Dr. Ma Wenzhe
Dr. Ma Wenzhe from the State Key Laboratory of Quality Research in Chinese Medicine (Macau University of Science and Technology), for the first time in clinic, described the increased oxidative metabolism in the Li–Fraumeni syndrome. The possible linkage between the gain of function in oxidative metabolism and tumorigenesis in the Li–Fraumeni syndrome implies that carriers may have a good response to interventions inhibiting mitochondrial respiration. The finding was published in The NEW ENGLAND JOURNAL of MEDICINE in March 2013, which is one of the most prestigious medical journals in the world and has the highest impact factor among research journals with an IF53.
The Li-Fraumeni syndrome is an autosomal dominant hereditary disorder caused by germline mutations in embryogenesis or in one of the parent's germ cells of the p53 tumor suppressor gene, which results in a variety of sarcomas and carcinomas. p53 is one of the most important tumor suppressors and clinically more than 50% tumors have p53 mutations. Furthermore, one of the hallmarks of tumors is the metabolic change and mitochondria, as the powerhouse of the cell, play important role in tumor metabolism. But what’s the relationship between p53 mutations in the Li-Fraumeni syndrome and mitochondrial function? This is the scientific contribution that Dr. Ma and his colleagues made by answering this question.
Dr. Ma and his colleagues developed a foot-exercise apparatus that, when used, would deplete phosphocreatine levels in the tibialis anterior. The recovery time constant (Tc) of phosphocreatine after exercise which was measured by magnetic resonance spectroscopy was significantly shorter in the carrier group than that for the non-carrier group, indicating the carriers have increased mitochondrial function. This was further attested by the increased capacity for mitochondrial oxidative phosphorylation in cultured lymphocytes and myoblasts from the carriers. Also, biochemical studies showed that myoblasts from the carriers have increased mitochondrial biogenesis. Data from an established mouse model of the syndrome also showed that these mice have increased mitochondrial biogenesis, oxygen consumption capacity and endurance during exercise. Based on these findings, Dr. Ma and his collogues, for the first time, made the conclusion that the p53 mutations associated with the Li-Fraumeni syndrome can promote oxidative metabolism by means of increased mitochondrial biogenesis. The finding provides important new insights into tumor prevention and drug development for the Li-Fraumeni syndrome.
Dr. Ma Wenzhe is the outstanding young scholar who joined MUST in August 2012 from the US National Institutes of Health (NIH). Chair professor Liu Liang, President of MUST, is very happy and inspired with Dr. Ma’s first-author publication in the world-class medical journal, which indicates that scholars in MUST have been competent of performing cutting-age research onto international excellence. He expressed his determination to attract the most extraordinary staff word wide to making MUST a renowned university in Asia with international influence, and particularly he wishes the State Key Laboratory of Quality Research in Chinese Medicine (MUST) to make more breakthrough discoveries in both quality research in Chinese medicines and innovative drug development by integrating the most advanced knowledge and the cutting-edge technologies from talented researchers in multidisciplinary background.