Prof SHUM Sau Wun Alisa - School of Biomedical Sciences, CUHK

Prof SHUM Sau Wun Alisa

Associate Professor

B.Sc. (University of Glasgow), D.Phil. (University of Oxford)

39436840

alisa-shum@cuhk.edu.hk

308A, Lo Kwee-Seong Integrated Biomedical Sciences Building, Area 39, CUHK

Biography

Prof. SHUM Sau Wun Alisa (沈秀媛) is an Associate Professor at the School of Biomedical Sciences of The Chinese University of Hong Kong (CUHK). She received her BSc degree in cell biology from University of Glasgow. She then obtained a DPhil degree in developmental biology from University of Oxford, studying the pathogenic mechanism of neural tube defects. After graduation, she was awarded a Croucher Fellowship to conduct postdoctoral research on genomic imprinting at University of Cambridge prior to joining CUHK.

Prof. Shum has used animal models to study different types of congenital malformations, including neural tube, heart and kidney defects, cleft palate and caudal regression. She has focused on the effect of retinoic acid and maternal diabetes on embryo development. Her group has unraveled a paradoxical teratogenic mechanism for retinoic acid, a key regulator of growth and development, which has important implications for retinoid-based therapies. Her group is the first to demonstrate a mechanistic link between perturbation of retinoid homeostasis and increased susceptibility to malformations in embryos exposed to diabetes. Recent findings from her group also support an association of subnormal retinoid levels with fetal programming of chronic diseases in adulthood. She aims to develop in utero therapeutic interventions to reduce the risk of birth defects and prevent the development of diabetes, obesity and related complications later in life in offspring of mothers with pregestational diabetes. Her current research also includes preclinical studies on novel drugs that have anti-obesity and insulin-sensitizing effects.

Research Interests

Development of drugs for prevention and treatment of metabesity (obesity, type 2 diabetes and related metabolic disorders) and neurodegenerative diseases.
Mechanisms underlying fetal programming of obesity, diabetes, hypertension and neurologic disorders.
In utero therapeutic interventions to combat against the adverse effects of maternal diabetes and obesity on embryo development.
Mechanisms underlying abnormal development of the central nervous system.

Selected Publications

Lee, L.M.Y., Leung Y.C., & Shum, A.S.W.(2023). Hyperglycemia alters retinoic acid catabolism in embryos exposed to a maternal diabetic milieu. PLoS One, 18(8):e0287253.
Lee, L.M.Y., Tam, S.T.K., McCaffery P.J., & Shum, A.S.W. (2019). Highly sensitive quantitative determination of retinoic acid levels, retinoic acid synthesis, and catabolism in embryonic tissue using a reporter cell-based method. In: Ray S. (eds) Retinoid and Rexinoid Signaling. Methods in Molecular Biology, 2019, 181-192.
Lee, L.M.Y., Leung, M.B.W., Kwok, R.C.Y., Leung, Y.C., Wang, C.C., McCaffery, P.J., Copp, A.J., & Shum, A.S.W. (2017). Perturbation of retinoid homeostasis increases malformation risk in embryos exposed to pregestational diabetes. Diabetes, 66, 1041-1051.
Lee, L.M.Y., Leung, C.Y., Tang, W.W.C., Choi, H.L., Leung, Y.C., McCaffery, P.J., Wang, C.C., Woolf, A.S., & Shum, A.S.W. (2012). A paradoxical teratogenic mechanism for retinoic acid. Proceedings of the National Academy of Sciences of the United States of America, 109, 13668-13673.
Shum, A.S.W., Tang, L.S.C., Copp, A.J., & Roelink, H. (2010). Lack of motor neuron differentiation is an intrinsic property of the mouse secondary neural tube. Developmental Dynamics, 239, 3192-3203.
Tse, H.K.W., Leung, M.B.W., Woolf, A.S., Menke, A.L., Hastie, N.D., Gosling, J.A., Pang, C.P., & Shum, A.S.W. (2005). Implication of Wt1 in the pathogenesis of nephrogenic failure in a mouse model of retinoic acid-induced caudal regression syndrome. American Journal of Pathology, 166, 1295-1307.
Leung, M.B.W., Choy, K.W., Copp, A.J., Pang, C.P., & Shum, A.S.W. (2004). Hyperglycemia potentiates the teratogenicity of retinoic acid in maternal diabetes. Diabetologia, 47, 515-522.
Chan, B.W.H., Chan, K.S., Koide, T., Yeung, S.M., Leung, M.B.W., Copp, A.J., Loeken, M.R., Shiroishi, T., & Shum, A.S.W. (2002). Maternal diabetes increases the risk of caudal regression caused by retinoic acid. Diabetes, 51, 2811-2816.
Shum, A.S.W., Poon, L.L.M., Tang, W.W.T., Koide, T., Chan, B.W.H., Leung, Y.C., Shiroishi, T., & Copp, A.J. (1999). Retinoic acid induces down-regulation of Wnt-3a, apoptosis and diversion of tail bud cells to a neural fate in the mouse embryo. Mechanisms of Development, 84, 17-30.
Shum A.S.W., & Copp, A.J. (1996). Regional differences in morphogenesis of the neuroepithelium suggest multiple mechanisms of spinal neurulation in the mouse. Anatomy and Embryology, 194, 65-73.
Sasaki, H., Ferguson-Smith, A.C., Shum, A.S.W., Barton, S.C., & Azim Surani, M. (1995). Temporal and spatial regulation of H19 imprinting in normal and uniparental mouse embryos. Development, 121, 4195-4202.
Brook, F.A.^#, Shum, A.S.W.^#, Van Straaten, H.W.M., & Copp, A.J. (1991). Curvature of the caudal region is responsible for failure of neural tube closure in the curly tail (ct) mouse embryo. Development, 113, 671-678.

^# Co-first author

Grants

RGC – General Research Fund [PI; 01-Jan-20 to 31-Dec-21]: “Dysregulation of retinoic acid homeostasis and signaling in fetal islet development under maternal diabetic or high glucose conditions” (HK$770,053).
RGC – General Research Fund [PI; 01-Oct-17 to 30-Sep-20]: “Association of retinoid deficiency with inborn nephron deficit in offspring exposed to maternal diabetes” (HK$1,212,780).
RGC – General Research Fund [PI; 01-Oct-14 to 31-Jan-18]: “A study on the association between oxidative stress and retinoic acid homeostasis” (HK$951,400).