In a new study, Sylvester researchers used mouse models to determine that promoting the activity of the p300 protein helps prevent myelodysplastic syndrome (MDS) from evolving into acute myeloid leukemia (AML). These findings could ultimately translate into new treatments that stall MDS progression. The study was published in the journal JCI Insight.
“Many MDS patients will progress to AML, which is more deadly, but we do not fully understand the mechanisms involved,” said Sylvester Director Stephen D. Nimer, M.D., senior author on the paper. “Now that we have identified an important role for p300 in preventing MDS progression, we can potentially manipulate its activity therapeutically.”
In the study, the researchers found that deleting or inhibiting p300 impairs the epigenetic machinery that controls gene expression triggering the development of AML. These findings indicated that losing p300 activity played a critical role in disease progression, increasing cell proliferation and giving the cells greater capacity to become increasingly malignant.