatment of metastatic triple-negative breast cancer (TNBC), which accounts for 10-15% of breast cancer diagnoses. It is a remarkable achievement, especially considering that the company’s breast cancer program did not yet exist when Dr. Karantza arrived.

Grants totaling nearly $4 million give early-career investigators independence to pursue brave and bold cancer research.

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.