Damon Runyon News

Patients with kidney disease who are undergoing dialysis often need to take a drug called a calcium-sensing receptor (CaSR) agonist to regain normal calcium levels in their blood. Unfortunately, inhibiting CaSR can sometimes reduce calcium levels too much, resulting in a condition known as hypocalcemia that carries serious adverse side effects. A major question in pharmacology, then, is how to modulate CaSR activity such that patients receive the benefits and not the risks.

The Damon Runyon Cancer Research Foundation has named 13 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 ($300,000 total) to investigate cancer causes, mechanisms, therapies, and prevention.

Metastatic tumors, which arise when a cancer spreads from the original tissue throughout the body, tend to be less responsive to therapy than primary tumors. Metastasis is often lethal for this reason, accounting for over 90 percent of cancer deaths. But given that primary and metastatic tumors within the same patient have the same genetic mutations, it is not clear why metastatic tumors are more aggressive.

The Damon Runyon Cancer Research Foundation is thrilled to continue our partnership with the Timmerman Traverse, an adventurous initiative that brings leaders and investors in biotech together to scale extraordinary heights.

The University of Texas MD Anderson Cancer Center, where former Damon Runyon Clinical Investigator Cassian Yee, MD, runs his lab, is home to the Moon Shots program, a cancer research initiative inspired by America's drive toward space in the 1960s. Recently, Dr. Yee and his colleagues announced a project that combines these two ambitions: sending T cells into space to inform the development of new cancer treatments.

In cancer treatment, “targeted therapies” refer to drugs that identify and attack specific proteins in cancer cells that help them survive and grow, while leaving normal cells alone. Due to their specificity, targeted therapies tend to be less toxic than chemotherapy or radiation therapies. Often, they take the form of small molecule inhibitors, which bind to the cancer-promoting proteins and disable them. Unfortunately, however, small molecule inhibitors only work for a subset of cancers.

Although many childhood cancers are now curable with chemotherapy, these lifesaving treatments often carry serious long-term side effects. Studies have shown, for example, that childhood cancer survivors are fifteen times more likely than the general population to suffer from congestive heart failure.  For patients and pediatric oncologists, the toxicity of chemotherapy drugs is tolerated only because there are no better options—in the United States, that is.

Each year, the Damon Runyon-Jake Wetchler Award for Pediatric Innovation is given to a third-year Damon Runyon Fellow whose research has the greatest potential to impact the prevention, diagnosis, or treatment of pediatric cancer. This year, the award recognizes the work of Yapeng Su, PhD, a Damon Runyon Quantitative Biology Fellow at Fred Hutchinson Cancer Research Center in Seattle.

Lung cancer is the leading cause of cancer death in the United States, and nearly a third of these cancers are driven by mutations in the KRAS gene. Long considered an “undruggable” cancer target, mutant KRAS proteins are known to rewire alveolar type II progenitor (AT2) cells, which line the lung surface and are responsible for repairing lung tissue after injury. KRAS inhibitors are now making their way to the clinic, but as yet only a subset of patients respond, highlighting the need to better understand the role of mutant KRAS in the development of lung cancer.