THE ROLE OF THE JAK PATHWAY IN MYELOFIBROSIS

Overactive JAK pathway is the hallmark of myelofibrosis—not the JAK2 mutation1-5

The discovery of the JAK2V617F mutation has greatly advanced the understanding of the pathogenesis of myeloproliferative neoplasms (MPNs).6

Mutation status may be relevant in the diagnosis of myelofibrosis, but for clinical decisions, it appears to have limited value.4,5


JAK=Janus kinase.

Implications for patients with myelofibrosis

An overactive JAK signaling pathway, which may be due to a number of causes including the JAK2V617F mutation, is important for the pathogenesis of MF.1,5

Nonetheless, the clinical application of the mutation status remains unclear.


What is the significance of the JAK2V617F mutation in myelofibrosis?

The JAK2V617F Mutation and Myeloproliferative Neoplasms

References

  1. Vainchenker W, Delhommeau F, Constantinescu SN, Bernard OA. Blood. 2011;118:1723-1735.
  2. Quintás-Cardama A, Vaddi K, Liu P, et al. Blood. 2010;115:3109-3117.
  3. Fourouclas N, Li J, Gilby DC, et al. Haematologica. 2008;93:1635-1644.
  4. Vardiman JW, Thiele J, Arber DA, et al. Blood. 2009;114:937-951.
  5. Verstovsek S, Kantarjian H, Mesa RA, et al. N Engl J Med. 2010;363:1117-1127.
  6. Vainchenker W, Constantinescu SN. Hematology. 2005:195-200.