By addressing fundamental scientific questions, CRI is improving our understanding of the biological basis of disease to cure people who would not be cured otherwise.


June 2024
Researchers identified a type of metabolic inflexibility during liver regeneration that prevents cells with dysfunctional mitochondria from proliferating, which demonstrates one way regenerative cells root out damage. When their mitochondria are damaged, hepatocytes turn on PDK4, a metabolic enzyme that stops the cells from shifting to an alternative source of acetyl-CoA, so they can’t proliferate. Science 384, ePub


April 2023
Extrachromosomal DNA (ecDNA) found to harbor cancer-associated oncogenes and immunomodulatory genes that promote cancer development in pre-cancerous cells. These findings raise the possibility of earlier interventions and preventive measures for patients with tumors containing ecDNA and provide a new understanding of ecDNA’s role in cancer development. Nature 616, 798-805
April 2023
Showed that clones of hepatocytes containing somatic mutations are selected for their ability to protect against the damaging effects of fatty liver disease. Through this elucidation of the biological basis for mutant clone expansion, the lab established a method by which adaptive pathways in metabolic disease can be identified. Cell 186, 1968-1984


October 2022
Identified markers that distinguish skeletal stem cells in the bone marrow from skeletal stem cells on the outside surface of bones and compared their functions. The Leptin Receptor-expressing skeletal stem cells in the bone marrow are responsible for the steady-state production of new bone cells that maintain the adult skeleton and repair certain types of bone injuries. The Gli1-expressing skeletal stem cells on the outside surfaces of bones (in the periosteum) are responsible for fracture repair. Cell Stem Cell 29, 1547-1561
August 2022
Discovered that mutations in IDH genes, which are common in adult and adolescent brain tumors, cause cells to become addicted to a metabolic process called de novo pyrimidine nucleotide synthesis. This addiction stems from the ability of IDH mutations to increase susceptibility to DNA damage, which provides new insights into the ways that these mutations reprogram brain cell biology. Cancer Cell 40, 939-956




December 2019
Found certain melanoma cells are more likely to spread through the body. Efficiently metastasizing melanoma cells take up more lactate because they have higher levels of a lactate transporter, called monocarboxylate transporter 1 (MCT1), on their cell surface as compared with inefficient metastasizers. This demonstrates that metabolic differences among melanoma cells confer differences in metastatic potential. Nature 577, 115-120





October 2015
Found that antioxidants promote the survival of cancer cells during metastasis. These results raised the possibility that cancer should be treated with pro-oxidants rather than antioxidants and explained why administration of antioxidants to patients led to worse outcomes in clinical trials. Nature 527, 186-91




January 2012
Identified the microenvironment, or niche, in which blood-forming stem cells are maintained within the bone marrow, a long-standing goal in the field of stem cell biology. This study also reported the discovery of Leptin Receptor-expressing stromal cells in the bone marrow that are the main source of growth factors required for the maintenance of blood-forming stem cells. Nature 481, 457–62

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