Damon Runyon News

Understanding molecular function in biological settings is essential for successful development of targeted therapies for cancer. Advances in biochemical profiling techniques have generated lists of molecules involved in cancer development and progression, but the mechanisms by which these molecules work together within cells and tumors remain largely unclear. Molecularly targeted cancer therapeutics based on incomplete understanding of the tumorigenic mechanisms often demonstrate initial response followed by cancer resistance.

Dr. Kircher's goal is to develop a new nanoparticle-based technology that will allow the detection and treatment of cancer based on in vivo tumor marker expression profiling. This would enable a single cancer cell to be both imaged and killed in a single process. To date this has not been achieved, in part due to inadequate sensitivity and inability to accurately visualize the expression of multiple tumor markers simultaneously.

Dr. Dodson is investigating how defects that are not strictly based on DNA mutations can be passed from parent to progeny for multiple generations. Germ cells, the producers of eggs and sperm in animals, normally transmit the blueprint for life from parent to progeny. When germ cells acquire defects, however, these defects may also pass from parent to progeny. These underexplored defects may contribute to the onset and inheritance of familial cancer syndromes, and a better understanding of them could result in new cancer therapies.

Glioblastoma remains the most aggressive brain tumor diagnosed in patients, and it is clear that new treatment strategies are needed. There is significant optimism around the use of approaches that stimulate a patient's immune system to treat brain tumors. Gavin focuses on identifying the specific components of a patient's brain tumor that the immune system recognizes and determining whether there are regional differences in this immune recognition.

Therapies that directly target cancer-promoting oncoproteins have revolutionized the treatment of cancer. Cancers, however, are primed to adapt and evolve in the presence of treatment, resulting in an ability to resume growth despite the presence of therapy. Utilizing cutting-edge new techniques that allow the determination of genetic alterations in single cancer cells, Piro aims to understand the principles that govern the evolution of resistance during therapy and identify novel therapeutic interventions that halt this process.

Leptomeningeal metastasis, or spread of cancer cells into the spinal fluid, is a devastating complication of cancer resulting in rapid neurologic disability and death. With little mechanistic information to guide treatment decisions, efforts at treatment are too often futile. To address this critical knowledge gap, Adrienne will employ a translational approach to analyze patient samples utilizing multiple, complementary, orthogonal molecular strategies as tools for discovery.

Mark is a cancer surgeon and health economist. He is examining one of the hidden barriers to surgical oncology access in head and neck cancer—that of non-medical costs. For 81 million people every year, surgery leads to catastrophic impoverishment, but only 40% of that is due to the direct medical costs of surgery. The rest is due to the hidden costs of transportation, food, and lodging necessary to get surgery. He proposes to design and optimize a cash transfer for patients with head and neck tumors in a low-income West African country.

Despite our best current treatments, 95% of patients with pancreatic cancer, including those at the earliest stages, die within 5 years of diagnosis. By 2020, pancreatic cancer will become the second leading cause of cancer-related death in the U.S., and new therapies are urgently needed. T cells are highly specialized cells of the immune system designed to protect the human body from infections and cancer. Very few T cells recognize pancreatic cancer; however, recent work showed that these T cells play a very important role in controlling the spread of pancreatic cancer.

Dr. Bowman focuses on acute myeloid leukemia (AML), which can be characterized by successive development of genetic mutations. While some mutations are found in nearly every cell of the disease, others are found in sub-populations and are thought to arise at later stages of disease development. It remains unclear if these late mutations are necessary for leukemic progression and are actionable therapeutic targets. He aims to develop models to test the oncogenic dependency of one of the most commonly mutated genes in AML, FLT3.

Pediatric acute myeloid leukemia (AML) has the lowest survival rate among all pediatric cancers. MLL gene rearrangements (MLL-r) occur in about 20% of children diagnosed with AML. This subtype of leukemia is exquisitely sensitive to inhibition of the interaction between MLL and the chromatin adaptor Menin. Dr. Soto-Feliciano is combining genetic, genomics, and mouse modeling approaches to identify factors that regulate the function of Menin in MLL-r and non-MLL-r leukemia.