Study illuminates precancerous 'clonal outgrowth' in bloodcells WeillCornell NatureGenet
The gene DNMT3A normally encodes an enzyme called a methyltransferase, which helps place methylations on DNA. The researchers found that the mutation's disruption of normal methylation led to a lack of these"off switches" across the genome and the abnormal activation of key genes.
"Our hope is that by uncovering molecular signatures like these we'll be able to target these clonal outgrowths and prevent cancer development in people who are still healthy," said study co-first-author Dr. Anna Nam, assistant professor of pathology and laboratory medicine in the Department of Pathology and Laboratory Medicine and a member of the Meyer Cancer Center at Weill Cornell Medicine, and a pathologist at NewYork-Presbyterian/Weill Cornell Medical Center.
The researchers plan to do further studies of clonal outgrowths resulting from other mutations. They are also developing their multi-omics techniques to increase the speed and scale of these studies. "We should soon be able to do studies of many more cells at a time, giving us a more complete picture of what is going on," said co-first author Neville Dusaj, a Tri-institutional MD-Ph.D. Program student in the Landau laboratory.
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