Benjamin D. Shogan, MD
Assistant Professor, Department of Surgery, University of Chicago
Urokinase Activation by Enterococcus. Faecalis to Promote Cancer Progress: a Novel Mechanism of Colorectal Cancer Recurrence Following Surgery.
Are certain intestinal bacteria to blame when colorectal cancer recurs after successful surgical resection?
Colorectal cancer is a major health concern with nearly 2 million new cases diagnosed worldwide in 2018. Currently surgical resection is the standard of care, and although surgery achieves a cure for some patients, up to half of those undergoing colorectal cancer surgery will have their cancer reoccur and will die from their disease. As a colorectal surgeon, Dr. Shogan grapples with these odds every day.
While many have studied how why people develop colorectal cancer in the first place, there is very little known about how and why it reoccurs. Using a live model, Dr. Shogan has observed that specific gut bacteria, namely Enterococcus faecalis, colonize at the surgical site and promote the formation of new tumors after surgery. The E. Faecalis seems to promote shed tumor cells that remain in the patient’s system after surgery back towards an aggressive phenotype, leading to migration and invasion of newly active cancer cells at the site of the surgery. This suggests that there is a microbial process driving cancer recurrence after surgery that could be blocked or countered.
Using this Cancer Research Foundation Young Investigator Award, Dr. Shogan hopes to identify the molecular mechanisms by which E. faecalis drives colorectal tumor cell migration and promotes tumor formation. Further, he hopes to identify the cellular pathways that are activated in certain cancer cells found in in tumors that have reoccurred after surgery and that have caused the cells to migrate back to the surgical site. Dr. Shogan’s project will provide novel insights into the host-microbe-cancer interactions that promote this invasive and metastatic phenotype of colorectal cancer cells and potentially those that drive other tumor types as well.