The enzyme TET2 play a key role in causing blood cancers, but how it become activated wasn’t known. In a study published online on April 3 in Cancer Discovery, co-senior authors Amit K. Verma, M.B.B.S., and Amittha Wickrema, Ph.D., of the University of Chicago report that the enzyme kinase JAK2 activates TET2 through phosphorylation. The researchers also discovered that JAK2V617F, a JAK2 mutation seen in blood cancers, is associated with increased TET2 activity, increased hydroxymethylation (an epigenetic alteration commonly found in blood cancers) and the overexpression of oncogenic genes. These findings indicate that the phosphorylation and consequent activation of TET2, mediated byJAK2V617F, leads to epigenetic and oncogenic changes that may underlie the development of blood cancers. Dr. Verma is professor of medicine and of developmental and molecular biology at Einstein and attending physician in oncology at Montefiore Einstein Center for Cancer Care.
Posted on: Wednesday, May 01, 2019