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.

Damon Runyon scientists and industry partners gathered in person on Thursday, March 9 for the 2023 Accelerating Cancer Cures Symposium, hosted by Amgen at their new campus in South San Francisco.

Human papillomavirus (HPV) was first identified as a cancer driver in the 1970s, when a German doctor named Harald zur Hausen discovered that the virus causes about 75% of human cervical cancers. HPV has since been linked to several other types of human cancer, including head and neck cancer, as discovered by then-Damon Runyon Clinical Investigator Maura L. Gillison, MD, PhD, in 2000.

Cancer cells are often assumed to be “hypermetabolic,” meaning their energy-producing cycles run on overdrive to fuel the uncontrolled division and growth that defines a tumor. But new findings from former Damon Runyon Fellow Caroline R. Bartman, PhD, and her colleagues at Princeton University challenge this assumption, revealing how much we still have to learn about cancer metabolism.