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1 rit, splenomegaly, and increased bone marrow reticulin.
2 e lobulated and contained dense, centralized reticulin.
3 typia, absence of biliary epithelia, loss of reticulin, alteration of normal perivenular glutamine sy
4 by bone marrow megakaryocytic proliferation, reticulin and/or collagen fibrosis, and presence of JAK2
6 im clinical trials, 10 were reported to have reticulin deposition; reticulin grade was increased in 4
8 v) of bFGF(+) MC and the density of collagen/reticulin fibers in silicotic nodules (rho = -0.80, p <
9 associated cells and the density of collagen/reticulin fibers in the hypocellular nodule centers (rho
10 rge, mature nodules, the density of collagen/reticulin fibers was higher, and bFGF(+) MC were found o
12 yh9(-/-) mice a much stronger increase in BM reticulin fibers was present after 4 weeks of romiplosti
15 ntain abundant pericapillary and parenchymal reticulin fibrils, which were shown by immunohistochemis
18 sessable responders who started therapy with reticulin fibrosis grade 4 experienced reductions to at
19 ations in myeloid and erythroid lineages and reticulin fibrosis identified a subclinical myeloprolife
20 ence and prognostic relevance of bone marrow reticulin fibrosis in 526 patients with World Health Org
24 se 2 features were inversely proportional to reticulin fibrosis, whereas increases in marrow angiogen
25 four patients (14%) displayed mostly grade 1 reticulin fibrosis, with only 2 cases showing higher-gra
27 Our results demonstrate that bone marrow reticulin grade at diagnosis represents an independent p
28 de showed significantly greater increases in reticulin grade compared with those allocated to hydroxy
32 were reported to have reticulin deposition; reticulin grade was increased in 4 of 5 patients with bo
34 y, evaluation of bone marrow progenitors and reticulin in nonaffected family members of patients with
35 and produces modest increases in bone marrow reticulin in some ITP patients that decrease when therap
36 topathology including the increase in marrow reticulin is completely and rapidly reversible upon the
37 that those who show substantially increasing reticulin levels are at risk of myelofibrotic transforma
40 im-treated rats, a retrospective analysis of reticulin observed in romiplostim ITP clinical trials, a
41 patients who developed increased bone marrow reticulin on anagrelide showed regression of fibrosis wh
43 iption factor 6, which, via induction of the reticulin protein Nogo, can lead to the disruption of th
44 ns include thrombosis, increased bone marrow reticulin, rebound worsening of thrombocytopenia upon di
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