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生命科学专题学术讲座 | 胡政:Deciphering tumor origin and evolution with deep lineage recording
时间
2024年11月26日(周二)
16:00-17:30
地点
云栖校区3#312会议室
主持
西湖大学生命科学学院特聘研究员 王寿文
受众
全体师生
分类
学术与研究
生命科学专题学术讲座 | 胡政:Deciphering tumor origin and evolution with deep lineage recording
时间:11月26日星期二16:00-17:30
Time:4:00-5:30 PM, Tuesday, November 26,2024
主持人:西湖大学生命科学学院特聘研究员 王寿文
Host:Dr. Shouwen Wang, Principal Investigator, School of Life Sciences
地点:云栖校区3#312会议室
Venue:Room 312, Building 3, Yunqi Campus
主讲嘉宾/Speaker:
Dr. Zheng Hu, Principal Investigator, Shenzhen Institute of Advanced Technology (SIAT), Chinese Academy of Sciences (CAS)
Dr. Zheng Hu is Principal Investigator at Shenzhen Institute of Advanced Technology (SIAT), Chinese Academy of Sciences (CAS). He is also the Director of Center for Synthetic Biology and Evolution at SIAT. Dr. Hu received his B.S. (2010) in Biomedical Engineering from Huazhong University of Science and Technology and received his Ph.D (2015) from Beijing Institute of Genomics CAS. Dr. Hu did his postdoctoral fellow at Stanford University School of Medicine with Christina Curtis. Dr Hu’s research interests span from cancer genomics, cancer evolution to lineage tracing and computational biology. His research on measuring cancer evolutionary dynamics has yielded novel insights into cancer formation and metastasis, facilitating biomarker discovery for risk prediction and treatment decision making.
讲座摘要/Abstract:
Unravelling the origin and evolution of precancerous lesions is crucial for effectively preventing malignant transformation, yet our knowledge remains limited. Here we used a base editor-enabled DNA barcoding system to comprehensively map single-cell phylogenies in mouse models of intestinal tumorigenesis induced by inflammation or loss of the Apc gene. Through quantitative analysis of high-resolution phylogenies including 260,922 single cells from normal, inflamed and neoplastic intestinal tissues, we identified tens of independent cell lineages undergoing parallel clonal expansions within each lesion. We also found polyclonal origins of human sporadic colorectal polyps through bulk exome sequencing and single-gland whole-genome sequencing. Genomic and clinical data support a model of polyclonal-to-monoclonal transition, with monoclonality representing a more advanced stage. Single-cell RNA-seq revealed extensive intercellular interactions in early polyclonal lesions, but there was significant loss of interactions during monoclonal transition. Therefore, our data suggest that colorectal precancer is often founded by many different lineages and highlight their cooperative interactions. These findings provide insights into opportunities for earlier intervention in colorectal cancer.
联系人/Contact:
生命科学学院
于文越 yuwenyue@westlake.edu.cn