One of the top priorities in the medical field is diagnosing and stopping the growth of cancer.
Dr. Ying Xu, a computational biologist at The University of Georgia is studying hypoxia, an affliction thought to be related to the development of cancer.
Dr. Ying Xu is a computational biologist with current research interests in cancer systems biology and microbial bioinformatics. He is a professor and endowed chair in computational biology and bioinformatics in the Department of Biochemistry and Molecular Biology and also adjunct professor in the departments of Computer Science and Statistics at the University of Georgia. Originally trained as a computer scientist with a Ph.D. degree from the University of Colorado at Boulder in 1991, he is currently studying fundamental biology problems using computer technology and statistics as tools. He has published over 300 research articles and five books in bioinformatics and computational biology. Learn more about his Computational Systems Biology Lab.
Hypoxia
Scientists have been trying to understand why humans develop cancer for centuries.
Multiple theories have been developed. The most popular one in the past three decades is that cancer is the result of genetic mutations.
While mutations do play roles in cancer development, we think that the issue goes deeper than that. We have been examining the issue from the perspective of energy demand and supply in our cellular systems under persistent hypoxic conditions since scientists have long known that cancer is often linked with inflammation-associated hypoxia, a condition that results in inadequate oxygen supply to specific tissues.
Our study revealed that under persistent hypoxia, there is a gap between energy demand and supply in the affected cells. It is well known that under hypoxia, our energy supply goes down but our cellular system does not know which part of the energy consuming components to shut down. Since our cells have not been trained for such conditions, an energy gap results and the cells go “hungry.”
Other organisms such as turtles or frogs do not have this problem. This energy gap will lead to increased uptake of glucose from blood circulation and accumulation of glucose metabolites, which, in conjunction with inflammation and hypoxia, will lead to the production of short hyaluronic acids.
But, in our tissue system, short hyaluronic acids serve as signals for tissue injury. Continuous production of such molecules will trigger our body to think that the tissue is injured and needs repair. So our body activates the tissue repair system, which involves cell proliferation, cell survival and angiogenesis, basically all the signals needed for cancer development.
As long as the hypoxic condition persists, this process continues, leading to persistent cell proliferation. Genetic mutations typically take place later in this process serving as more efficient replacements for ongoing functions which are triggered by the hyaluronic acid-induced cell proliferation.
