Hypothesis: a possible role for interferon in the treatment of idiopathic myelofibrosis.
It is proposed that interferon may be an active agent in the treatment of patients with idiopathic myelofibrosis. In this disorder the megakaryocyte cell lineage plays a major role in the deposition of bone marrow collagen by the release of growth promoting factors, including platelet-derived growth factor, which are mitogenic for fibroblast proliferation. Interferon reduces collagen deposition in the bone marrow by suppressing the activity of the proto-oncogene, which is involved in the production of growth factors from abnormal megakaryocytes and platelets. A direct myeloid cytoreductive effect of interferon upon the megakaryocyte proliferation contributes to reducing growth factor activity in the bone marrow. Finally, interferon induces monocytoid differentiation, thereby increasing bone marrow collagenase-activity. Thus, interferon has several actions, which in concert might reduce bone marrow collagen in myelofibrosis.
Hasselbalch
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Department of Medical-Haematology C, Gentofte University Hospital, Hellerup/Copenhagen, Denmark.
D001853:Bone Marrow / Q000378:metabolism; D003094:Collagen / Q000378:metabolism; D006801:Humans; D007370:Interferon Type I / Q000627:therapeutic use*; D008954:Models, Biological; D010982:Platelet-Derived Growth Factor / Q000096:biosynthesis / Q000235:genetics; D055728:Primary Myelofibrosis / Q000235:genetics / Q000378:metabolism / Q000628:therapy*; D000090063:Proto-Oncogene Mas; D011519:Proto-Oncogenes / Q000187:drug effects
D007370:Interferon Type I; C000715470:MAS1 protein, human; D010982:Platelet-Derived Growth Factor; D000090063:Proto-Oncogene Mas; D003094:Collagen