Blast Cell

14,000,000 Leading Edge Experts on the ideXlab platform

Scan Science and Technology

Contact Leading Edge Experts & Companies

Scan Science and Technology

Contact Leading Edge Experts & Companies

The Experts below are selected from a list of 216 Experts worldwide ranked by ideXlab platform

Pirjo Koistinen - One of the best experts on this subject based on the ideXlab platform.

  • The soluble form of interleukin-6 receptor modulates Cell proliferation by acute myeloBlastic leukemia Blast Cells.
    Annals of Hematology, 1999
    Co-Authors: Marjaana Säily, Pirjo Koistinen, Eevariitta Savolainen
    Abstract:

    As interleukin-6 (IL-6) has been shown to have diverse effects on Blast Cell growth in acute myeloBlastic leukemia (AML), and as a soluble (s) form of IL-6 receptor (IL-6R) agonizes IL-6 effects in many Cell types, we investigated whether sIL-6R was able to modulate clonogenic Blast Cell growth in AML. The proliferation responses of eight autonomously growing AML Cell lines and eight primary AML Blast Cell samples were compared with their IL-6 and sIL-6R expression. Only three of the 16 AML samples were influenced by IL-6, two of them being stimulated and one inhibited by it. The sIL-6R-induced responses were more frequent, however, and, in contrast to those by IL-6, always stimulatory: clonogenic Cell growth in six of the 16 AML samples was stimulated by sIL-6R treatment. All the Cell lines and four of the seven primary Blast Cell samples analyzed expressed IL-6, and the expression was associated with unresponsiveness to exogenous IL-6. sIL-6R was also frequently expressed by AML Cells: only one of the samples was negative for it. However, there was no correlation between sIL-6R expression and the responsiveness of Cells to exogenous sIL-6R. The work presented here shows that sIL-6R is able to stimulate Blast Cell growth in AML. As AML Blast Cells are provided by exogenous IL-6 and sIL-6R in a bone marrow environment, and as many of them also express IL-6 and sIL-6R themselves in vitro, it is possible that signaling through the IL-6/sIL-6R system plays a role in maintaining their growth also in vivo.

  • effect of mast Cell growth factor on clonogenic Blast Cell growth in acute myelogenous leukemia
    Annals of Hematology, 1996
    Co-Authors: Timo Siitonen, M Lundstrom, Aiping Zheng, Eevariitta Savolainen, Pirjo Koistinen
    Abstract:

    The effect of the mast Cell growth factor (MGF), also known as stem Cell factor, steel factor, and kit ligand, alone or in combination with other GFs on clonogenic Blast Cell growth in 23 patients with acute myeloBlastic leukemia (AML) was investigated. MGF alone enhanced colony formation by about 35%, being clearly stimulatory (>20% increase in colony numbers) in nine patients. The additive effect of MGF on colony growth was observed in combination with interleukin-3 (IL-3). Preincubation of the Cells with MGF in suspension did not sensitize them to the effect of IL-3, granulocyte-macrophage colony-stimulating factor (GM-CSF), G-CSF, or IL-4 in a clonogenic Cell culture assay. Although almost all the Blast Cell samples expressed the c-kit the receptor for MGF, at the mRNA and/or the protein level, the Cells did not necessarily respond to exogenous MGF. On the other hand, Blast Cells were able to respond to exogenous MGF even when the Cells themselves expressed MGF. Neither the expression of MGF nor the response of Blast Cells to exogenous MGF was related to the capability of the Cells to form colonies spontaneously. In conclusion, MGF alone, but especially combined with IL-3, was a potent growth factor for clonogenic Blast Cells in AML. Autocrine production of MGF by AML Blast Cells analyzed at the mRNA level was not related to autonomous growth of the Cells.

D Metcalf - One of the best experts on this subject based on the ideXlab platform.

  • lineage commitment of hemopoietic progenitor Cells in developing Blast Cell colonies influence of colony stimulating factors
    Proceedings of the National Academy of Sciences of the United States of America, 1991
    Co-Authors: D Metcalf
    Abstract:

    Abstract In clonal cultures of normal mouse marrow Cells, combination of granulocyte, granulocyte-macrophage, or multipotential colony-stimulating factor (G-CSF, GM-CSF, or multi-CSF, respectively) with stem Cell factor (SCF) did not alter the number of Blast colonies stimulated to develop compared with SCF alone but induced an up to 25-fold increase in their mean Cell content and an up to 6-fold increase in their mean progenitor Cell content. Costimulation of Blast colony formation by SCF plus G-CSF did not change the relative frequency of progenitor Cells of different types within the colonies compared with colonies stimulated by SCF alone. However, combination of GM-CSF or multi-CSF with SCF significantly increased the relative frequency of granulocytic progenitors and, for multi-CSF, also of eosinophil progenitor Cells. These changes in the relative frequencies of progenitor Cells committed to the various lineages support the hypothesis that hemopoietic regulators have some ability to induce selective lineage commitment in the progeny of multipotential Cells.

Makio Ogawa - One of the best experts on this subject based on the ideXlab platform.

  • enhancement of murine Blast Cell colony formation in culture by recombinant rat stem Cell factor ligand for c kit
    Blood, 1991
    Co-Authors: K Tsuji, K M Zsebo, Makio Ogawa
    Abstract:

    Mice with W mutations characterized by hypopigmentation, sterility, anemia, and mast Cell deficiency have abnormalities in c-kit, a receptor with tyrosine kinase activity. Recently, the ligand for c-kit was cloned by investigators in several laboratories. Zsebo et al identified and cloned a gene for a cytokine termed stem Cell factor (SCF) in the medium conditioned by buffalo rat liver Cells, and this cytokine proved to be c-kit ligand. We have examined the effects of recombinant rat SCF (rrSCF) on colony formation from primitive hematopoietic progenitors in culture. rrSCF and erythropoietin (Ep) supported formation of granulocyte/macrophage (GM) colonies as well as a small number of multilineage and Blast Cell colonies from marrow Cells of normal mice. We then examined the effects of rrSCF using marrow and spleen Cells of mice that had been treated with 150 mg/kg 5- fluorouracil (5-FU). Unlike single factors, combinations of factors such as rrSCF plus interleukin-3 (IL-3), rrSCF plus IL-6, and rrSCF plus granulocyte colony-stimulating factor (G-CSF) markedly stimulated the growth of multilineage colonies. In contrast to these factor combinations and a combination of IL-3 and IL-6, a combination of rrSCF and IL-4 did not support multilineage colony formation. Mapping studies of the development of multipotential Blast Cell colonies further indicated that rrSCF, like IL-6, G-CSF, and IL-11, shortens the dormant period in which the stem Cells reside. When we tested the effects of rrSCF using pooled Blast Cells, which are highly enriched for progenitors and are devoid of stromal Cells, rrSCF plus Ep supported formation of only a few multilineage colonies, indicating that rrSCF itself is ineffective in support of the proliferation of multipotential progenitors. However, rrSCF supported formation of a significant number of neutrophil and neutrophil/macrophage colonies from pooled Blast Cells, indicating that rrSCF is able to support directly the proliferation of progenitors in neutrophil/monocyte lineages. c-kit ligand may play important roles in adult hematopoiesis.

Chenxi Tian - One of the best experts on this subject based on the ideXlab platform.

  • the c elegans spalt like protein sem 4 functions through the soxc transcription factor sem 2 to promote a proliferative Blast Cell fate in the postembryonic mesoderm
    Developmental Biology, 2017
    Co-Authors: Qinfang Shen, Chenxi Tian, Vikas Ghai
    Abstract:

    Proper development of a multiCellular organism relies on well-coordinated regulation of Cell fate specification, Cell proliferation and Cell differentiation. The C. elegans postembryonic mesoderm provides a useful system for uncovering factors involved in these processes and for further dissecting their regulatory relationships. The single Spalt-like zinc finger containing protein SEM-4/SALL is known to be involved in specifying the proliferative sex myoBlast (SM) fate. We have found that SEM-4/SALL is sufficient to promote the SM fate and that it does so in a Cell autonomous manner. We further showed that SEM-4/SALL acts through the SoxC transcription factor SEM-2 to promote the SM fate. SEM-2 is known to promote the SM fate by inhibiting the expression of two BWM-specifying transcription factors. In light of recent findings in mammals showing that Sall4, one of the mammalian homologs of SEM-4, contributes to pluripotency regulation by inhibiting differentiation, our work suggests that the function of SEM-4/SALL proteins in regulating pluripotency versus differentiation appears to be evolutionarily conserved.

  • the c elegans soxc protein sem 2 opposes differentiation factors to promote a proliferative Blast Cell fate in the postembryonic mesoderm
    Development, 2011
    Co-Authors: Chenxi Tian, Clark Colledge, Michael J Stern, Robert H Waterston
    Abstract:

    The proper development of multiCellular organisms requires precise regulation and coordination of Cell fate specification, Cell proliferation and differentiation. Abnormal regulation and coordination of these processes could lead to disease, including cancer. We have examined the function of the sole C. elegans SoxC protein, SEM-2, in the M lineage, which produces the postembryonic mesoderm. We found that SEM-2/SoxC is both necessary and sufficient to promote a proliferating Blast Cell fate, the sex myoBlast fate, over a differentiated striated bodywall muscle fate. A number of factors control the specific expression of sem-2 in the sex myoBlast precursors and their descendants. This includes direct control of sem-2 expression by a Hox-PBC complex. The crucial nature of the HOX/PBC factors in directly enhancing expression of this proliferative factor in the C. elegans M lineage suggests a possible more general link between Hox-PBC factors and SoxC proteins in regulating Cell proliferation.

Wolfgang R. Sperr - One of the best experts on this subject based on the ideXlab platform.

  • prognostic impact of Blast Cell counts in dysplastic bone marrow disorders mds and cmml i with concomitant fibrosis
    Annals of Hematology, 2014
    Co-Authors: Sigrid Machherndlspandl, Wolfgang R. Sperr, W Sega, H Bosmuller, Ulrich Germing, Ch Gruber, Kathrin Nachtkamp, P Reinecke, Friedrich Wimazal, Leonhard Mullauer
    Abstract:

    In a retrospective study, 43 patients with dysplastic neoplasms of the bone marrow (myelodysplastic syndromes and myelodysplastic/myeloproliferative-overlap neoplasms) associated with marked (grades 2–3) fibrosis were examined. Histopathologic and morphologic findings as well as cytogenetic and molecular results were correlated with clinical endpoints. Multilineage dysplasia (34 of 43 patients, 79 %) and hyperCellular bone marrow (64 %) were found in most patients. In ten of 35 patients, poor risk karyotypes according to the International Prognostic Scoring System (IPSS) were recorded. The JAK2 V617F mutation was detected in four of 30 patients (13 %), and the KIT D816V mutation was found in two of 30 patients (6 %). Patients were mainly treated with palliative drugs and best supportive care. After an observation time of 1–41 (median 21) months, ten of 43 patients (23 %) had developed a secondary acute leukemia. The median survival of all 43 patients was 21.4 months (range 1.8–88.2 months). Of all prognostic parameters examined, the Blast Cell count at diagnosis was found to be a most reliable and most predictive marker concerning survival and leukemia progression. This confirms previous studies in dysplastic bone marrow neoplasms without fibrosis.

  • expression of mast Cell tryptase by myeloBlasts in a group of patients with acute myeloid leukemia
    Blood, 2001
    Co-Authors: Wolfgang R. Sperr, Alexander W. Hauswirth, Mehrdad Baghestanian, John-hendrik Jordan, Andreas Chott, Hanspeter Kiener, Puchit Samorapoompichit, Hans Semper, Geritholger Schernthaner, Susanne Natter
    Abstract:

    α- and β-tryptase genes encode serine proteases that are abundantly expressed by mast Cells. Under physiologic conditions other myeloid Cells are virtually tryptase negative. However, tryptases are also expressed in several myeloid leukemia Cell lines. In this study, serum total tryptase levels were determined in 150 patients with acute leukemias (de novo acute myeloid leukemia [AML], n = 108; secondary AML, n = 25; acute lymphoid leukemia [ALL], n = 17) by fluoroenzyme immunoassay. In healthy subjects (n = 30), tryptase levels ranged between 2.0 and 12.6 ng/mL. Elevated tryptase levels (> 15) were detected in 42 (39%) of 108 patients with de novo AML and in 11 (44%) of 25 patients with secondary AML. No elevated tryptase levels were found in patients with ALL. In de novo AML, elevated tryptase levels were frequently detected in patients with French-American-British classification M0 (6 of 9), M2 (9 of 14), M3 (4 of 6), and M4eo (7 of 7), and less frequently in M1 (7 of 20), M4 (6 of 26), M5 (2 of 18), M6 (0 of 5), or M7 (1 of 3). The highest tryptase levels were found in M4eo. Immunohistochemical staining of bone marrow sections with anti-tryptase antibody as well as immunoelectron microscopy revealed tryptase expression in the cytoplasm of myeloBlasts. As assessed by Northern blotting and reverse transcriptase–polymerase chain reaction, AML Cells expressed α-tryptase messenger RNA (mRNA) but little or no β-tryptase mRNA. In AML patients with elevated serum tryptase before chemotherapy, who entered complete remission, tryptase levels returned to normal or near normal values. Blast Cell persistence or regrowth was associated with a persistently elevated level or recurrent increase of tryptase. Together, tryptase is expressed in myeloBlasts in a group of AML and may serve as a useful disease-related marker.