Cytogenetic Differences between Bone Marrow and Spleen in a Case of Agnogenic Myeloid Metaplasia Developing Blast Crisis

2009 ◽  
Vol 15 (3) ◽  
pp. 187-191 ◽  
Author(s):  
L. Brandt ◽  
F. Mitelman ◽  
A. Panani
Keyword(s):  
Bone Marrow ◽  
Blast Crisis ◽  
Myeloid Metaplasia ◽  
Agnogenic Myeloid Metaplasia

scholarly journals Allogeneic bone marrow transplantation for agnogenic myeloid metaplasia

1997 ◽  
Vol 98 (4) ◽  
pp. 1004-1009 ◽  
Author(s):  
Philippe Guardiola ◽  
Helene Esperou ◽  
Dominique Cazals-Hatem ◽  
Norbert Ifrah ◽  
Jean-Pierre Jouet ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Transplantation ◽  
Marrow Transplantation ◽  
Allogeneic Bone Marrow Transplantation ◽  
Allogeneic Bone Marrow ◽  
Allogeneic Bone ◽  
Myeloid Metaplasia ◽  
Agnogenic Myeloid Metaplasia

scholarly journals Urinary hydroxyproline excretion in myelofibrosis

Blood ◽  
1980 ◽  
Vol 55 (3) ◽  
pp. 383-385 ◽  
Author(s):  
JC Wang ◽  
MK Aung ◽  
MS Tobin
Keyword(s):  
Bone Marrow ◽  
Control Group ◽  
Urinary Hydroxyproline ◽  
Myeloid Metaplasia ◽  
Patients With Cancer ◽  
Diagnostic Problems ◽  
Agnogenic Myeloid Metaplasia ◽  
Metastatic Involvement ◽  
Hydroxyproline Excretion ◽  
Marrow Fibrosis

Abstract Urinary hydroxyproline measurements were performed in a group of health volunteers as well as patients with cancer and myelofibrosis. Patients in whom there was no metastatic involvement of bone marrow excreted an amount of hydroxyproline not different from that of the control group. Those who had marrow metastasis produced elevated levels of hydroxyproline; the highest excretions were observed when marrow fibrosis was associated with metastasis. These results contrasted with those observed in agnogenic myeloid metaplasia patients whose excretions were equivalent to the control group. The result suggests differences in the pathogenesis of myelofibrosis and a technique potentially useful for distinguishing between patients who may otherwise be diagnostic problems.

scholarly journals Chromosomal Evidence for the Secondary Role of Fibroblastic Proliferation in Acute Myelofibrosis

Blood ◽  
1970 ◽  
Vol 36 (6) ◽  
pp. 729-735 ◽  
Author(s):  
ELLIS J. VAN SLYCK ◽  
LESTER WEISS ◽  
MARILYN DULLY
Keyword(s):  
Bone Marrow ◽  
White Woman ◽  
Normal Karyotype ◽  
Myeloid Metaplasia ◽  
Secondary Role ◽  
Agnogenic Myeloid Metaplasia ◽  
Bone Marrow Fibroblasts ◽  
Hematopoietic Cell Lines ◽  
Fibroblastic Proliferation

Abstract A 22-year-old white woman with acute myelofibrosis and agnogenic myeloid metaplasia is reported. She was found to have a consistent chromosomal aberration in her myeloblasts, interpreted as a 1-3 translocation. Bone marrow fibroblasts were successfully cultured, yielding a normal karyotype. The lymphocyte karyotype in this patient was also normal. It is proposed that these findings favor a secondary role of the fibroblastic proliferation in myelofibrosis and suggest that the primary cellular disturbance resides only in the hematopoietic cell lines.

Quantitative Analysis of Growth Factor Production in the Mechanism of Fibrosis in Agnogenic Myeloid Metaplasia.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 4272-4272
Author(s):  
Jen-Chin Wang ◽  
Tsong S. Chang ◽  
Amit Goldberg ◽  
Allan D. Novetsky ◽  
Jeffrey Lipton
Keyword(s):  
Bone Marrow ◽  
Growth Factors ◽  
Quantitative Analysis ◽  
Growth Factor ◽  
Bone Marrow Fibrosis ◽  
Myeloid Metaplasia ◽  
Agnogenic Myeloid Metaplasia ◽  
Growth Factor Production ◽  
Tgf Β1 ◽  
Marrow Fibrosis

Abstract There are previous reports that growth factors including TGF-β1, PDGF and FGF produced by megakaryocytes are responsible for the etiology of fibrosis in agnogenic myeloid metaplasia (AMM). Due to the technical difficulty in isolating enough megakaryocytes from the inaspirable bone marrow from patients with AMM, a quantitative analysis of these growth factors produced by the megakaryocytes and correlated to the degree of myelofibrosis has not been able to be performed. The present study employed the cell culture technique to grow megakaryocytes from blood CD 34+ cells and then perform the quantitative analysis of these growth factors, compared with other sources such as monocyte-macrophage lineages and correlated to the degree of bone marrow fibrosis. We found TGF-β1, PDGF and FGF produced by the megakaryocytes were significantly elevated in AMM compared with normal controls (p<0.05) and TGF-β1 was more abundantly produced than PDGF or FGF. While these growth factors are several fold elevated in AMM compared with other MPD including essential thrombocythemia (ET), polycythemia vera (PV), it was not statistically significant. A quantitative analysis of these growth factors produced by the CD 14+ cells in the blood and bone marrow showed that these growth factors were not significantly elevated in AMM compared with other MPD or controls and were significantly elevated only in some patients (defined as elevation of more than 2 SD of the controls). The correlation of these growth factors produced by the megakaryocytes or monocyte-macrophage lineages with degree of myelofibrosis in 12 patients with AMM were r=0.73 and 0.23 respectively (Non parametric (Spearman) correlation with two-tailed analysis was used to calculate the correlation). We concluded: In AMM, these fibrosing growth factors are mainly produced by the megakaryocytes and in some patients, monocyte-macrophage lineages may contribute to the production of these growth factor production. TGF-β1 is more abundantly produced from the megakaryocytes than PDGF or FGF confirming TGF-β1 is the most important fibrosing growth factor in the pathogenesis of myelofibrosis in AMM. A statistically significant correlation of the growth factor and degree of myelofibrosis in AMM suggests that these fibroing growth factors produced by the megakaryocytes are main etiology of bone marrow fibrosis in AMM.

Increased circulating CSF-1 (M-CSF) in myeloproliferative disease: association with myeloid metaplasia and peripheral bone marrow extension

Blood ◽  
1989 ◽  
Vol 74 (4) ◽  
pp. 1231-1234 ◽  
Author(s):  
HS Gilbert ◽  
V Praloran ◽  
ER Stanley
Keyword(s):  
Bone Marrow ◽  
Phenotypic Expression ◽  
Elevated Serum ◽  
Serum Levels ◽  
Myeloproliferative Disease ◽  
Myeloid Metaplasia ◽  
Macrophage Population ◽  
Agnogenic Myeloid Metaplasia ◽  
Peripheral Bone

Abstract Myeloproliferative disease (MPD) is heterogeneous in phenotypic expression and may display features consistent with expansion and activation of the monocyte/macrophage population during its course. The role of colony-stimulating factor-1 (CSF-1) in the pathophysiology of MPD was investigated by measuring circulating CSF-1 levels and examining their relationship to disease phenotype. Serum CSF-1 concentrations, measured by radioimmunoassay, were elevated in all MPD phenotypes. CSF-1 levels differed significantly between groups of patients with essential thrombocythemia, polycythemia vera, and postpolycythemic or agnogenic myeloid metaplasia (in ascending order). CSF-1 serum levels were positively correlated with spleen size and the degree of peripheral bone marrow extension, determined by scintigraphy using a macrophage-seeking isotope. There was no correlation between CSF-1 concentration and circulating levels of erythrocytes, neutrophils or platelets, or the presence of bone marrow fibrosis. Elevated serum CSF-1 levels appear to be associated with an expanded monocyte/macrophage population in MPD. In view of the known cooperativity between CSF-1 and other growth factors in regulating hematopoiesis, the finding of increased serum CSF-1 concentrations and its association with myeloid metaplasia and bone marrow extension may indicate a pathophysiologic role for CSF-1 in determining the phenotypic expression of MPD.

scholarly journals Urinary hydroxyproline excretion in myelofibrosis

Blood ◽  
1980 ◽  
Vol 55 (3) ◽  
pp. 383-385
Author(s):  
JC Wang ◽  
MK Aung ◽  
MS Tobin
Keyword(s):  
Bone Marrow ◽  
Control Group ◽  
Urinary Hydroxyproline ◽  
Myeloid Metaplasia ◽  
Patients With Cancer ◽  
Diagnostic Problems ◽  
Agnogenic Myeloid Metaplasia ◽  
Metastatic Involvement ◽  
Hydroxyproline Excretion ◽  
Marrow Fibrosis

Urinary hydroxyproline measurements were performed in a group of health volunteers as well as patients with cancer and myelofibrosis. Patients in whom there was no metastatic involvement of bone marrow excreted an amount of hydroxyproline not different from that of the control group. Those who had marrow metastasis produced elevated levels of hydroxyproline; the highest excretions were observed when marrow fibrosis was associated with metastasis. These results contrasted with those observed in agnogenic myeloid metaplasia patients whose excretions were equivalent to the control group. The result suggests differences in the pathogenesis of myelofibrosis and a technique potentially useful for distinguishing between patients who may otherwise be diagnostic problems.

Sign in / Sign up

Export Citation Format

Share Document