Damon Runyon News
View New Articles By
View New Articles By
Over twenty years ago, scientists at the Broad Institute, including Matthew Meyerson, MD, PhD (Damon Runyon Fellow ’95-’98), William R. Sellers, MD (Damon Runyon Clinical Investigator '01-'05, Board Member), and Todd R. Golub, MD (Innovation Award Committee Member, Board Member), set out to understand why some patients with lung cancer did not respond to existing treatments. Now, these decades of work have paid off: the FDA has approved a new oral treatment for non-small-cell lung cancer, the most common form of the disease.
The Damon Runyon Cancer Research Foundation has named 14 new Damon Runyon Fellows, brilliant postdoctoral scientists conducting basic and translational cancer research in the laboratories of leading senior investigators. This prestigious Fellowship encourages the nation's most promising young scientists to pursue careers in cancer research by providing them with independent funding ($300,000 total over four years) to investigate cancer causes, mechanisms, therapies, and prevention.
Purines, namely adenine and guanine, are one of two chemical compounds that cells use to make the building blocks of DNA and RNA. (The other are pyrimidines, cytosine and thymine.) Cells can make purines in two ways: by building them from scratch, known as “de novo purine biosynthesis,” or by recycling them from existing molecules, known as “purine salvage.” When the salvage pathway is active, it signals to the cell to slow down the biosynthesis pathway so that the cell does not make too many purines. Until recently, scientists did not fully understand how this slowdown happens.
Rhabdomyosarcoma (RMS) is a cancer of the soft tissue that predominantly affects children. Under the microscope, these tumors resemble developing skeletal muscle, but they appear in parts of the body where skeletal muscle does not exist, such as the bladder and salivary gland. For years, this has raised two fundamental questions: what types of cells give rise to RMS, and why does this cancer mainly occur in children?
Acute myeloid leukemia (AML) is diagnosed in more than 20,000 people in the U.S. each year, and the five-year survival rate remains around 30%. For patients whose disease is driven by mutations in the gene NPM1, the most common mutation in adult AML, treatment options have long been limited.
Cancer drugs often target a molecule that cancer cells rely on for survival but, crucially, healthy cells do not. When they are first identified, this type of molecule is known as a therapeutic vulnerability—and what previously made the cancer cell especially fit now makes it an easier target.
In 2021, Damon Runyon scientists Michael E. Pacold, MD, PhD, Robert S. Banh, PhD, and their colleagues at New York University Langone Health discovered how the enzyme CoQ10 is made, a synthesis pathway that scientists had been seeking for over two decades. CoQ10 is crucial for energy production in cells (which is why it is popular as a dietary supplement, though evidence of the health benefits is scant).
New research from Damon Runyon-Dale F. Frey Breakthrough Scientist Abigail E. Overacre-Delgoffe, PhD, and her lab at the University of Pittsburgh suggests that sucralose—the sugar substitute found in many “sugar-free” sodas, yogurts, and snack foods—may interfere with cancer immunotherapy. Their findings indicate that the widely used artificial sweetener changes the composition of the gut microbiome in ways that weaken patients’ immune systems and blunt the effectiveness of immune checkpoint inhibitors, a class of drugs that unleash T cells to attack tumors.