We are interested in the mutational mechanisms and clonal evolution of cancer, in particular mechanisms of structural variants and the impact on 3D chromatin organization. Through close collaborations with clinicians, we are working towards the long-term goal to provide improved therapeutic intervention options for clinical decision-making.
Keywords: Cancer genomics, structural variants, 3D chromatin organization, tumor evolution, precision medicine, bioinformatics, prostate cancer, glioblastoma, medulloblastoma, leukemia
Cancer is a genetic disease and is fueled by the accumulation of genomic alterations that improve the fitness of the cell. A tumor cell is exposed to a plethora of intrinsic and extrinsic stimuli that can act to stimulate or inhibit the progression of the disease. How a tumor cell escapes and evolves in time and space to cause treatment-resistance and lethal disease is a fundamental question in cancer research. We are interested in the mutational mechanisms during tumor evolution (Figure 1), in particular, the mechanisms and functional consequences of large-scale genomic structural variations (SV) (e.g. deletions, duplications, and translocations) in cancer.