Three scientists with exceptional promise and novel approaches to fighting cancer have been named the 2023 recipients of the Damon Runyon Physician-Scientist Training Award. The awardees were selected through a highly competitive and rigorous process by a scientific committee comprised of leading cancer researchers who are themselves physician-scientists.

The Damon Runyon Cancer Research Foundation and St. Jude Children’s Research Hospital announced a new pediatric-focused fellowship today. The initiative aims to help address the critical shortage of top young scientists who often seek more prevalent opportunities in adult cancer research or the pharmaceutical sector. The Damon Runyon–St. Jude Pediatric Cancer Research Fellowship will fund up to 25 fellowships over eight years, a $9 million investment.

Imagine you have just learned that you are genetically predisposed to developing blood cancer. Everyone acquires mutations in their blood as they age, your doctor explains, but certain mutations carry higher risk than others. When a mutation occurs in a blood stem cell and confers an evolutionary advantage, that mutant blood stem cell will give rise to a whole subpopulation of cells with the same mutation. This is known as clonal hematopoiesis (CH), and again, it is a normal age-related phenomenon.

In the context of cancer, “drug addiction” has a different meaning—counterintuitively, it’s when cancer cells, not patients, depend on continuous treatment for survival. This can happen if, after the drug target is inhibited, some compensatory signaling pathway is turned on that serves a similar function in the cancer cell. When drug treatment stops, the cell goes into “withdrawal” and this alternative pathway becomes overactive, so much so that it leads to cell death.

Due to their critical role in so many cellular functions, proteins that span the cell membrane are the target of more than half of all FDA-approved drugs. Some of these transmembrane proteins are single-pass, meaning they cross the membrane only once, while others are more complex, multipass proteins, meaning they cross the membrane in at least two places. Drugs targeting the latter are primarily small molecule inhibitors, named for their size relative to antibodies and other large proteins.

A major challenge in treating brain cancer is delivering drugs across the blood-brain barrier (BBB), the dense network of cells and blood vessels that prevents toxins and pathogens from entering the brain. Unfortunately, the BBB also bars entry to therapeutic molecules, leaving highly toxic radiation or chemotherapy treatment as the only recourse for many patients with brain cancer.

Cancer immunotherapies work by triggering the body’s immune response against tumors. Tumor cells can evade destruction by the immune system, however, by attracting helper T cells, the “peacekeepers” of the immune system.

Glioblastomas (GBMs) are the most common—and the most aggressive—type of cancer originating in the brain. Part of the reason these tumors are so hard to treat is that the cancer cells suppress the immune cells that enter their environment. Not only can they outcompete immune cells for critical nutrients, effectively starving the immune cells, but some GBMs can even adjust their metabolism to produce metabolites that directly inhibit immune cell activity.

Damon Runyon has announced its 2023 Quantitative Biology Fellows, three exceptional early-career scientists who are applying the tools of computational science to generate and interpret cancer research data at extraordinary scale and resolution. Whether constructing synthetic synapses to study cellular communication or engineering tumor models to predict treatment response, their projects seek to extend the boundaries of what is possible in cancer research by approaching fundamental biology questions from a new direction.

P53, the most frequently mutated gene across all human cancers, is mutated in the majority of pancreatic cancers. But despite the overwhelming evidence that p53 mutations contribute to cancer progression, therapies targeting mutant p53 have had limited success, suggesting an incomplete understanding of the protein’s function. In order to understand what goes wrong when p53 mutates, researchers need a clearer picture of how normal p53 prevents tumor development in the first place.