The balance of power in B-cells tips in cancer's favor when a gene now understood to block tumor activity is mutated or deleted, researchers reported Nov. 23 in the journal Nature. The group believes the discovery offers a new treatment target for the most common form of lymphoma in adults.
In lab tests, researchers found the fate of the FBXO11 gene in B-cells had an impact on the activity of a known misfit protein (B-cell lymphoma 6, or BCL6) in cases of diffuse large B-cell lymphoma. When the FBXO11 gene was mutated or deleted, the activity of the cancer-causing protein increased. Conversely, when scientists dialed up FBXO11 activity, the tumor cells perished. It turns out FBXO11 is a key part of a system that takes out the garbage in cells and degrades the bad-acting protein BCL6.
This finding provides a new pathway to pursue for treatments of diffuse large B-cell lymphoma, which is the most common form of lymphoma in adults, according to a statement. The study included contributions from cancer research hubs New York University School of Medicine, Dana-Farber Cancer Institute and Howard Hughes Medical Institute.
"We have discovered that the protein FBXO11 is a novel tumor suppressor in B-cells," said senior study author Dr. Michele Pagano, the May Ellen and Gerald Jay Ritter professor of oncology and professor of pathology at NYU Langone Medical Center and a Howard Hughes Medical Institute investigator, in a statement. "Our new research findings show deletion or mutation of the FBXO11 gene in B-cells may lead to the formation of Diffuse Large B-Cell Lymphoma."
- here's the release