Cells within the tumor are highly heterogeneous. Only small portion of the cells within tumor are capable to generate a new tumor. These cells called cancer stem cells.  Theoretically, cancer stem cells are originally from normal stem cells or early progenitor cells which accumulate the random mutations and undergo an altered version of the normal differentiation process. The cancer stem cell will drive tumor progression and its recurrence. Thus, further elucidation of the role and molecular mechanisms by which tumor promoter and tumor suppresser (such as c-Jun, CCR5, cyclin D1, Notch, p21, Dach etc.) on breast and prostate cancer stem cell self-renewal, expansion and differentiation will shed a light on the mechanism of breast cancer formation and invasion, leading to more effective treatments.

 Current Research Projects

• The role of c-Jun and CCR5 on breast cancer tumor metastasis and stem cell self-renewal, expansion and differentiation
• In vivo study of the role of cyclin D1 on prostate cancer tumorigenesis
• Establishment of light controlled in vivo temporal and spatial gene expression system

Future Plans

To determine the role of c-Jun and cyclin D1 in prostate cancer tumorigenisis in conditional knock-out mouse model.