Professor Tang graduated MB ChB from The Chinese University of Hong Kong in 1991. He was admitted to Fellow of the Royal College of Pathologists of Australasia (FRCPA) in 1997 after training in both histopathology and chemical pathology in the Departments of Anatomical & Cellular Pathology and Chemical Pathology at the Prince of Wales Hospital. Professor Tang joined the University in 1996. He was then conferred the degree of Doctor of Medicine. In 2003/04, he was awarded a scholarship from the Sir Robert Black Trust Fund for a study leave at the Strangeways Research Laboratory of the University of Cambridge, UK. He is currently serving in the Advisory Committee of Genetic Pathology in the Royal College of Pathologists of Australasia. He has been examiner for RCPA and also serves as editor of RCPA Catalogue of Genetic Tests and Laboratories.

Professor Tang is a member of the joint metabolic clinic of the New Territories East Cluster hospitals which provides clinical service for patients with inherited metabolic diseases (IMD, also known as inborn errors of metabolism). His research interest covers both single gene diseases and genetic predisposition of common diseases. His research team contributed to the discovery of the disease gene causing Primary Carnitine Deficiency (named by him as 卡尼丁缺乏症, which has now become a commonly used Chinese medical term). The disease gene is known as OCTN2 or SLC22A5 and the discovery has been recognized as an Outstanding Research Project by the University. He continues to provide molecular genetic tests and develop new assays for Primary Carnitine Deficiency and other defects in the fatty acid beta -oxidation pathway.

Professor Tang is also the principal investigator of the Laboratory for Genetics of Disease Susceptibility in the recently established Li Ka Shing Institute of Health Sciences. The group focuses on studies of genetic predisposition to common diseases in the Chinese population. Our track records include genetic studies of Scoliosis, Diabetes, Alzheimer's disease, and infectious diseases (particularly SARS and tuberculosis). We first proposed a complex trait model of genetic susceptibility for idiopathic scoliosis since 2007 which is now confirmed by many GWAS and sequencing studies. He is also active in development of new analysis algorithms in bioinformatics and genetic statistics.

Patent:

Determination of gene expression levels of a cell type, US9589099B2

Links to publications:

Publons.com/researcher/2047982/nelson-l-tang

Google Scholar

ResearchGate

Pubmed

ORCID ID: 0000-0002-3607-5819

Book Editor:

Chemical Diagnostics: From Bench to Bedside (in the series of Topics in Current Chemistry, Vol. 336). L.S. Tang, Nelson; Poon, Terence (Eds.) Publisher: Springer; 2014. ISBN-10: 364239941X (Top 25% most downloaded eBooks in the relevant Springer eBook Collection)

10 selected publication among > 300 publications Tang, N. L. S., & Hui, J. (2020). 20 Years After Discovery of the Causative Gene of Primary Carnitine Deficiency, How Much More Have We Known About the Disease? HK J Paediatr (new series), 25:23-29. http://www.hkjpaed.org/pdf/2020;25;23-29.pdf Styrkarsdottir, U., Stefansson, O. A., Gunnarsdottir, K., et al. (2019). GWAS of bone size yields twelve loci that also affect height, BMD, osteoarthritis or fractures. Nature Communications, 10(1), 2054. https://doi.org/10.1038/s41467-019-09860-0 Styrkarsdottir, U., Helgason, H., Sigurdsson, A., et al. (2017). Whole-genome sequencing identifies rare genotypes in COMP and CHADL associated with high risk of hip osteoarthritis. Nature Genetics, 49(5), 801–805. https://doi.org/10.1038/ng.3816 Styrkarsdottir, U., Thorleifsson, G., Gudjonsson, S. A., et al. (2016). Sequence variants in the PTCH1 gene associate with spine bone mineral density and osteoporotic fractures. Nature Communications, 7, 10129. https://doi.org/10.1038/ncomms10129 Zhu, Z., Tang, N. L.-S., Xu, L., et al. (2015). Genome-wide association study identifies new susceptibility loci for adolescent idiopathic scoliosis in Chinese girls. Nature Communications, 6, 8355. https://doi.org/10.1038/ncomms9355 Estrada, K., Styrkarsdottir, U., Evangelou, E., et al. (2012). Genome-wide meta-analysis identifies 56 bone mineral density loci and reveals 14 loci associated with risk of fracture. Nature Genetics, 44(5), 491–501. https://doi.org/10.1038/ng.2249 Wan, X., Yang, C., Yang, Q., Xue, H., Fan, X., Tang, N. L. S., & Yu, W. (2010). BOOST: A fast approach to detecting gene-gene interactions in genome-wide case-control studies. American Journal of Human Genetics, 87(3), 325–340. https://doi.org/10.1016/j.ajhg.2010.07.021 Khor, C. C., Vannberg, F. O., Chapman, S. J., et al. (2010). CISH and susceptibility to infectious diseases. The New England Journal of Medicine, 362(22), 2092–2101. https://doi.org/10.1056/NEJMoa0905606 Woo, J., Tang, N., Suen, E., Leung, J., & Wong, M. (2009). Green space, psychological restoration, and telomere length. Lancet (London, England), 373(9660), 299–300. https://doi.org/10.1016/S0140-6736(09)60094-5 Tang, N. L.-S., Chan, P. K.-S., Hui, D. S.-C., To, K.-F., Zhang, W., Chan, F. K. L., Sung, J. J.-Y., & Lo, Y. M. D. (2007). Lack of support for an association between CLEC4M homozygosity and protection against SARS coronavirus infection. Nature Genetics, 39(6), 691–692. https://doi.org/10.1038/ng0607-691