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Results for “MYELOFIBROSIS”

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At least 1,297 records · Page 72Linked to original sources
PubMed1993

Transplantation of autologous peripheral blood stem cells mobilized using GM-CSF for acute leukemia with myelofibrosis.

A patient with acute mixed lineage leukemia had marked marrow fibrosis at presentation. The fibrosis persisted despite achievement of complete remission. Because the marrow was inaspirable, granulocyte-monocyte colony-stimulating factor (GM-CSF) was used to mobilize stem cells into the peripheral blood which were used for autologous transplantation. Myeloid engraftment was rapid. The extent of the fibrosis decreased after transplantation. GM-CSF-mobilized peripheral blood stem cells may be used for autologous transplantation in patients with fibrotic marrows who are not candidates for allografting.

Acute Disease↗
PubMed2000

NF-kappa B as a central mediator in the induction of TGF-beta in monocytes from patients with idiopathic myelofibrosis: an inflammatory response beyond the realm of homeostasis.

Immune-mediated mechanisms have been implicated in the etiology of idiopathic bone marrow fibrosis (IMF). However, the mechanism remains poorly defined. Compared with healthy controls, IMF monocytes are overactivated, with increased production of TGF-beta and IL-1. TGF-beta is central to the progression of fibrosis in different organs. In the lung, fibrosis is associated with up-regulation of TGF-beta-inducible genes. Because IL-1 and TGF-beta have pro- and antiinflammatory properties and neither appears to regulate the high levels of each other in IMF, we studied the mechanism of this paradigm. We focused on the role of RelA, a subunit of the transcription factor, NF-kappaB that is associated with inflammatory responses. We transiently knocked out RelA from IMF monocytes with antisense oligonucleotides and showed that RelA is central to IL-1 and TGF-beta production and to the adhesion of IMF monocytes. Because the NF-kappaB family comprises subunits other than RelA, we used aspirin and sodium salicylate to inhibit kinases that activate NF-kappaB and showed effects similar to those of the RelA knockout system. It is unlikely that RelA could be interacting directly with the TGF-beta gene. Therefore, we determined its role in TGF-beta production and showed that exogenous IL-1 could induce TGF-beta and adherence of IMF monocytes despite the depletion of NF-kappaB. The results indicate that IL-1 is necessary for TGF-beta production in IMF monocytes, but NF-kappaB activation is required for the production of endogenous IL-1. Initial adhesion activates NF-kappaB, which led to IL-1 production. Through autocrine means, IL-1 induces TGF-beta production. In total, these reactions maintain overactivation of IMF monocytes.

Adult↗