Dr. Bynoe is an immunologist and a leading expert on the blood-brain barrier. In 2011, her team discovered that a drug called Lexiscan briefly opens the blood-brain barrier, allowing drugs to more effectively treat brain diseases.

Dr. Bynoe is originally from Saint Vincent and the Grenadines. She received her B.S. from Long Island University, and her Ph.D. from Albert Einstein College of Medicine. She was a postdoctoral fellow in the lab of Dr. Charles Janeway, a very famous immunologist at Yale, and was promoted to an Associate Research Scientist before coming to Cornell. She is currently the Director of Graduate Studies for the Immunology and Infectious Disease Ph.D. program at Cornell.

In a recent study, Dr. Bynoe showed the importance of a protein called CD73 in the development of glioblastoma. Glioblastoma is the most common type of brain cancer, and it is also the most deadly because it is extremely hard to treat. Even with treatment, patients survive only 16 months on average. By showing the importance of CD73 and examining what role it is playing in glioblastoma, Dr. Bynoe’s research has identified a new drug target for this very severe disease.

To do this, Dr. Bynoe first showed that brain tumor cells express high levels of CD73. She then took those brain tumor cells and transplanted them into mice that couldn’t make CD73. She found that the level of CD73 was even higher in the tumors of those mice than normal mice. However, in the mice without CD73, the tumors weren’t able to grow as well - they barely grew or expanded over the course of 3 weeks - and the mice lived much longer. Thus, it was the CD73 from the mouse itself and not from the tumor that mattered for the outcome.

Looking at this more closely, Dr. Bynoe noticed that tumors in the mice without CD73 were less good at creating new blood vessels, which are needed to nourish the growing tumor. However, those tumors also created many more blood vessels. That led her to look at the adenosine receptor A2B, which is known to indirectly stimulate blood vessel growth. Tumors in mice without CD73 had higher levels of A2B activity, which is consistent with higher levels of inflammation. However, when she blocked A2B with a drug, the tumor cells were more susceptible to chemotherapy.

Thus, Dr. Bynoe was able to show that reducing the levels of CD73 in the brain of a glioblastoma patient and/or blocking the activity of A2B are promising new directions for treatment.