Location: Conference Hall, Biotechnology Division, Dalian Institute of Chemical Physics
Time: 2015.12.1 (Tuesday)13:30- 14:30 p.m.
Lecturer：Prof. Dr. Jane Yu
University of Cincinnati-College of Medicine
Cincinnati, USA
Abstract：
Hyperactivation of mTOR is a common defect in a variety of cancer and diseases. mTOR regulates cell growth, protein translation, autophagy and cellular metabolism. Loss of tumor suppressor protein TSC2 results in activation of mTOR. Through a combination of bioinformatic, genomic and metabolic analyses, we identify dysregulation of specific metabolic pathways in cell models, preclinical models and human clinical materials. We investigate the translational potentials of targeting mTOR singly or in combination with other drugs affecting metabolic processes.
CV of the speaker:
Prof. Dr. Jane Yu
Department of Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, University of Cincinnati-College of Medicine
Cincinnati, OH 45267, USA
Tel: 513-558-4114, Fax: 513-558-4858
Email: jane.yu@uc.edu
Prof. Dr. Jane Yu graduated from Department of Biology of Peking University, China. She received Ph.D. in Biochemistry in The Graduate School and University Center of The City University of New York. Subsequently, she joined the Fox Chase Cancer Center in Philadelphia for her postdoctoral training under the mentorship of Dr. Elizabeth Petri Henske. From December 2008 to June 2015, Dr. Yu was an Independent Principal Investigator at the Brigham and Women’s Hospital-Harvard Medical School. Recently, Dr. Yu joined the Division of Pulmonary, Critical Care and Sleep Medicine Department of Medicine at the University of Cincinnati.
Dr. Yu’s research focuses are to study mechanisms through tumor suppressor proteins hamartin (TSC1) and tuberin (TSC2) regulate cellular metabolism and cell survival, identify potential biomarkers, establish preclinical models for translational research, perform bioinformatic and network analyses, conduct high-throughput drug screens, and develop pathway targeted therapies for tuberous sclerosis complex (TSC), lymphangioleiomyomatosis (LAM) and cancers.
Dr. Yu’s most important scientific achievements include 1) development of the first metastatic mouse model of lymphangioleiomyomatosis (LAM), a female predominant lung disease and demonstration that estrogen promotes the survival and lung metastasis of TSC2-deficient cells via MAPK pathway; 2) demonstration of the efficacy of FDA-approved agents in preclinical models; 3) discovery of the role of autophagy and metabolic reprogramming in tumorigenesis and set the stage for the first phase I clinical trial of autophagy inhibitor hydroxychloroquine and mTOR inhibitor Sirolimus at the BWH/HMS clinics; 4) discovery that TSC2 negatively regulates arachidonate metabolism and inflammation, demonstration of the efficacy of aspirin in suppressing tumorigenesis in preclinical models, and development of using plasma prostaglandins as diagnostic and therapeutic biomarkers for patients with TSC. This discovery has been translated into a Phase I Clinical Trial at BWH/HMS. Currently, Dr. Yu’s research has been funded by The LAM Foundation, The Adler Foundation, Department of Defense, Dana-Farber Cancer Institute/Harvard Medical School, Broad Institute of MIT-Harvard, NIH/NHLBI RO1, and NIH/NIDDK RO1.
Contact: Group 1808, Prof. Guowang Xu(9530)