![Investigating the Cause of Myelodysplastic Syndrome]()
Within the bone marrow, hematopoietic stem cells (HSCs) occupy niches that include stromal and mesenchymal cells. In myelodysplastic syndromes (MDS), which precede acute myeloid leukemia, HSCs behave abnormally, either because of genetic aberrations or epigenetic alterations to DNA that influence whether genes are expressed or not. In a study published online on July 6 in Cancer Research, collaborators found that novel epigenetic alterations in the bone marrow microenvironment are critically important in causing MDS to progress. More specifically, the presence of an abnormally high number of methyl groups (hypermethylation) in stromal cells activated the Wnt/β-catenin signaling pathway in MDS stem cells, stimulating their progression to leukemia. The findings suggest that drugs that inhibit DNA methyltransferases (DNMTs) that are used to treat MDS can exert their beneficial actions via influencing the surrounding cells of the bone marrow. Senior author, Amit Verma, M.B.B.S., is professor of medicine and of developmental and molecular biology. First author Tushar Bhagat, Ph.D., is a postdoctoral fellow in Dr. Verma’s lab at Einstein.
Posted on: Tuesday, September 26, 2017