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Results for “MYELOFIBROSIS”

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At least 1,063 records · Page 59Linked to original sources
PubMed1985

Avian monocytic leukemia cells release fibroblast growth factor: implications to associated myelofibrosis.

The marrow of chicks with leukemia induced by avian 'myeloblastosis' virus (AMV) exhibited a 5-10-fold increase in the number of fibroblast colony-forming cells (CFU-F). The increased CFU-F correlated with a mild fibrosis which can be seen in the marrow of these animals. Fibroblast proliferation likely was not simply due to the presence of leukemic cells because addition of formaldehyde-fixed peripheral leukemic cells failed to initiate CFU-F growth. Conditioned medium (CM) from day-4 cultures of peripheral leukemic cells was markedly stimulatory to CFU-F growth. The stimulatory activity was not due to virus released from the leukemic cells as, (1) removal of virus by pelleting had no effect on the CM activity and (2) direct inoculation of CFU-F cultures with virus failed to stimulate CFU-F growth. Normal avian marrow macrophage monolayers also released high levels of a fibroblast growth factor and both the macrophage-derived and leukemic cell-derived factors were heat-labile (65 degrees, 30 min).

Animals↗
PubMed1990

Myelofibrosis: a review of clinical and pathologic features and treatment.

The purpose of this review is to discuss and clarify the current understanding of the pathogenesis, clinical manifestations, and treatment of MF. MF may be either a primary or secondary disorder. It is characterized by an increased deposition of bone marrow collagen, fibronectin, and laminin. Present evidence indicates that MF may be mediated by platelet or megakaryocyte growth factors, decreased prostaglandin mediated stem cell inhibition, immune complex deposition, and both fibroblast and endothelial cell proliferation. Recently acute MF has been recognized to be identical to acute megakaryocytic leukemia. Secondary MF usually responds to appropriate treatment of the underlying disease. Primary MF is usually treated by blood product support, but may be responsive to androgens, splenectomy, splenic irradiation, chemotherapy, or bone marrow ablation with marrow reconstitution.

Combined Modality Therapy↗
PubMed2004

Osteosclerosis in idiopathic myelofibrosis is related to the overproduction of osteoprotegerin (OPG).

OBJECTIVE: The aim of this study is to investigate the mechanism of osteosclerosis in IMF in relation to OPG derangement. METHODS: Plasma OPG level was assayed by OPG ELISA in 19 patients with IMF, 15 patients with other myeloproliferative disorders (MPDs), and 12 normal volunteers as controls and correlated with the degree of osteosclerosis. Furthermore, the level of OPG mRNA, in the cultured bone marrow stromal (BMS) cells of patients with IMF and anemia patients used as controls, in the presence or absence of TGF-beta1, was studied by real-time RT-PCR. RESULTS: The present study showed that blood OPG level was significantly elevated in patients with IMF as compared to patients with other MPDs (p < 0.01) or normal volunteer controls (p < 0.05), and there was no significant difference in the level between patients with MPDs and controls. In addition, there was a positive correlation (r=0.67, p=0.04) between plasma OPG levels and the degree of osteosclerosis. There was no difference in the OPG mRNA in patients with IMF as compared with controls even on TGF-beta1 stimulation. CONCLUSION: These results suggest that osteosclerosis in IMF may be related to overproduction of OPG and enhanced level of OPG is not due to the effect of TGF-beta1 on the BMS cells. It could be due to the effect of TGF-beta1 or other growth factors on cells other than BMS cells such as the osteoblasts.

Bone Marrow Cells↗