The American Society of Clinical Oncologists hosted their annual meeting this past weekend (June 4th-8th, 2021), giving oncology professionals from around the globe the chance to present cutting-edge research on new cancer therapies, ongoing clinical trials, and standards of patient care. Among the studies presented were those of several former and current Damon Runyon Clinical Investigators, whose research unites lab inquiry with clinical application.

One of the many ways tumor cells evade capture by the immune system is by presenting proteins on their surface that signal “don’t touch me” to immune T-cells. These proteins are called immune checkpoints. Therapies that block them—known as immune checkpoint blockades (ICB)—are remarkably effective, but they only work for a minority of cancer patients. In search of more widely beneficial immunotherapies, Damon Runyon Physician-Scientist Gabriel Griffin, MD, and colleagues at the Broad Institute of MIT and Harvard are investigating other mechanisms of immune system evasion to target in combination with ICB. Specifically, they have set out to find epigenetic regulators—proteins that turn genes “on” and “off”—that play a role in helping cancer cells avoid detection.

Prostate cancer (PCa), second only to skin cancer in prevalence among American men, has multiple subtypes defined by which key gene was mutated early in disease progression. Molecular analysis of PCa tumors has illuminated these subtype-defining genetic events, yet it remains unclear how these early alterations influence later genetic events and, eventually, result in different clinical outcomes. While molecular characterization often guides treatment decisions in breast and other cancers, more clarity is needed about these pathways for PCa subtyping to be clinically relevant. At Weill Cornell Medicine, Damon Runyon Clinical Investigator Chris Barbieri, MD, PhD, and colleagues are leading this charge.

Established by an Act of Congress in 1863, the National Academy of Sciences (NAS) is the body of distinguished researchers “charged with providing independent, objective advice to the nation on matters related to science and technology.” Election to membership is among the highest honors a scientist can receive. This year, three Damon Runyon alumni join the NAS ranks, bringing the total number of Damon Runyon alumni in NAS to 89.

By the time patients experience symptoms, their tumors contain a genetically diverse collection of cancer cells, each with an accumulation of mutations. If we could better understand the sequence of events that leads from a single mutation to a heterogeneous population of tumor cells, earlier detection and intervention might be possible. However, attempts to trace this evolution where it has already occurred (in model organisms, immortalized cell lines, or patient samples) face significant challenges.

The KRAS gene, responsible for encoding a protein that serves as an “on/off” switch for cell growth, is one of the most commonly mutated genes in cancer. The frequency and nature of its mutation differ across cancer types, however, with the highest occurrence of mutation found in cancers of the colorectum, pancreas, lung, and blood plasma.

The tumor, once an indistinct mass of heterogeneous cells, is gaining single-cell resolution. Until recently, even distinguishing between healthy cells and malignant cells within a tumor sample presented a challenge.