By searching for hyperactive cell signals in primary effusion lymphoma, researchers were able to find a pathway that can be blocked to limit tumor growth.
Researchers from the UNC Lineberger Comprehensive Cancer Center have discovered a hyperactive cell signal that contributes to tumor growth in primary effusion lymphoma and developed an experimental therapeutic, UNC3810A, to block the signal and slow tumor growth.
In the report, published in the journal Proceedings of the National Academy of Sciences, researchers searched for kinases that were hyperactive in primary effusion lymphoma, as well as in other types of non-Hodgkin lymphoma. They then characterized the activity of the kinase signals, which help to control cell signaling, in the cancer cells.
Their studies showed that Tyro3 kinase, a protein that is highly upregulated and expressed in primary effusion lymphoma, was uniquely hyperactive in those cells compared with normal cells. The study authors also found that the protein could activate a pathway that promotes the cancer’s survival.
When cells were treated with UNC3810A, the researchers observed a dose-dependent activation of cell death and a significant suppression of tumor growth. The compound was used as an in vivo tool to understand the biological roles of Tyro3 in primary effusion lymphoma, and the researchers are currently working toward optimizing UNC3810A to preclinical candidate.
The study authors noted that since the target that they identified in primary effusion lymphoma is also upregulated in other types of cancers besides lymphomas, the drug they developed may be used for multiple cancers.