Lydia Finley, PhD (Damon Runyon Jack Sorrell Fellow ‘13-‘17) of Memorial Sloan Kettering Cancer Center, New York, and colleagues, demonstrated that stem cells can rewire their metabolism to enhance a mechanism that helps them avoid committing to a specific fate; in turn, this improves stem cells’ ability to renew themselves. She showed that the nutrients a stem cell uses, and how it uses them, can contribute to a cell’s fate by influencing gene expression through epigenetic modifications.

Peter D. Cole, MD (Damon Runyon-Sohn Pediatric Cancer Fellowship Award Committee, Damon Runyon Clinical Investigator ‘03-‘08) of Albert Einstein College of Medicine, Bronx, and colleagues, reported that common variations in four genes related to brain inflammation or cells’ response to damage from oxidation may contribute to the problems with memory, learning and other cognitive functions seen in children treated for acute lymphoblastic leukemia (ALL).

Catherine J. Wu, MD (Damon Runyon Clinical Investigator ‘07-‘12) and colleagues at Dana-Farber Cancer Institute, Boston, found that in patients with chronic lymphocytic leukemia (CLL), treatment produced shorter remissions if the tumor tissue showed signs of highly disorganized methylation, chemical modifications on the DNA that regulate gene expression. The findings demonstrate that such disorganization can actually benefit tumors and render them less vulnerable to anti-cancer drugs. The study was published in the journal Cancer Cell.

John M. Timmerman, MD (Damon Runyon Clinical Investigator ‘05-‘10) of University of California, Los Angeles, Gordon J. Freeman, PhD (Damon Runyon Fellow ‘79-‘81), of Dana-Farber Cancer Institute, Boston, and colleagues, reported that an immunotherapy drug called Opdivo/nivolumab, which inhibits the PD-1 pathway, is effective in treatment of relapsed or refractory Hodgkin’s lymphoma.  In a Phase I clinical trial of 23 patients with Hodgkin’s lymphoma treated with the drug, the rate of progression-free survival was 86%.

Jedd D. Wolchok, MD, PhD (Damon Runyon-Lilly Clinical Investigator ‘03-‘08) and colleagues at Memorial Sloan Kettering Cancer Center, New York, reported a key discovery that explains why some patients respond to Yervoy/ipilimumab, an immunotherapy drug, while others do not. They found that the cancer cells from patients who respond to the drug carry a high number of genetic mutations—some of which make tumors more visible to the immune system, and therefore easier to fight.

Election to the Institute of Medicine is one of the highest honors that can be earned in the fields of medicine and health.  In recognition of their outstanding achievements, members of the Damon Runyon Cancer Research Foundation community were inducted this month:

Feng Zhang, PhD (Damon Runyon-Rachleff Innovator ‘12-‘14) of the Broad Institute and Massachusetts Institute of Technology, Cambridge, is one of six promising early career scientists named as 2014 NYSCF-Robertson Stem Cell Investigators. The award is designed to support scientists engaged in novel neuroscience and cutting-edge translational stem cell research. Each Investigator will receive a generous five-year award.

Matthew G. Vander Heiden, MD, PhD (Damon Runyon-Rachleff Innovator ‘11-‘13, Damon Runyon Fellow ‘06-‘08) of MIT, Cambridge, and colleagues, reported the discovery of a sign of the early development of pancreatic cancer – an increase in certain amino acids due to changes in metabolism. This occurs before the disease is diagnosed and symptoms appear, and the researchers hope that eventually they may be able to use this information to detect the disease earlier. These findings were published in the journal Nature Medicine.

Sidi Chen, PhD (Damon Runyon Fellow ‘12-‘15) and Feng Zhang, PhD (Damon Runyon-Rachleff Innovator ‘12-‘14) of the Broad Institute and Massachusetts Institute of Technology, Cambridge, developed a new mouse model that allows scientists to use the CRISPR-Cas9 system for in vivo genome editing experiments. They demonstrated the utility of the new “Cas9 mouse” model to edit multiple genes in a variety of cell types, and to model lung adenocarcinoma. The mouse has already been made available to the entire scientific community.

Bradley L. Pentelute, PhD (Damon Runyon-Rachleff Innovator '13-'15), and colleagues at Massachusetts Institute of Technology, Cambridge, used a disarmed version of the anthrax toxin to deliver two proteins known as antibody mimics, which can kill cancer cells by disrupting specific proteins inside the cells. In this study, they successfully targeted Bcr-Abl and hRaf-1, which both have known functions in cancer. This is the first demonstration of effective delivery of antibody mimics into cells, which could be applied to develop new drugs for cancer and other diseases.