讲座题目: Signaling Pathway in the Bone Development and Cancer Stem Cell
主讲人: Jianning Tao, Ph.D. Assistant Professor, Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, USA
主持人:廖鲁剑 教授
开始时间: 2015-6-15 9:30-10:30
讲座地址: 闵行生科院534报告厅
主办单位: 天美娱乐 科技处
报告人简介：Jianning Tao’s laboratory studies skeletal development and pediatric bone tumors. Specifically, Dr. Tao focuses on understanding cancer stem cell and metastasis of osteogenic sarcoma, one of the most common type of cancer in children. As a PI faculty, Dr. Tao plans to contribute his expertise to clinical, educational, scholarly or service efforts by providing laboratory experience and knowledge to the pediatric research. He is also looking forward to opportunities to collaborate with other scientists in the world to develop patient-related research projects. Moreover, Dr. Tao has also been trained as a developmental biologist and molecular biologist, so he can contribute his expertise by giving lectures/seminars and providing lab training to help trainees to understand disease pathogenesis and therapy. In addition, Dr. Tao has published high impact research articles in journals such as Cancer Cell and Development, and he hopes to continue producing high impact publication and share his research discovery with the broader pediatric and academic society. Furthermore, Dr, Tao would like to serve as a mentor and advocate for education, scholarship, and service activities.
报告摘要：Osteogenic sarcoma (OS) is the most common malignant tumor of bone with a predilection for adolescents and young adults. Human OS occurs sporadically and bone tumor initiation and progression are poorly understood. We describe here the generation and characterization of a genetically engineered mouse model of OS based on conditional expression of truncated Notch1 protein. All animals spontaneously developed bone tumors including OS-like with 100% penetrance. The tumors, developed through Rbpj-dependent canonical pathway, model human OS including morphology, metastatic behavior, cytogenetic complexity, and genome-wide expression profiling. We demonstrated that Notch activation combined with p53 loss synergistically accelerates OS development in mice, though p53 driven OS is not dependent on canonical Notch signaling, revealing a dual dominance of Notch oncogene and p53 mutation in the development of OS. Because of similarity between murine OS and human OS, our authenticated model can be used not only to address cancer mechanisms of OS but also as a valuable platform for developing novel therapeutic strategies.
