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Jedd D. Wolchok, MD, PhD (Damon Runyon-Lilly Clinical Investigator ‘03-‘08) at Memorial Sloan Kettering Cancer Center, New York, and colleagues, reported that matching the size of a tumor to the body's immune response could help doctors tailor immunotherapy treatments for melanoma patients whose disease has spread.
David M. Livingston, MD (Damon Runyon Board Member), of Dana-Farber Cancer Institute, Boston, has been named the 20th recipient of the Pezcoller Foundation-AACR International Award for Cancer Research. Dr. Livingston is honored for his fundamental contributions to the field of basic cancer research. His work has been pivotal to the understanding of retinoblastoma pathway of cell cycle control as well as the transcriptional co-activation function of the key regulatory proteins, p300 and CBP.
At the junction of growth and starvation stands a signaling protein called mechanistic Target of Rapamycin Complex 1 (mTORC1). Inside the cell, mTORC1 regulates metabolism, growth, protein and organelle recycling (autophagy), proliferation, and survival. When something goes wrong in the pathway, various diseases such as cancer, obesity, and type 2 diabetes, can develop. An outstanding challenge is to understand how mTORC1 becomes activated in response to a wide variety of stimuli including nutrients, growth factors, and stressors, in normal and cancer states.
Anjana Rao, PhD (Damon Runyon Fellow ’79), and James Scott-Browne, PhD (Damon Runyon Fellow ’11-’13), at the La Jolla Institute for Allergy and Immunology, La Jolla, and colleagues, are focusing on a key issue of how tumor-fighting T cells can lose their effectiveness or become “exhausted.” The researchers identified two proteins, NFAT and Nr4a, that can bind to the DNA of T cells and shut down their tumor-fighting activity. Next steps will be to determine if these processes can be interfered with or reversed in order to re-motivate immune cells to eradicate a pati
Don X. Nguyen, PhD (Damon Runyon Fellow ’05-’08), of Yale Cancer Center, New Haven, and colleagues, reported new findings that explain the propensity of latent lung adenocarcinoma (LUAD) to relapse. They showed that differential expression of extracellular matrix (ECM) molecules and their interacting proteins contributes to risk of relapse in distinct LUAD subtypes. One protein called hyaluronan receptor HMMR, when overexpressed, was associated with inflammation and poor prognosis.
Christine Iok In Chio, PhD (Damon Runyon Shirley Stein Fellow ’13-’17), in the laboratory of her sponsor David Tuveson, MD, PhD, and colleagues at Cold Spring Harbor Laboratory, Cold Spring Harbor, created a new 3D model of pancreatic cancer, which allowed them to identify two distinct stroma cell populations called cancer-associated fibroblasts (CAF’s), that work together with cancer cells to protect and help the tumor grow.
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. CCL2 levels increased further after the mice received radiotherapy.
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. She is recognized for her groundbreaking contributions including the development of new methods to study evolutionary selection in humans and viruses; the creation of new collaborative models for combatting emerging diseases across disciplinary and national borders; and leadership of global efforts to increase data sharing in pandemics such as Ebola and Lassa Fever.
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.
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