Dr Terry R. Medler

Dr Terry R. Medler

Dr Medler aims to determine to what extent activation of the complement pathway contributes to cancer

Terry R. Medler, PhD grew up in Marseilles, Illinois and received his B.S. in Chemistry and Biology at Valparaiso University. He then moved to The Johns Hopkins University to pursue his interest in medical research and also received his M.S. in Biotechnology from Hopkins. After deciding that a career in research was his aspiration, he moved to Chicago to pursue his PhD in Cancer Biology at Northwestern University.

The realization that cellular programs in tumor cells alone are not sufficient to drive and sustain tumor growth brought him to the laboratory of Lisa M. Coussens, Ph.D. at Oregon Health & Science University. Her lab has pioneered groundbreaking research showing that tumor growth is supported by chronic inflammation that was initially intended to clear damaged/cancerous cells. By understanding how these immune cells are recruited and activated in solid tumors, the lab hopes to find new treatments for cancer.

As a central mediator of inflammation in tissues, activation of the complement pathway is critical for clearance of “damaged” cells, in addition to recruiting and activating immune cells to “damaged” tissues. Thus, the focus of his research is to determine whether activation of this pathway also regulates chronic inflammation associated with solid tumor development. To address this hypothesis, he is using a human papillomavirus (HPV) – mediated mouse model of cancer that effectively models cervical cancer, some head and neck cancers, skin cancer, and cancers of the anogenital region (anal, penile, vulva) in humans.

Complement C5a Regulates Squamous Carcinogenesis

The goals of Dr. Medler’s research project titled “Complement C5a Regulates Squamous Carcinogenesis” are to determine to what extent activation of the complement pathway contributes to cancer, how complement is activated in these cancers, and whether therapeutics targeting this pathway might extend to an enhanced response to current standard-of-care chemotherapy.