Damon Runyon is delighted to announce the election of Lori J. Pierce, MD, to its Board of Directors.

Despite the best efforts of cancer researchers and clinicians, pancreatic cancer remains a highly lethal disease, with only 5% of patients surviving 5 years after their diagnosis. This is in part because pancreatic cancer cells have relatively few mutations, meaning fewer strange-looking proteins, or neoantigens, on their surface to attract the attention of cancer-killing immune T cells. This makes most pancreatic tumors “immune cold,” safe from detection by the body’s defense system.

The Damon Runyon Cancer Research Foundation has named 16 new Damon Runyon Fellows, exceptional postdoctoral scientists conducting basic and translational cancer research in the laboratories of leading senior investigators. The prestigious, four-year Fellowship encourages the nation's most promising young scientists to pursue careers in cancer research by providing them with independent funding ($260,000 total) to investigate cancer causes, mechanisms, therapies, and prevention.

Amid growing calls for academic and funding institutions to recognize the financial hardships faced by postdoctoral researchers across the country, the Damon Runyon Cancer Research Foundation has announced that it will increase its Fellowship stipend by 12.5% over the award’s four-year term. The stipend increase will be effective for all Damon Runyon Fellows whose awards begin or renew on or after July 1, 2022.

Ras proteins, present in all mammalian cells, are molecular switches that control the processes of cell survival and proliferation. Unsurprisingly, mutations in any of the three RAS genes (KRAS, NRAS, or HRAS) can lead to uncontrolled cell growth, or cancer. Since these cancer drivers were first identified in the 1980s, it has been clear that different types of cancer are coupled with specific RAS mutants. For example, nearly 90% of pancreatic tumors display KRAS mutations, while NRAS mutations are more likely to appear in blood cancers. Why these associations exist, however, is not well understood.

Colorectal cancer is among the leading causes of cancer deaths worldwide, second only to lung cancer. As with many cancers, the primary cause of death in this type of cancer is metastasis, or when the cancer spreads from its original tissue to another organ in the body. In colorectal cancer, the liver is most common site of metastasis—more than half of all colorectal cancer patients will develop tumors in their liver during the course of their disease. Targeting the genes and pathways that promote liver metastasis may be key to developing better treatments for colorectal cancer, but until recently, these genetic mechanisms were not well defined.

Like living species, cancer cell populations undergo evolution. They accumulate mutations and become heterogeneous, and the mutations that increase chances of survival become more common. In this way, a single genetic alteration can evolve into a tumor and eventually spread throughout the body. Understanding the evolutionary path that tumors follow, from a single-cell mutation to metastatic cancer, is essential for designing effective clinical interventions. However, environmental factors and other variables can confound efforts to trace a cancer’s development from beginning to end.

Cancer treatment decision-making depends on an accurate understanding of a patient’s prognosis. Mistaking a cancer’s aggressiveness can lead to either under- or overtreatment, both of which carry increased risk of fatality. Current methods of prognostication, which usually rely on examining cancerous tissue via X-ray or microscope, involve subjective judgments and sometimes fail to predict disease course. With the rise of DNA sequencing technologies, clinicians are increasingly looking to patients’ genomes for clues about how their cancer will behave.

The Damon Runyon Cancer Research Foundation has named five new Damon Runyon Clinical Investigators. The recipients of this prestigious award are outstanding, early-career physician-scientists conducting patient-oriented cancer research at major research centers under the mentorship of the nation's leading scientists and clinicians.

Last fall, we published the story of Damon Runyon Clinical Investigator Jennifer M. Kalish, MD, PhD, a pediatric geneticist at the Children’s Hospital of Philadelphia who has dedicated her career to the study of Beckwith-Wiedemann Syndrome (BWS), a rare genetic condition that causes overgrowth in certain parts of the body and predisposes children to cancers of the kidney and liver. As Founding Director of the hospital’s Beckwith-Wiedemann Syndrome Clinic, Dr. Kalish established the country’s first and only active BWS patient registry and biorepository storing blood and tissue samples necessary for research. In December 2020, her lab unveiled the first human cell-based model of the syndrome, developed using cells from patients in the registry.