Research in our lab is broken down into four fields: systems biology for biofuel study, cancer bioinformatics, comparative genomics, and structural bioinformatics. We are interested in developing computational tools for solving biological problems. Particular areas of work include cancer computation and systems biology, plant cell-wall synthesis genes and pathways, microbial genome structure, pathway and network inference, and protein structure prediction.
Composition changes in microbial communities in human guts have been known to be associated with colorectal cancer development. However the causal relationship between such changes and cancer development remain elusive. We have recently conducted extensive transcriptomic data analyses of cancer-prone chronic inflammations, namely Crohn’s disease and ulcerative colitis coupled with the matching microbial communities as well as of early colon cancer tissues and associated microbial communities, and made a number of exciting discoveries. First we observed that certain microbial species have their population sizes increase with the level of oxidative stress in the inflammatory microenvironment and they seem to be directly involved in electron transfer from the diseased human tissues as electron receptors, suggesting that these microbes benefit from the influx of electrons. Interestingly some of these microbes secrete metabolites that may contribute to the altered immune responses, which are known to be cancer related. On the other hand, the most significantly increased subpopulations of microbes in human guts observed and reported previously, are known polysaccharide degraders. Knowing that cancer cells tend to have substantially increased polysaccharides on their cell surfaces, this observation strongly suggests that these increased microbial populations are the result of cancer development rather than its cause. Detailed analysis results will be presented and discussed in the context of co-evolution of diseased human cells and microbial community.