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.

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 second class of Damon Runyon Quantitative Biology Fellows, announced this month, will apply the tools of computational biology to generate and interpret cancer research data at extraordinary scale and resolution. From RNA sequencing data that pinpoints tumor cells to their exact location to three-dimensional models of cell-cell interaction, their projects extend the boundaries of what is possible in cancer research, allowing them to tackle fundamental biological and clinical questions.

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.