Our research focuses on understanding how alterations in tissue development, regeneration, and cellular states contribute to cancer initiation and progression, particularly in ovarian and endometrial cancers. Our laboratory established the first autochthonous mouse model of high-grade serous ovarian carcinoma (HGSC) and identified the transcriptional regulation of the miR-34 family by p53. We demonstrated that miR-34 is frequently downregulated in ovarian cancer and uncovered a critical role for the p53/miR-34/MET feed-forward loop in regulating cell motility and invasion. We also identified a previously unrecognized cancer-prone stem cell niche in the ovarian surface epithelium and discovered a pre-ciliogenic cell state in the uterine (Fallopian) tube epithelium that is particularly susceptible to ovarian cancer initiation.

More recently, our group developed a mouse model of serous endometrial carcinoma (SEC) driven by combined p53 and Rb1 deficiency. Using this model, we showed that the loss of differentiated cellular states is accompanied by the emergence of a clinically significant single-cell and spatial transcriptomic dysregulation signature. These HGSC and SEC models, together with several other highly accurate mouse models of human cancer developed by our laboratory, have provided important conceptual and technical insights into stem cell biology and cancer genomics and have helped advance the field of stem cell pathology.

Our research is strengthened by collaborations with developmental biologists and by cross-disciplinary partnerships in technology-driven areas, including high-throughput single-cell profiling, spatial transcriptomics, nonlinear microscopy, intravital imaging, and nanotechnology. My training as a human pathologist and extensive expertise in comparative mouse pathology further enhance our investigations into the cellular and molecular mechanisms of cancer pathogenesis.