Blood and spleen haematopoiesis in patients with myelofibrosis

Douay, Luc; Laporte, Jean-Philippe; Lefrançois, G.; Najman, A; Dupuy-Montbrun, Marie-Christine; Lopez, M.; Giarratana, Marie‐Catherine; Gorin, Norbert‐Claude

doi:10.1016/0145-2126(87)90009-9

Cited by 30 publications

(9 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…[1][2][3][4][5][6][7][8][9][10][11][12] In myelofibrosis with myeloid metaplasia (MMM), a CMD characterized by bone marrow fibrosis and constitutive myeloid metaplasia, 13 the number of circulating hematopoietic precursors has always been reported to be consistently high, with the mean levels being from 8-to 167-fold higher than those found in control subjects. [1][2][3][4][5][6][7][8][9] When cells are measured by flow cytometry, the average CD34 ϩ cell recovery from peripheral blood is higher in patients with MMM than in those with other Philadelphia-negative (Ph Ϫ ) CMDs. [10][11][12] These observations suggest that the circulating pool of CD34 ϩ cells in Ph Ϫ CMDs increases along with the proliferative capacity of the individual disease, and that this pool might have the potential to portray the proliferative patterns of such diseases.…”

Section: Introductionmentioning

confidence: 99%

Diagnostic and clinical relevance of the number of circulating CD34+ cells in myelofibrosis with myeloid metaplasia

Barosi

Viarengo

Pecci

et al. 2001

Blood

200

161

View full text Add to dashboard Cite

The absolute content of CD34 ؉ cells in the peripheral blood of 84 patients with myelofibrosis with myeloid metaplasia (MMM) and 23 patients with other Philadelphia-negative (Ph ؊ ) chronic myeloproliferative disorders (CMDs) was investigated. In MMM, the median absolute number of circulating CD34 ؉ cells was consistently high (91.6 ؋ 10 6 /L; range, 0-2460 ؋ 10 6 /L). Receiver operating characteristic curve analysis showed that 15 ؋ 10 6 /L as a decision criterion for CD34 ؉ cells produced an almost complete discrimination between MMM patients out of therapy and other Ph ؊ CMDs (positive predictive value, 98.4%; negative predictive value, 85.0%). MMM patients with higher numbers of CD34 ؉ cells had a significantly longer disease duration (P ‫؍‬ .019) and higher spleen volume index (P ‫؍‬ .014), liver volume (P ‫؍‬ .000), percentage of circulating immature myeloid cells (P ‫؍‬ .020), and percentage of myeloid blasts (P ‫؍‬ .000). When CD34 ؉ cells were correlated with the use of Dupriez risk stratification, CD34 ؉ cells increased significantly from low-risk (median, 68.1 ؋ 10 6 /L) to intermediate-risk (median, 112.8 ؋ 10 6 /L) and high-risk patients (median 666.1 ؋ 10 6 /L) (F ‫؍‬ 4.95; P ‫؍‬ .009). When CD34 ؉ cells were correlated with a severity score on the basis of both myeloproliferative and myelodepletive characteristics of the disease, only the myeloproliferation index was significantly associated with CD34 ؉ cell level (F ‫؍‬ 5.7; P ‫؍‬ .000). Overall survival and interval to blast transformation from the time of CD34 ؉ cell analysis were significantly shorter in patients with more than 300 ؋ 10 6 /L CD34 ؉ cells (P ‫؍‬ .005 and .0005, respectively). In conclusion, the absolute number of CD34 ؉ circulating cells allows MMM to be distinguished from other Ph ؊ CMDs; it is strongly associated with the extent of myeloproliferation and predicts evolution toward blast transformation. (Blood. 2001;98:3249-3255)

show abstract

Section: Introductionmentioning

confidence: 99%

Diagnostic and clinical relevance of the number of circulating CD34+ cells in myelofibrosis with myeloid metaplasia

Barosi

Viarengo

Pecci

et al. 2001

Blood

200

161

View full text Add to dashboard Cite

show abstract

“…Many observations support the fact that circulating committed progenitors in PMF largely arise from and circulate from the spleen (Douay et al, 1987). Thus, in the patient reported in this study the failure to detect circulating erythroid progenitors is due to either a defect in the capacity of haemopoietic stem cells to undergo commitment to the erythroid lineage or the ability of committed erythroid progenitors to undergo erythropoiesis or that erythroid progenitors are generated and sequestered in the spleen.…”

Section: Discussionmentioning

confidence: 56%

“…Douay and co-workers have shown that, in PMF patients, CFU-GM can be maintained in liquid suspension culture in the absence of a substantial stromal layer over a 10-week period and concluded that primitive stem cells circulated in PMF patients (Douay et al, 1987). In our study, PBMNC were co-cultured with normal marrow stroma to maintain circulating primitive stem cells and assess whether they were able to give rise to ery-…”

Section: Discussionmentioning

confidence: 99%

Defective erythropoiesis in primary myelofibrosis associated with a chromosome 11 abnormality

Patton

Bunce²,

Larkins³

et al. 1991

Br J Cancer

View full text Add to dashboard Cite

Summary A case of primary myelofibrosis was identified with a previously unreported complex karyotype with two abnormal clones in addition to a proportion of normal cells: 46,XY, -2, -1 1, + der(2)t(2; 1) (q24/31;q13), + mar and 45,XY, -2, -1 1, + der(2)t(2;1 1)(q24/31;q13), + mar, -17,del(7q). Study of circulating committed progenitors from this patient consistently showed (1) an absence of erythroid progenitors which is uncommon and (2) greatly increased granulocyte-monocyte progenitors (CFU-GM) which is generally observed in myelofibrosis. Further study showed that peripheral blood mononuclear cells co-cultured with irradiated normal bone marrow stroma generated increased numbers of CFU-GM compared with controls but failed to generate erythroid progenitors, providing evidence for an intrinsic defect in erythropoiesis. Only once previously has the absence of erythroid progenitors in primary myelofibrosis been studied in relation to cytogenetic abnormalities. This case also revealed a complex karyotype which, however, shared with our case a defect on chromosome 11. The identification of two cases of primary myelofibrosis which lack committed erythroid progenitor cells and which show in common a chromosomal defect on chromosome 11 point to the existence of genes on this chromosome which play a key role during erythropoiesis.

show abstract

“…Extramedullary hematopoiesis can be seen in a wide range of splenic conditions varying from benign hematologic conditions, hematopoietic neoplasms, nonhematopoietic tumors and other disorders of the spleen and circulation. [4][5][6][7][8][9][10][11][12][13][14][15][16][17] The splenic environment is uniquely suited as a site for extramedullary hematopoiesis. It is likely that the stromal microenvironment is similar enough to bone marrow to allow for near-normal development of hematopoietic cell lines.…”

mentioning

confidence: 99%

“…It is likely that the stromal microenvironment is similar enough to bone marrow to allow for near-normal development of hematopoietic cell lines. 5,7 However, differentiation of neoplastic hematopoietic proliferations, such as those seen commonly in chronic myeloproliferative disorders, from extramedullary hematopoiesis associated with benign conditions may be difficult in some cases. 18 In most, the degree of extramedullary hematopoiesis seen in spleens with non-neoplastic conditions or in association with nonhematopoietic neoplasms is inconspicuous enough to not raise concern for possible involvement by a myeloid disease.…”

mentioning

confidence: 99%

Morphologic and immunohistochemical evaluation of splenic hematopoietic proliferations in neoplastic and benign disorders

et al. 2005

View full text Add to dashboard Cite

Spleen is a common site of extramedullary hematopoiesis. Extramedullary hematopoiesis seen in nonneoplastic conditions can occasionally be extensive and raise concerns for a myeloid neoplasm. We compared the morphologic and immunohistochemical features of splenic hematopoietic proliferations seen in neoplastic myeloid disorders (eg chronic myeloproliferative disorders, myelodysplastic/myeloproliferative disorders and acute myeloid leukemias) to extramedullary hematopoiesis seen in a variety of reactive conditions. In all, 80 spleen specimens were reviewed. The presence of each marrow-derived lineage, dysplasia and immunohistochemical results were evaluated (CD34, CD117, myeloperoxidase, CD68, p53, TdT, CD42b and hemoglobin). Neoplastic hematopoietic proliferations in chronic myeloproliferative disorders are characterized by trilineage hematopoiesis with significant dysplasia in all cell lineages. Acute myeloid leukemia showed an increase in immature forms, which were highlighted by immunohistochemistry. Reactive extramedullary hematopoiesis showed variability in histologic features. Post-bone marrow transplant and thrombotic thrombocytopenic purpura/hemolytic-uremic syndrome spleens showed extramedullary hematopoiesis with some morphologic features of immaturity, which could simulate chronic myeloproliferative disorder. However, they lacked characteristic immunohistochemical features of neoplastic myeloid disorders such as positivity for CD34 or CD117. Modern Pathology (2005) 18, 1550-1561.

show abstract

Blood and spleen haematopoiesis in patients with myelofibrosis

Cited by 30 publications

References 20 publications

Diagnostic and clinical relevance of the number of circulating CD34+ cells in myelofibrosis with myeloid metaplasia

Diagnostic and clinical relevance of the number of circulating CD34+ cells in myelofibrosis with myeloid metaplasia

Defective erythropoiesis in primary myelofibrosis associated with a chromosome 11 abnormality

Morphologic and immunohistochemical evaluation of splenic hematopoietic proliferations in neoplastic and benign disorders

Contact Info

Product

Resources

About