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Chinweike Ukomadu, MD, PhD

Assistant Professor, Department of Medicine, Harvard Medical School

Associate Physician, Medicine, Brigham And Women's Hospital

Contact Info

Chinweike Ukomadu
Brigham and Women's Hospital
75 Francis St

Boston, MA, 02115
Mailstop: Thorn 1404
Phone: 617-732-6287
Fax: 617-730-5807
cukomadu@partners.org

Assistant

Michele Pelosi
Administrative Assistant
Medicine
Brigham And Women's Hospital
20 Shattuck Street
Boston, MA, 02115
Phone: 617-732-7429
mpelosi@partners.org

DF/HCC Program Affiliation

Gastrointestinal Malignancies
Cancer Cell Biology

Research Abstract

Physiologic hepatocyte proliferation, as occurs in embryos during hepatic outgrowth and in adults during liver regeneration, is a tightly regulated process. In contrast, many liver diseases are accompanied by uncontrolled hepatocyte proliferation that can lead to hepatocellular carcinoma (HCC). We believe that similar genes control hepatocyte proliferation under physiologic and pathologic settings. By identifying genes important for liver development we can probe for contribution of these factors in liver cancer development and progression. The importance of a thorough dissection of the events that control pathologic hepatocyte proliferation is underscored by the enormous burden of liver disease: chronic liver disease is currently the 12th most common cause of death in the United States. Among patients with chronic liver disease, HCC is a frequent and accompanying complication and prognosis is dire, with resection or transplantation the only curative therapies . In fact, HCC is the fifth most common cancer worldwide and the third leading cause of cancer-related death.
Our recent studies have focused on the role of the ubiquitin-like with PHD and Ringer Fingers domain protein 1 (UHRF1) in liver development, regeneration and cancer development. We have acquired zebrafish lines deficient in UHRF1 and have generated specific antibodies to UHRF1. In collaboration with Dr Kirsten Edepli at Mount Sinai School of Medicine, we have generated liver specific transgenic mutants that express wild type and a specific phosphorylation deficient mutant form of UHRF1. Our goal is to understand the role of this protein in liver cancer formation.

Publications

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