My lab studies genetic alterations in cancer. The past decade has seen a burst of high-throughput sequencing data, especially out of the whole genomes of many different types of tumors. Researchers can now take advantage of that data to explore why genetic alterations occur, what roles they play during tumor progression and how they impact responses to treatment. The particular genetic alterations we study are called genomic rearrangements, large scale structural changes of DNA and chromosomes that occur frequently in tumor cells. The best known genomic rearrangement is the Philadelphia chromosome, which is a reciprocal translocation between chromosome 9 and 22 frequently found in chronic myeloid leukemia and some other types of leukemia. This translocation results in two genes being fused into one (BCR-ABL1 fusion). The fusion gene drives the cancer cells to divide uncontrollably. Researchers are trying to develop targeted therapies to block the effects of these and many other fusion genes now known to drive cancer. We are developing computational algorithms to identify new cancer-driving genomic rearrangements through the analysis of large-scale sequencing data from many cancer patients and with the aim of identifying novel drug targets. We are also trying to understand what causes these rearrangements. Better understanding of such mechanisms could provide clues to disease prevention, early detection and patient monitoring. My team also collaborates with physician-scientists to study the impact of genetic alteration on drug response and identify biomarkers that can be used to predict treatment outcome.

My main appointment is in the University of Chicago’s Ben May Department for Cancer Research. I also hold a joint appointment in the Department of Human Genetics. I have won the National Cancer Institute Transition Career Development Award, Cancer Research Foundation Young Investigator Award and the Mary Kay Foundation Innovative/Translational Cancer Research Award.