Not all cancers respond to the same treatments or have the same genetic origins.
Epstein-Barr virus (EBV), a common and highly contagious virus, has been found to cause certain cancers, including non-Hodgkin lymphoma (NHL). The aggressive blood cancer is incredibly common, carrying a lifetime risk of 1 in 46 for men and about 1 in 55 for women.
But a new study, led by researchers in the lab of Blossom Damania, PhD at the UNC School of Medicine and UNC Lineberger Comprehensive Cancer Center, has identified a new "weak spot" in EBV-positive non-Hodgkin lymphoma that could shape the next generation of cancer treatments.
The study was published in the journal, Proceedings of the National Academy of Sciences.
Blossom Damania, PhD
"Many EBV-positive lymphomas can rapidly develop resistance to treatment, leading to poor patient outcomes," said Maria White, PhD, a postdoctoral researcher in the Damania lab and lead author on the paper. "Our research indicates that targeting a single enzyme may offer a more effective approach for the treatment of EBV-positive NHL."
The enzyme, called NEK2, plays a large role in cancer cell division. High levels of the enzyme have been associated with aggressive types of cancers and serve as a biomarker of poor prognosis. Given the enzyme's prominent role in EBV-positive NHL, White and Damania wanted to see what would happen if they selectively "turned off" the enzyme in cellular models.
They found that inactivating NEK2 resulted in the death of some lymphoma cells and also made the lymphoma cells more vulnerable to other anti-cancer treatments. Importantly, NEK2 inhibition had no effect on non-cancerous cells.
They then tested the inactivation of NEK2 in EBV-associated NHL using a preclinical cancer model and showed that the NEK2 inhibitor significantly prolonged survival and decreased the level of tumor cells throughout the body, with a few who were completely rid of all observable traces of lymphoma. Future studies include testing NEK2 inhibitors in clinical trials for NHL.
This research was funded by the National Institutes of Health (NIH).
