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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.
ArvCon, now in its seventh year, is a weekend featuring multiple tabletop roleplaying game sessions, a concert, giveaways, and other surprises, benefiting the Damon Runyon Cancer Research Foundation. Damon Runyon’s award programs are targeted to have the greatest impact on cancer research, providing critical early career support to researchers pursuing work with a high potential to impact all types of cancer. Damon Runyon’s mission is to foster new generations of elite scientists and fill gaps in traditional research funding that threaten future breakthroughs.
Five scientists with exceptional promise and novel approaches to fighting cancer have been named the 2021 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.
In addition to his Damon Runyon-funded research project, which aims to optimize the delivery of the chemotherapy drug cisplatin, Quantitative Biology Fellow Vitor Mori, PhD, has dedicated some of his efforts over the past year to addressing the COVID-19 crisis in his home city of Sao Paulo, Brazil. The most populous city in the Western and Southern hemispheres, Sao Paolo has been struck particularly hard by the pandemic – Brazil’s COVID-19 death toll is second only to the United States.
While some cancers are known to be caused by mutations in key genes, genetic mutation does not always tell the full story. Epigenetic changes—which do not affect the DNA sequence itself, but rather the degree to which a gene is expressed—can play an important role in cancer as well. Such is the case with acute lymphoblastic leukemia (ALL), the most common form of cancer in children, which has a low incidence of genetic mutation but often coincides with abnormal epigenetic behavior.
There are two types of genes that, if mutated, can lead to cancer. One set of genes directs cell growth – a mutation in one of these genes can cause cells to grow uncontrollably, like a gas pedal stuck to the car floor. The other set of genes function as the “brakes,” telling cells when to slow down, correct replication mistakes, or undergo apoptosis (programmed cell death). These are called tumor suppressor genes, and as the name implies, a disruption in their function can allow the growth of tumors.
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.
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