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Because cancer cells proliferate at a higher rate than normal cells, they require more energy than normal cells, and thus need to rewire the cell’s energy-producing processes to meet this excessive demand. Think of spoiled Veruca Salt in Charlie and the Chocolate Factory rerouting the chocolate bar supply directly to her father’s factory, where his workers unwrapped them faster than any normal child could, expediting her discovery of a Golden Ticket.
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.
Pancreatic cancer, which will affect an estimated 60,430 Americans this year, is notoriously hard to treat. Chemotherapy and immunotherapy drugs sometimes work at first, but often the tumors develop resistance and continue to grow. This makes it one of the most lethal types of cancer, with the average five-year survival rate after diagnosis hovering around 10%.
A range of genetic disturbances can result in the same type of cancer, the way an off-tasting dish might result from any number of bad ingredients or missteps in the preparation process. Often, variation in clinical features—tumor appearance, location, behavior—is what defines cancer subtypes, while the genetic origins of each subtype remain unclear. But to make sense of this variation, and thus refine diagnosis and develop more precise treatments, researchers must trace these clinical features back to their genetic origins.
Clear cell renal cell carcinoma (ccRCC), which accounts for over 75% of kidney cancer diagnoses, gets its name from how the tumor cells look under a microscope. Their clear appearance, as if the tissue were studded with air bubbles, is due to an accumulation of cholesterol in the cells. Studies have shown that ccRCC cells contain at least twice as much cholesterol as normal kidney cells, and in some cases up to 35 times more. How this accumulation occurs and how it contributes to cancer progression, however, is poorly understood.
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.
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