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职业迁徙
个人简介
We are interested in noncoding and epigenetic regulation of hematopoiesis and cancer. Currently, we are focusing on 1. Epigenetic mechanisms that control solid cancer and immune cell cross talks, 2. Noncoding RNAs in normal hematopoiesis and leukemia, 3. Finding novel functional noncoding sequences in the genome.
In our laboratory, we use the amazing blood-forming system, or hematopoiesis, as a model to study the noncoding and epigenetic controls. In a normal adult human being, ~100 to 200 billion new blood cells are generated every day to replace similar numbers of existing blood cells. These mature blood cells originate from hematopoietic stem cells and exhibit vastly different forms, shapes and functions, regulating processes such as innate and adaptive immune responses, oxygen transport and coagulation. Mature blood cells, such as macrophages and neutrophils, can also be found in tumor tissues to control tumor cell behavior and anti-cancer immune responses. During aging, hematopoietic stem cells accumulate mutations in key tumor suppressor genes, most frequently those regulating DNA methylation. Mutant hematopoietic stem cells out-compete normal stem cells in a process termed clonal hematopoiesis. Clonal hematopoiesis is a near universal feature of human aging, increases the risk of diseases such as leukemia, and can have wider impacts on other aging-associated diseases such as vascular defects and solid cancer.
In our laboratory, we use the amazing blood-forming system, or hematopoiesis, as a model to study the noncoding and epigenetic controls. In a normal adult human being, ~100 to 200 billion new blood cells are generated every day to replace similar numbers of existing blood cells. These mature blood cells originate from hematopoietic stem cells and exhibit vastly different forms, shapes and functions, regulating processes such as innate and adaptive immune responses, oxygen transport and coagulation. Mature blood cells, such as macrophages and neutrophils, can also be found in tumor tissues to control tumor cell behavior and anti-cancer immune responses. During aging, hematopoietic stem cells accumulate mutations in key tumor suppressor genes, most frequently those regulating DNA methylation. Mutant hematopoietic stem cells out-compete normal stem cells in a process termed clonal hematopoiesis. Clonal hematopoiesis is a near universal feature of human aging, increases the risk of diseases such as leukemia, and can have wider impacts on other aging-associated diseases such as vascular defects and solid cancer.
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PANCREASno. 2 (2024): e157-e163
JOURNAL OF CLINICAL INVESTIGATIONno. 3 (2024)
Huihui Zhang,Jun Lu,Jie Gao,Wenjun Sha, Xinhua Cai, Mai Re Yan Mu Rouzi, Yuanying Xu,Wenjun Tang,Tao Lei
Journal of Diabetes Research (2024): 5287580-5287580
Acta Diabetologicano. 5 (2024): 1-11
Zongwei Huang, Zihan Chen,Ying Li,Ting Lin,Sunqin Cai,Wenxi Wu, Lishui Wu, Siqi Xu,Jun Lu,Sufang Qiu
SCIENTIFIC REPORTSno. 1 (2024): 7686-7686
Yi Luan,Jiajia Hu,Qijun Wang,Xujun Wang,Wenxue Li,Rihao Qu, Chuan Yang,Barani Kumar Rajendran,Hongyue Zhou, Peng Liu, Ningning Zhang, Yu Shi,
Cell Reportsno. 3 (2024): 113934-113934
DIABETES METABOLIC SYNDROME AND OBESITY (2024): 997-1011
Zhiliang Bai,Dingyao Zhang,Yan Gao,Bo Tao,Shuozhen Bao,Archibald Enninful,Daiwei Zhang,Graham Su, Xiaolong Tian, Ningning Zhang,Yang Xiao,Yang Liu,
bioRxiv the preprint server for biology (2024)
Journal of Clinical Investigationno. 3 (2024)
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