We have examined changes in metastatic sites of HGSOC using mass spectrometry to define the matrisome (with collaborator Alexandra Naba, UIC). Through immunostaining and analysis of collagen fibers, we have demonstrated how the ECM changes in the primary tumor and metastatic sites. Current work is examining the premetastatic niche to determine if the ECM changes before the tumor is established in metastatic sites.

The ECM surrounding tumors is much more fibrotic than healthy tissue, which results in a change to the physical properties of the tumor. We have previously developed materials to decouple stiffness from other properties of the ECM (with collaborator Kristyn Masters, UC-Denver). We are examining how this increase in stiffness regulates invasion of USC tumor cells (with collaborator Dan Matson, UW-Madison).

While most HGSOC patients respond to chemotherapy initially, many suffer relapses and ultimately develop chemoresistant disease. Using our materials, we are examining how changes in the ECM influence this process.

Two of the most common sites of metastasis for HGSOC are the omentum and mesentery, which are adipose-rich structures in the peritoneum. The physical and biochemical environment of these tissues is altered in conditions such as obesity, and is further changed with metastasis. Using in vitro and in vivo models, we are studying how this unique microenvironment impacts metastasis.