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Study identifies mechanisms underlying osteochondroma formation


Osteochondromas are cartilage-capped benign bone tumors that form on the surface of bones near growth plates. These growths typically occur in adolescents and can result in growth impairment, pain, and fractures. In hereditary forms of the disease, 80-90% of patients have mutations in the genes exostosin 1 and 2; however, these mutations are not found in all patients. In this issue of JCI Insight, Antonios Aliprantis and colleagues at Brigham and Women's Hospital and Harvard Medical School in Boston demonstrate that loss of the genes encoding nuclear factor of activated T cells c1 and c2 (known as NFATs) induce osteochondroma formation in mice. Moroever, Aliprantis and colleagues identified the specific population of cells that give rise to these growths, known as aggrecan-expressing cells. Although mutations in the NFATs have yet to be identified in human osteochondromas, these studies indicate that therapeutic strategies targeting NFATs could potentially be used to treat skeletal diseases characterized by excessive growth of this cell population.



NFAT restricts osteochondroma formation from entheseal progenitors


Antonios Aliprantis
Brigham & Womans Hospital and Harvard University
Email:[email protected]

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JCI Insight is the newest publication from the American Society of Clinical Investigation, a nonprofit honor organization of physician-scientists. JCI Insight is dedicated to publishing a range of translational biomedical research with an emphasis on rigorous experimental methods and data reporting. All articles published in JCI Insight are freely available at the time of publication. For more information about JCI Insight and all of the latest articles go to

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