The Starr Cancer Consortium has awarded grant funding to three Weill Cornell Medicine-led multi-institution teams to advance their groundbreaking cancer research projects. The grants will support studies on mechanisms that drive lymphoma and urothelial cancers, and the effects of radiation therapy.
Established by the Starr Foundation in 2006, the Starr Cancer Consortium is a collaboration among five leading research institutions: The Broad Institute of MIT and Harvard, Cold Spring Harbor Laboratory, Memorial Sloan Kettering Cancer Center, The Rockefeller University and Weill Cornell Medicine.
Each year, investigators from these institutions propose new strategies to improve the prevention, diagnosis, treatment and fundamental understanding of cancer. A review board of scientists from institutions outside the consortium selects the best of these proposals for funding, with an emphasis on identifying ambitious projects that have the potential to transform the field. This year, the winners include projects led by Drs. Lewis Cantley, Bishoy Faltas and Steven Josefowicz of Weill Cornell Medicine.
"Weill Cornell Medicine investigators have excelled once again in receiving grant funding from The Starr Foundation's annual competition, with members of our faculty leading three of the 10 funded projects," said Dr. Hugh Hemmings, senior associate dean for research and chair of the Department of Anesthesiology. "The generous support of the foundation enables these talented investigators to pursue innovative and collaborative approaches to tackle some of the toughest problems in cancer research."
Assistant Professor of Pathology and Laboratory Medicine; member of the Drukier Institute for Children’s Health; member of the Meyer Cancer Center
Mechanisms of Dynamic Chromatin Reorganization Regulating B Cell Differentiation and Lymphomagenesis
Activated B-cell-like diffuse large B-cell lymphomas (ABC-DLBCLs) are aggressive blood cancers. The affected cells carry mutations that activate cascading molecular signals inside the cells, allowing them to escape normal controls on multiplication and become cancerous. Therapies that target early steps in these signaling cascades have only been modestly effective. Based on preliminary results, Dr. Josefowicz and his colleagues hypothesize that ABC-DLBCLs are addicted to a downstream step in the signaling process, mediated by chromatin kinases that phosphorylate histones, DNA-packaging material, to activate oncogenes. They plan to test this hypothesis with inhibitors of these kinases, which should selectively kill the lymphoma cells by striking at the root of the lymphoma's addiction to active chromatin states at genes that drive pathology.
Co-principal investigators include Drs. Christina Leslie from Memorial Sloan Kettering Cancer Center, Ari Melnick from Weill Cornell Medicine, and Shixin Liu from The Rockefeller University.
Source: WCM Newsroom, 1/15/21