More than one mechanism may promote MF.1,2
Considering the influence of driver mutations and other high-risk mutations, there is a need to continue developing a better understanding of additional cellular pathways and the distinct factors involved in primary MF.5,6 By doing so, researchers are focusing more on what may drive disease progression in each individual patient.1,2
Focusing exclusively on the JAK-STAT pathway may not adequately address the inflammatory aspects of the disease, such as NFκB activation and alternative pathways for STAT phosphorylation.1,7 However, some specific targets that are distinct from the JAK-STAT pathway—such as TLR/IL1R, ROCK, and FLT3—may require a closer look at the role they play in the inflammatory cascade of MF.1,2,8-10
How do you know when JAK inhibition may not be enough for your patients?4
By understanding each patient's type of myelofibrosis (primary or secondary), clinical phenotype (noncytopenic or cytopenic), and the genetic mutations/pathways involved, physicians can create a more appropriate management plan designed around each patient's needs.11,12
Research has shown that multiple pathways may be involved in MF.
Finding new perspective starts by
discovering other pathways.
Watch John Mascarenhas, MD, discuss how discovering complementary JAK-independent pathways has shaped his view of MF prognosis and progression.
Exploring new pathways further develops insights around managing MF.1,2,8-10
As researchers continue to explore the complexity and evolving biology of MF, they discover different targets for future management of this disease. Research has brought to light potential complementary JAK‑independent pathways and somatic mutations, which may warrant further investigation.