Do “driver” mutations really come first in myelofibrosis?
Researchers look deeper into the role of inflammation.
Pinpointing the pathogenesis of myelofibrosis (MF) has been described as a chicken-or-the-egg scenario. Chronic inflammation and the JAK2 clone have become so intertwined in the literature, researchers have questioned which comes first.
But the latest research suggests inflammation plays a central role in MF whether a JAK mutation exists or not. “In cancer, we generally think that the mutant cell is the whole problem, and therefore the target,” says Angela Fleischman, associate professor of hematology/oncology at University of California Irvine. “But in myeloproliferative neoplasms [MPNs], getting rid of the clone doesn’t fix the problem.” The JAK2 clone, at least in some people, she says, is a consequence and not necessarily the root cause of MF.
