Interferohn is effective in myeloproliferative disorders, which include myelofibrosis. Pegylated interferon is more convenient that interferon because it can be given weekly. However, in the one study in which marrow histology was examined, progression of myelofibrosis was not inhibited by pegylated interferon. Many patients with myelofibrosis are JAK2 positive and pegylated interferon has been shown to reduce Jak2 expression. However, the extent of evidence and number of publications is much smaller for myelofibrosis than for P. Vera and Essential Thrombocytosis. A recent (Nordic) guideline says: “JAK2-mutation is found in about half those patients with PMF. The findings of a steady decrease in the level of the JAK2-mutation in a large number of PV-patients during treatment with pegylated interferon α-2a supports the contention that IFN-treatment may influence the disease at the molecular level, at least in half of the patients (JAK2-positive). A prospective, randomised study of pegylated interferon versus HU in patients with PMF is warranted to clarify this issue”.
There is still an ongoing study: Pegasys® in Patients With Myeloproliferative Diseases, NCT00452023. The goal of this clinical research study is to see if Pegasys (IFN-alpha2a) can help to control the disease in patients with essential thrombocytosis (ET), polycythemia vera (PV), agnogenic myeloid metaplasia/myelofibrosis (AMM/MF), or Philadelphia chromosome-negative chronic myeloid leukemia (Ph-negative CML). The safety of this treatment will also be studied
Verstovsek S, Lawhorn K, Giles F, et al. PEG-intron for myeloproliferative diseases: an update on ongoing phase II study. Blood. 2004;104:11. Abstract 1517.
Nordic MPD Study Group, http://www.legeforeningen.no/asset/38584/1/38584_1.pdf,
Interferohn is effective in myeloproliferative disorders, which include myelofibrosis. Pegylated interferon is more convenient that interferon because it can be given weekly. However, in the one study in which marrow histology was examined, progression of myelofibrosis was not inhibited by pegylated interferon. Many patients with myelofibrosis are JAK2 positive and pegylated interferon has been shown to reduce Jak2 expression. However, the extent of evidence and number of publications is much smaller for myelofibrosis than for P. Vera and Essential Thrombocytosis. A recent (Nordic) guideline says: “JAK2-mutation is found in about half those patients with PMF. The findings of a steady decrease in the level of the JAK2-mutation in a large number of PV-patients during treatment with pegylated interferon α-2a supports the contention that IFN-treatment may influence the disease at the molecular level, at least in half of the patients (JAK2-positive). A prospective, randomised study of pegylated interferon versus HU in patients with PMF is warranted to clarify this issue”.
There is still an ongoing study: Pegasys® in Patients With Myeloproliferative Diseases, NCT00452023. The goal of this clinical research study is to see if Pegasys (IFN-alpha2a) can help to control the disease in patients with essential thrombocytosis (ET), polycythemia vera (PV), agnogenic myeloid metaplasia/myelofibrosis (AMM/MF), or Philadelphia chromosome-negative chronic myeloid leukemia (Ph-negative CML). The safety of this treatment will also be studied
Verstovsek S, Lawhorn K, Giles F, et al. PEG-intron for myeloproliferative diseases: an update on ongoing phase II study. Blood. 2004;104:11. Abstract 1517.
Nordic MPD Study Group, http://www.legeforeningen.no/asset/38584/1/38584_1.pdf,