Targeting uracil-DNA glycosylase (UNG) may help to prevent the onset and proliferation of B-cell lymphoma, according to a study published in The Journal of Experimental Medicine.1
An enzyme, activation-induced deaminase (AID), contributes to the immune system’s ability to fight unfamiliar infections. AID can, however, create DNA mutations that play a causal role in the development of B-cell lymphoma.
Researchers showed in a mouse model that UNG allows both normal B cells and lymphoma cells to proliferate. RNA mismatching created by AID at chromosomal telomeres can cause genomic instability in B cells; unstable cells are, however, normally destroyed by a mechanism identified by the study’s authors.
Continue Reading
The presence of UNG allows for the proliferation of all B cells, including those with genomic instability, which can lead to B-cell lymphoma. Targeting UNG, therefore, may prevent lymphoma cells from proliferating.
RELATED: Adding CVP ± Rituximab After IFRT Improves PFS vs IFRT Alone in Stage 1-2 Follicular Lymphoma
The authors suggest that UNG inhibition may be an effective way to treat lymphoma. It is unclear, however, under what conditions this treatment might effectively be used, or whether preventing the proliferation of abnormal B cells would also introduce problems by preventing the proliferation of normal B cells.
Reference
- Cortizas EM, Zahn A, Safavi S, et al. UNG protects B cells from AID-induced telomere loss. J Exp Med. 2016 Oct 3. doi: 10.1084/jem.20160635 [Epub ahead of print]
