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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 628 (1991), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 718 (1994), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 330 (1987), S. 765-767 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] K562 cells provide a model system for studying human erythroid differentiation as they can be induced by haemin or other chemicals to undergo differentiation and accumulate haemoglobins8"11. We have purified inhibin from ovine rete testis fluid by immunoaffinity chromatography (J.V. et al. ...
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  • 4
    ISSN: 0730-2312
    Keywords: prolongation of G1 ; activin A ; RB protein ; cell cycle ; differentiation ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The human erythroleukemic cell line, K562, can be induced to differentiate by the addition of activin A, a newly purified protein belonging to the TGF-β1 family. The present studies used flow cytometric cell cycle analysis, indirect immunofluorescence staining of the proliferating cell nuclear antigen (PCNA), and thymidine incorporation assay of cell proliferation to study the effects of activin A on the cell cycle during differentiation in K652 cells. Activin phase. The latter can be observed after approximately 24 hr of incubation with activin A and then disappears after this early stage of induction of differentiation. Cell cycle kinetics analysis using synchronized K562 cells also confirms that in the presence of activin A, K562 cells progress normally through various phases of cell, except that there is prolongation of the G1 phase between 10 to 24 hr of culture. Furthermore, this transient arrest in G1 is correlated with dephosphorylation of a nucleoprotein, the RB gene product, which occurs within 9-24 hr of incubation with activin A; and phosphorylation of RB protein then develops afterward. In addition, these cell cycle-related events are observed to occur earlier than the accumulation of hemoglobins in K562 cells. It is concluded that transient dephosphorylation of RB protein and prolongation of G1 phase of cell cycle precede and accompany erythroid differentiation caused by activin A and chemical inducers, thus constituting part of the mechanism for induction of differentiation in the erythroleukemia cells. © 1992 Wiley-Liss, Inc.
    Additional Material: 7 Ill.
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  • 5
    Electronic Resource
    Electronic Resource
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 70 (1998), S. 8-21 
    ISSN: 0730-2312
    Keywords: activin A ; bone marrow stromal cells ; gene regulation ; promoter activity ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Activin A, a member of the TGF-β superfamily, plays roles in differentiation and development, including hematopoiesis. Our previous studies indicated that the expression of activin A by human bone marrow cells and monocytes is highly regulated by inflammatory cytokines and glucocorticoids. The present study was undertaken to investigate the regulation of activin A gene expression in the human bone marrow stromal cell lines L87/4 and HS-5, as well as in primary stromal cells. Northern blots demonstrated that, like primary stromal cells, the cell lines expressed four activin A RNA transcripts (6.4, 4.0, 2.8, and 1.6 kb), although distribution of the RNA among the four sizes varied. The locations of the 5′ ends of the RNAs were investigated by Northern blots and RNase protection assays. The results identified a transcription start site at 212 nucleotides upstream of the translation start codon. In addition, luciferase expression assays of a series of deletion constructs were used to identify regulatory sequences upstream of the activin A gene. A 58 bp upstream sequence exhibits promoter activity. However, severalfold higher expression requires a positive element consisting of an additional 71 bp of the upstream region. Promoter activity was also identified between 2.5 and 3.6 kb upstream of the start codon. These findings suggest that expression of activin A at the transcriptional level follows complex patterns of regulation. J. Cell. Biochem. 70:8-21, 1998. © 1998 Wiley-Liss, Inc.
    Additional Material: 11 Ill.
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  • 6
    Publication Date: 2004-11-16
    Description: Acute or chronic leukemias resist apoptosis in vitro when co-cultured with marrow stromal cells, suggesting that the growth/survival of leukemia cells relies in part on interactions with stromal cells in the microenvironment. We have recently demonstrated that consistent and high-level engraftment of human primary leukemia obtained from patients can be achieved in NOD/scid mice by preconditioning with either adherent cord blood or marrow mesenchymal stem cells. High success rate of engraftment (84.9 ± 2.9 % leukemia blasts in mouse marrow) was obtained with many lineages of leukemia including acute T- or B-cell lymphoblastic and myeloid leukemia. In general, leukemia blasts were detectable in peripheral blood of mice by week 4–5, leading to fatal outcome by week 6 (42 ± 4 days). Furthermore, cells from the marrow of these preconditioned mice were found to secrete leukemia-promoting activities, suggesting that the mouse marrow had been altered to favor the proliferation/survival of leukemic cells in vivo. We also showed that the human leukemia cells harvested from mice could be serially transferred to other mice for many generations with ~100 fold increase in the number of leukemic and clonogenic cells in mice, while retaining properties similar to primary leukemia samples obtained from patients. Several lines of evidence in our studies including the appearance of leukemia blasts in marrow and blood, the dissemination to other tissues, and gene expression profiling in microarray analysis confirm that this xenograft model recapitulates key features of human leukemia. Furthermore, weekly i.p. injections of NOD/scid mice with vincristine at 0.5 mg/kg for three weeks, starting at second week after inoculation of patients primary leukemia, resulted in a significant delay in the appearance of human leukemia blasts in blood, doubly the length of mouse survival. In addition, pairs of primary leukemia samples collected at diagnosis and at relapse from the same patients were engrafted into NOD/scid mice. The NOD/scid mice transplanted with either samples developed leukemia in mouse peripheral blood at week 4–5 with similar kinetics after inoculation. However, weekly vincristine treatment x 3 of the mice transplanted with diagnosis leukemia samples, prevented the appearance of leukemia blast cells in the circulating peripheral blood for at least 5 weeks. In contrast, similar treatment of mice engrafted with relapse leukemia samples had 50% leukemia blasts in blood at week 5 and subsequently developed fatal leukemia dissemination at week 7. These findings indicate that this robust high level engraftment model of human primary leukemia may be useful in predicting clinical response to chemotherapy. Evidence has further suggested that these human leukemia in NOD/scid mice may be derived from a small subset of immature stem cells in the samples that give rise to leukemia expansion and phenotypic diversity in these mice. Therefore, we had developed a robust and predictive animal model of human primary leukemia, which is valuable for studying leukemia stem cells and for testing or prioritizing new agents/regimens in vivo.
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
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  • 7
    Publication Date: 2001-05-15
    Description: Childhood T-cell acute lymphoblastic leukemia (T-ALL) is one of the most common childhood cancers. It is reported that preconditioning sublethally irradiated immunodeficient NOD/SCID (nonobese diabetic/X-linked severe combined immunodeficient) mice with human cord blood mononuclear cells facilitates the engraftment, expansion, and dissemination in these mice of primary T-ALL cells obtained from patients at the time of diagnosis. Cells recovered from mouse bone marrow or spleen resembled the original leukemia cells from patients with respect to surface lineage markers and T-cell receptor Vβ gene rearrangements. Moreover, the pattern of leukemia dissemination in mouse tissues, resulting in universally fatal leukemia, is reminiscent of the human clinical disease. In addition, the fidelity of the model to the human disease is documented with regard to the presence of morphologically identifiable human leukemia cells in mouse bone marrow and blood and the maintenance of leukemia-initiating capacity within the leukemia-engrafted mouse. Therefore, several lines of independent approaches are used to suggest that the engrafted cells are of human leukemia origin and are not derived from cord blood. The in vivo model described here should enable the study of the growth properties of primary T-ALL cells obtained from patients and should prove useful in evaluating the potential efficacy of therapeutic strategies directed toward T-ALL.
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
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  • 8
    Publication Date: 2002-11-01
    Description: The novel prodrug of butyric acid, pivaloyloxymethyl butyrate (AN-9), a histone deacetylase inhibitor, shows great promise as an effective and relatively nontoxic anticancer agent for solid malignancies. However, little is known about its effects on hematopoietic malignancies. In this study, we show that 21 primary samples of acute leukemia were sensitive to the antiproliferative effects of AN-9, with a 50% inhibitory concentration (IC50) of 45.8 ± 4.1 μM. In colony-forming assays, primary T-cell acute lymphoblastic leukemia (T-ALL) cells were 3-fold more sensitive to AN-9 than the normal hematopoietic progenitors, erythroid burst-forming units and granulocyte/monocyte colony-forming units. AN-9 induced apoptosis in the T-ALL cell line CEM. A common problem with cancer is chemoresistance, which is often typical of relapsed cancers. Remarkably, a T-ALL sample at diagnosis and an acute myeloid leukemia sample at relapse that were resistant to doxorubicin in vitro were sensitive to AN-9, with an IC50 of 50 μM for both samples. More strikingly, samples from 2 infants with t(4;11) ALL obtained at diagnosis and relapse each were the most sensitive to AN-9, with IC50values of 25 μM and 17 μM, respectively. Furthermore, a doxorubicin-resistant clone of HL60, HL60/ADR, obtained by the transfection of the MDR-1 gene, was equally sensitive to AN-9 cytotoxicity as the parental cells. AN-9 induced the expression of p21 in an infant leukemia sample with 11q23 rearrangement, but not in T- or B-precursor ALL. Collectively, our results suggest that AN-9 is a selective agent for hematopoietic malignancies that can circumvent the mechanisms of chemoresistance limiting most conventional chemotherapy.
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
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  • 9
    Publication Date: 1987-12-01
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Springer Nature
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  • 10
    Publication Date: 1992-11-01
    Print ISSN: 0730-2312
    Electronic ISSN: 1097-4644
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Published by Wiley
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