We continue to expand our clinical research in pharmacokinetic, pharmacodynamic and, more recently, pharmacogenomics studies of investigational drugs, which enable us to obtain a clear picture of how these drugs impact the patient. The department aims to bridge the gap between the development of promising new drugs and their application in the clinic.
Understanding how cancer advances by altering cell metabolism. Tumorigenesis is often associated with altered nucleotide metabolism, characterized by dysregulated Ribonucleotide Reductase (RR), and altered carbohydrate metabolism, characterized by increased glucose uptake and elevated lactic acid production under aerobic conditions. Notably, it was recently reported that RRM2B, the small subunit of RR, serves a crucial role in maintaining chromosomal stability and preventing chronic inflammation-associated tumorigenesis. We are also focused on understanding the autophagy regulatory mechanisms and biological functions in cancer. Autophagy is cell catabolic process in response to stress. Special emphases are focused on the involvement of ROS and oxidative stress from mitochondria to induce autophagy.
Understanding how cancer cells survive against therapeutics by altering cell signaling. Original DNA damage & Repair, add Ub and SUMO.
Understanding how cancer progresses by promoting cell survival. We are investigating how changes in androgen receptor (AR) signaling cause prostate tumorigenesis as well as progression from androgen-sensitive to castration-resistant prostate cancer. In conjunction, we are developing drugs that inhibit AR signaling by novel mechanisms.