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PubMedDate not supplied

[Postradiation dynamics in the bone marrow of mice of the granulocyte and macrophage cell precursors cloned in agar diffusion chambers].

It was shown that a bone marrow CFUc population was considerably depleted during 24 h following gamma-irradiation of mice with a dose of 4 Gy. The number of CFUc started rapidly normalizing on day 2 after irradiation and reached the control level by the 11 th day. During the regeneration period CFUdc were more sensitive to the cytotoxic action of hydroxyurea.

Agar↗
PubMed1977

Myeloid membrane markers. I. Expression of marker antigens specific for murine granulocytes and their precursor cells.

Bone marrow cells were investigated by immunoelectromicroscopy and by quantitative photometric immunoradioautography with a rabbit antiserum against murine bone marrow cells. The serum was absorbed with murine spleen, liver and thymus cells until it no longer reacted with thymocytes and lymph node cells in a quantitative complement fixation test. The antiserum stained granulopoietic but not erythropoietic or lymphopoietic cells. The density of the myeloid antigen on single cells increased with the differentiation from immature to mature granulopoietic cells. While the increase of label was statistically not significant at the level of differentiation from promyelocyte to myelocyte and metamyelocyte to band neutrophil, there was a remarkable gain of label from myeloblast to promyelocyte and from band neutrophil to segmented neutrophil. This was evident under the electron microscopy using peroxidase-labeled antibodies and could be measured quantitatively with photometric immunoradioautography using 125I-labeled antibodies.

Absorption↗
PubMed1995

Recombinant human granulocyte-macrophage colony-stimulating factor in septic neutropenic pediatric cancer patients: detection of circulating hematopoietic precursor cells correlates with rapid granulocyte recovery.

Cycling intensive chemotherapy currently used to treat pediatric solid tumors induces severe neutropenia. Prolonged neutropenia is a major risk factor for septic death which occurs in up to 5% of febrile or septic neutropenic episodes. We treated 18 neutropenic pediatric cancer patients (eight females, 10 males) during 30 febrile and/or septic episodes with single daily doses of E. coli-derived non-glycosylated recombinant human granulocyte-macrophage colony-stimulating factor (rh-GM-CSF, 5 micrograms per kg of body weight). The cytokine was administered for a median period of 6.5 days (2-12 days). Analysis of circulating hematopoietic progenitor cells was performed at day 1 (baseline) and day 5 of rh-GM-CSF treatment and included flow cytometric CD34 analysis as well as the methylcellulose-based clonogenic assay. Prompt hematopoietic recovery and resolution of septic problems was observed in all children. The counts of leukocytes (WBC), absolute neutrophils (ANC), and platelets (PLT) rose above 1,000/microL, 1,000/microL, and 50,000/microL within 4 days (0-9), 5.5 days (2-13), and 6 days (0-14), respectively. Faster granulocyte recovery and improved recruitment of circulating hemopoietic precursors was observed in children with detectable amounts (> 0.1%) of CD34-positive mononuclear cells prior to rh-GM-CSF treatment. We conclude that, to some extent, the efficacy of rh-GM-CSF treatment in neutropenic cancer patients is influenced by the hematopoietic recovery status on the progenitor cell level. Although they respond more slowly to the treatment, patients without circulating CD34-positive progenitor cells may gain most from growth factor therapy. Rh-GM-CSF can be safely administered to febrile and/or septic neutropenic children treated for cancer.

Adolescent↗
PubMed2003

G-CSF signaling can differentiate promyelocytes expressing a defective retinoic acid receptor: evidence for divergent pathways regulating neutrophil differentiation.

Several lines of investigation suggest that granulocyte colony-stimulating factor (G-CSF) augments all-trans retinoic acid (ATRA)-induced neutrophil differentiation in acute promyelocytic leukemia (APL). We sought to characterize the relationship between G-CSF- and ATRA-mediated neutrophil differentiation. We established a G-CSF receptor-transduced promyelocytic cell line, EPRO-Gr, derived from the granulocyte-macrophage colony-stimulating factor (GM-CSF)-dependent EPRO cell line harboring a dominant-negative retinoic acid receptor alpha (RARalpha). In EPRO-Gr, neutrophil differentiation occurs either in GM-CSF upon addition of ATRA or upon induction with G-CSF alone. Transient transfection of EPRO-Gr cells with a RARE-containing reporter plasmid demonstrates increased activity in the presence of ATRA, but not G-CSF, while STAT3 phosphorylation occurs only in response to G-CSF. This suggests that ATRA-mediated differentiation of EPRO-Gr cells occurs via a RARE-dependent, STAT3-independent pathway, while G-CSF-mediated differentiation occurs via a RARE-independent, STAT3-dependent pathway. ATRA and G-CSF thus regulate differentiation by divergent pathways. We characterized these pathways in the APL cell line, NB4. ATRA induction of NB4 cells resulted in morphologic differentiation and up-regulation of C/EBPepsilon and G-CSFR, but not in STAT3 phosphorylation. The addition of G-CSF with ATRA during NB4 induction resulted in STAT3 phosphorylation but did not enhance differentiation. These results may elucidate how G-CSF and ATRA affect the differentiation of primary and ATRA-resistant APL cells.

Animals↗
PubMed1999

Prolonged release and c-kit expression of haemopoietic precursor cells mobilized by stem cell factor and granulocyte colony stimulating factor.

Mobilization of haemopoietic precursor cells into the circulation by the combination of cytokines, stem cell factor (SCF) and G-CSF in previously untreated patients with carcinoma of the breast resulted in increased yield of collected peripheral blood precursor cells (PBPC). This mobilization of PBPC by SCF with G-CSF lasted several days after ceasing the cytokines in comparison to the rapid fall of PBPC after ceasing G-CSF. Possible mechanisms for this increased and prolonged mobilization were investigated. Immunological phenotyping with CD38, Thy-1 and MDR-1 of the CD34-positive mobilized PBPC detected no difference in maturity compared to PBPC mobilized by G-CSF alone. However, the down-regulation of c-kit, which is associated with the mechanism of mobilization, was much greater in the PBPC mobilized by SCF and G-CSF. The potential clinical implication of increased and prolonged mobilization is increased yield, allowing transplantation of heavily pre-treated patients, transplantation with PBPC from a single apheresis, or PBSC support for multiple courses of high-dose therapy from one mobilization procedure.

Antigens, CD34↗
PubMed2004

Keeping track of pro-B cells: a new model for the effects of IL-7 during B cell development.

Trophic and instructive models have been invoked to explain how various cytokines influence the survival, proliferation and differentiation of lymphoid progenitors. There is evidence that IL-7 can act in either a trophic or an instructive manner during B and T cell development although its roles in B cell development in the fetus versus the adult mouse and in the mouse versus the human may vary. Here we outline the stages of B cell development and the conventional model of the role of IL-7 in the transitions from pro-B cells to pre-B cells and then to immature B cells. We also discuss the implications of recent data that have led to a new model for this process.

Animals↗
PubMed2005

Hemogram and myelogram in progressing non-Hodgkin's lymphomas.

Parameters of hemogram and myelogram were studied in patients with aggressive and indolent non-Hodgkin's lymphomas: the relationships between the parameters recorded before treatment and during remission or progress 6 months after chemotherapy were studied by multifactorial analysis. The progress of indolent non-Hodgkin's lymphomas was associated with changes caused by tumor infiltration of the bone marrow; lymphocytosis in the myelogram or hemogram was associated with a relative decrease in the count of granulocytic hemopoietic stem cells. A sign associated with the absence of remission in aggressive non-Hodgkin's lymphomas was decreased level of hemoglobin and erythroid cells. Changes in myelogram attesting to anemia and suppressed erythropoiesis before chemotherapy are additional prognostic factors indicating obligatory intensification of chemotherapy for patients with aggressive non-Hodgkin's lymphomas.

Analysis of Variance↗
PubMed2006

A close developmental relationship between the lymphoid and myeloid lineages.

The classic dichotomy model of hematopoiesis postulates that the first step of differentiation beyond the multipotent hematopoietic stem cell generates the common myelo-erythroid progenitors and common lymphoid progenitors (CLPs). Previous studies in fetal mice showed, however, that myeloid potential persists in the T- and B-cell branches even after these lineages have diverged, indicating that the simple dichotomy model is invalid, at least for fetal hematopoiesis. Nevertheless, CLPs have persisted in models of adult hematopoiesis; results from several groups support the presence of CLPs in bone marrow. Recent evidence challenges the dichotomy model in the adult, and it is proposed here that the alternative myeloid-based model is applicable to both fetal and adult hematopoiesis.

Animals↗
PubMed2004

Induction of anti-leukemic cytotoxic T lymphocytes by fusion of patient-derived dendritic cells with autologous myeloblasts.

Presentation of AML antigens by dendritic cells (DC) could potentially induce a T cell-mediated anti-leukemic immune response. In the present study, we generated DC from adherent (AD-DC) and non-adherent (NAD-DC) myeloblasts obtained from bone marrows of AML patients. Both cell populations displayed morphological, phenotypic and functional properties of DC. The functions of NAD-DC were compared to AD-DC that had been fused with autologous AML blasts (FC/AML). The FC/AML induced greater T cell proliferation and CTL activity against autologous AML blasts (9/10 cases) as compared to NAD-DC. FC/AML may thus represent a promising strategy for DC-based immunotherapy of patients with AML.

Adult↗
PubMed2003

Morphological and cytochemical characteristics of leukaemic promyelocytes.

Evaluation of cell morphology is usually sufficient to diagnose acute promyelocytic leukaemia (APL). In this chapter we discuss the features of classical hypergranular APL, the APL variant, hyperbasophilic promyelocytic leukaemia, APL with basophil-like granules, acute eosinophilic leukaemia with PML/RARalpha positivity and the morphology of APL cells lacking t(15;17). In addition to morphological examination, cytochemical investigations (peroxidase chloroacetate-esterase, etc.) may help further in defining the cytology of leukaemic cells in APL.

Cell Size↗
PubMed2005

Aberrant subcellular targeting of the G185R neutrophil elastase mutant associated with severe congenital neutropenia induces premature apoptosis of differentiating promyelocytes.

Mutations in the ELA2 gene encoding neutrophil elastase (NE) are present in most patients with severe congenital neutropenia (SCN). However, the mechanisms by which these mutations cause neutropenia remain unknown. To investigate the effects of mutant NE expression on granulopoiesis, we used the HL-60 promyelocytic cell line retrovirally transduced with the G185R NE mutant that is associated with a severe SCN phenotype. We show that the mutant enzyme accelerates apoptosis of differentiating but not of proliferating cells. Using metabolic labeling, confocal immunofluorescence microscopy, and immunoblot analysis of subcellular fractions, we also demonstrate that the G185R mutant is abnormally processed and localizes predominantly to the nuclear and plasma membranes rather than to the cytoplasmic compartment observed with the wild-type (WT) enzyme. Expression of the G185R mutant appeared to alter the subcellular distribution and expression of adaptor protein 3 (AP3), which traffics proteins from the trans-Golgi apparatus to the endosome. These observations provide further insight into potential mechanisms by which NE mutations cause neutropenia and suggest that abnormal protein trafficking and accelerated apoptosis of differentiating myeloid cells contribute to the severe SCN phenotype resulting from the G185R mutation.

Adaptor Protein Complex 3↗