Gregory L. Beatty, MD, PhD (Damon Runyon-Nadia’s Gift Foundation Innovator ’12-’15) and colleagues at the Abramson Cancer Center at University of Pennsylvania, Philadelphia, reported high levels of inflammatory compounds in mice with pancreatic tumors. These included CCL2, a signaling molecule that promotes recruitment of inflammatory white blood cells by tumors. This likely contributes to the protective tumor microenvironment that makes most pancreatic tumors resistant to treatment.

By Giada Bianchi, MD, Damon Runyon-Celgene Physician-Scientist

The Damon Runyon Cancer Research Foundation recently asked some of our current award recipients how cancer will be prevented, diagnosed, and/or treated differently in the future. What can a future cancer patient, say 10-20 years from now, expect to experience? Their responses were fascinating, and over the next few months we will share their visions for the future on this blog.

Theodora S. Ross, MD, PhD (Damon Runyon Scholar ’01-’03), and colleagues at UT Southwestern, Dallas, reported that the BRCA1 gene is required for the survival of blood forming stem cells. This could explain why patients with BRCA1 mutations do not have an elevated risk for leukemia; the stem cells die before they have an opportunity to transform into a blood cancer. These results also suggest that these patients may be at higher risk for the serious side effects of chemotherapy. The study was published in Cell Reports.

Pardis C. Sabeti, MD, DPhil (Damon Runyon Fellow ‘04-‘06) of Harvard University, Cambridge, will receive the 2017 Richard Lounsbery Award from the National Academy of Sciences.

Elaine V. Fuchs, PhD (Damon Runyon Board Member, Damon Runyon Fellow ‘77-‘79) of The Rockefeller University, New York, has been named the recipient of the 2017 McEwen Award for Innovation. The prize, given by the International Society for Stem Cell Research, recognizes groundbreaking work pertaining to stem cells or regenerative medicine. Dr. Fuchs studies adult skin stem cells, how they make and repair tissues, and how cancers develop.

Akinyemi I. Ojesina, MBBS, PhD (Damon Runyon Fellow ’08-’11), of University of Alabama at Birmingham, worked with The Cancer Genome Atlas Research Network to identify novel genomic and molecular characteristics of cervical cancer that will aid in the subclassification of the disease and may help define personalized therapies for each individual patient.

By Ralph Kleiner, PhD, Damon Runyon - Dale F. Frey Breakthrough Scientist; Assistant Professor, Princeton University

As a chemical biologist, my work is motivated by a desire to understand the natural world. While pursuing basic research may seem far removed from the clinic, fundamental advances in our molecular understanding of biology have transformed our ability to diagnose and treat cancer as well as other diseases. Since scientific progress is often slow and can follow a circuitous path, it is absolutely critical that organizations like Damon Runyon are willing to play the ‘long game’, and invest in early stage and basic research.

By Daniel Webster, PhD, Damon Runyon-Philip O’Bryan Montgomery Jr. MD Fellow

The Damon Runyon Cancer Research Foundation recently asked some of our current award recipients how cancer will be prevented, diagnosed, and/or treated differently in the future. What can a future cancer patient, say 10-20 years from now, expect to experience? Their responses were fascinating, and over the next few months we will share their visions for the future on this blog. 

Elaine V. Fuchs, PhD (Damon Runyon Board Member, Damon Runyon Fellow ‘77-‘79) and Shruti Naik, PhD (Damon Runyon Fellow ’14-’18) at The Rockefeller University, New York, and colleagues, found that skin squamous cell carcinomas alter the protein-making machinery to preferentially use tumor-related mRNAs, leading to the production of proteins important for cancer progression. This switch is linked to a ribosome initiation factor called eIF2 and transition initiation factor eIF2A.

Trudy G. Oliver, PhD (Damon Runyon-Rachleff Innovator ’13-’15), and colleagues at the Huntsman Cancer Institute at the University of Utah, Salt Lake City, reported the generation of a new mouse model for studying small cell lung cancer (SCLC). They demonstrated that Myc oncogene expression cooperates with Rb1 and Trp53 loss in the mouse lung to promote aggressive, highly metastatic tumors that are initially sensitive to chemotherapy followed by relapse.