Lin Xi
Postdoc Research Associate
Dr.Jiang Chang’s Lab
Center for Translational Cancer Research
Institute of Biosciences and technology
Texas A&M Health, Science Center
Houston, Texas
USA
His Professional/ Employment 2007 – 2012 Research assistant, Texas A&M Health Sciences Center 2012 – Present Post-Doctorate, Texas A&M Health Sciences Center Honors 2004 – 2007 Xiamen University Graduate Studies Fellowship 2004 – 2007 Third Institute of Oceanography Graduate studies Fellowship 2006 Model Student (top academic, virtue and physical condition) 2002 – 2003 Annual Excellent Undergraduate Scholarship 2000 – 2004 Tuition Scholarship for Students majoring in Fundamental Sciences
Hydrocephalus in humans is a severe neurological disorder characterized by an excessive accumulation of CSF in the brain. It affects about 1 in every 500 children based on an estimation by the National Institute of Neurological Disorders and Stroke in the USA. The precise causes of hydrocephalus remain largely unknown. Accumulating evidence suggests that genetic factors are critical for the pathogenesis of hydrocephalus. Congenital hydrocephalus, caused by genetic abnormalities, is the most common type of hydrocephalus. There were at least nine genes identified to be closely associated with congenital hydrocephalus pathogenesis in animal studies, but few of them were verified in humans. My research is continual identification of new genes/loci linked to this medical disorder and expand our knowledge of the genetic components of the disease. Gliomas, tumors from glial origin, are the most prevalent primary tumors in the brain. Glioblastoma multiforme (GBM, World Health Organization grade IV), the highest grade of gliomas, are the most common malignant primary brain tumors with rapid and invasive growth, and fast development of resistance to chemoradiotherapy. Despite significant advances in neurosurgery and multiple therapeutic strategies, the median overall survival of glioblastoma patients remains just over 1 year. There is a critical need for new molecular targets, concepts, and approaches to treat this devastating disease. We found, in our study, that RND3 (also called RhoE), a small GTPase, as an endogenous inhibitor of Notch and snail signaling, downregulated in human GBM and responsible for the hyperactivation of Notch and snail signaling, which promotes gliomagenesis and invasion respectively. My research interests is to continually explore pathological role of RND3 in human GBM progression and invasion as well as the associated animal studies.
