Ligation of CD44 with low-molecular-weight hyaluronan and a monoclonal antibody leads to inhibition of drug-induced apoptosis in a human myeloid cell line

Hematology ◽  
2009 ◽  
Vol 14 (4) ◽  
pp. 213-219 ◽  
Author(s):  
Masahiro Onoda ◽  
Chiaki Nakaseko ◽  
Akira Yokota ◽  
Yasushi Saito
Keyword(s):  
Molecular Weight ◽  
Monoclonal Antibody ◽  
Cell Line ◽  
Myeloid Cell ◽  
Low Molecular Weight ◽  
Drug Induced ◽  
Myeloid Cell Line ◽  
Induced Apoptosis

Cotreatment with Pioglitazone, a Synthetic Ligand for Peroxisome Proliferator-Activated Receptor γ (PPARγ), Enhances Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand (TRAIL)-Induced Apoptosis of Human Leukemia Cells.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 4377-4377
Author(s):  
Joo-In Park ◽  
Hoon Han ◽  
Ji-Seon Han ◽  
Hyuk-Chan Kwon ◽  
Jin-Yeong Han ◽  
...  
Keyword(s):  
Cell Growth ◽  
Cell Line ◽  
Myeloid Cell ◽  
Leukemia Cells ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Myeloid Cell Line ◽  
Synthetic Ligand ◽  
Induced Apoptosis ◽  
Acute Myeloid

Abstract Imatinib (STI571, Glivec) is the choice treatment for Bcr/Abl-positive malignancies. Emergence of resistance to Imatinib warrants the exploration of novel well-tolerated anticancer agents. Peroxisome proliferator-activated receptor γ (PPARγ) is a nuclear receptor family, which mainly associates with the adipocyte differentiation, but also appears to facilitate cell differentiation or apoptosis in certain malignant cells. Previous studies imply that the PPARγ activation pathway may be a possible intervention mode for treatment of leukemia, which is resistant to imatinib (STI571). In this study, we investigated the effects of pioglitazone, a synthetic ligand for PPARg, on the cell growth and TRAIL-induced apoptosis in a novel imatinib (STI571) resistant acute myeloid cell line (SR-1), which we have established from an STI571 resistant blast crisis patient, as well as HL-60 cells. HL-60 and SR-1 cells are relatively resistant to TRAIL-induced apoptosis. Pioglitazone alone inhibited the cell growth of SR-1 and HL-60 cells, but did not induce the apoptosis of these cell lines. However, simultaneous exposure of cells to 100 ng/ml TRAIL with either 25 μM pioglitazone or 50 μM piogliazone resulted in a striking increase in apoptosis. To clarify the mechanism of pioglitazone to sensitize the leukemia cells to TRAIL-induced apoptosis, we investigated the change of the proteins related to cell cycle and apoptosis by western blot. As results, we observed the significant decrease of X-linked inhibitor of apoptosis (XIAP) and the increased expression of p21 by cotreatment of pioglitazone with TRAIL. Taken together, these findings indicate that pioglitazone may have promising activity in augmenting TRAIL-induced apoptosis of human acute leukemia cells including the imatinib (STI571) resistant acute myeloid cell line.

Nonchemotherapy Drug-Induced Neutropenia and Agranulocytosis

2014 ◽  
Vol 27 (5) ◽  
pp. 447-452 ◽  
Author(s):  
Amy M. Pick ◽  
Kelly K. Nystrom
Keyword(s):  
High Risk ◽  
Cell Line ◽  
Broad Spectrum ◽  
Myeloid Cell ◽  
Drug Induced ◽  
Colony Stimulating Factors ◽  
Immune Mediated ◽  
Myeloid Cell Line ◽  
Risk Patients ◽  
Direct Toxicity

Drug-induced agranulocytosis is a severe complication that has been implicated with most classes of medications. Medications such as clozapine, trimethoprim-sulfamethoxazole and methimazole have been more commonly associated with agranulocytosis than other agents. Although the pathogenesis isn't fully elucidated, it appears to be two-fold with a direct toxicity to the myeloid cell line and immune-mediated destruction. Patients may be asymptomatic at the time neutropenia is discovered or may present with more severe complications such as sepsis. In approximately 5% of cases drug-induced agranulocytosis may be fatal. Management of drug-induced agranulocytosis includes the immediate discontinuation of the offending medication, initiation of broad-spectrum antibiotics and consideration of the use of granulocyte colony-stimulating factors in high-risk patients.

AZT Incorporation into Mitochondria: Study in a Human Myeloid Cell Line

1996 ◽  
Vol 15 (5) ◽  
pp. 363-366 ◽  
Author(s):  
NEIL J. NUSBAUM ◽  
PHILLIP E. JOSEPH
Keyword(s):  
Cell Line ◽  
Myeloid Cell ◽  
Myeloid Cell Line

scholarly journals Direct demonstration of an HLA-DR allotypic determinant on the low molecular weight (beta) subunit using a mouse monoclonal antibody specific for DR3

1982 ◽  
Vol 156 (1) ◽  
pp. 104-111 ◽  
Author(s):  
JP Johnson ◽  
T Meo ◽  
G Reithmuller ◽  
DJ Schendel ◽  
R Wank
Keyword(s):  
Molecular Weight ◽  
Monoclonal Antibody ◽  
Cell Surface ◽  
B Cell ◽  
Beta Subunit ◽  
Low Molecular Weight ◽  
Β Subunit ◽  
Direct Demonstration ◽  
Hla Dr ◽  
Human B Cell

A murine monoclonal antibody directed against a human B cell surface antigen with the characteristics of HLA-DR is described. The antigen detected is tightly linked to HLA and is correlated with the alloantigen HLA-Dw/DR3. Reactivity with a fraction of Dw/DRw6 cells is also observed. The determinant recognized by this antibody has been shown to be present on the smaller molecular weight β subunit of the HLA-DR antigen.

scholarly journals Detailed molecular cytogenetic characterisation of the myeloid cell line U937 reveals the fate of homologous chromosomes and shows that centromere capture is a feature of genome instability

2020 ◽  
Vol 13 (1) ◽  
Author(s):  
Ruth N. MacKinnon ◽  
Joanne Peverall ◽  
Lynda J. Campbell ◽  
Meaghan Wall
Keyword(s):  
Cell Line ◽  
Chromosome Pair ◽  
Fusion Gene ◽  
Genome Instability ◽  
Snp Array ◽  
Myeloid Cell ◽  
Chromosome 20 ◽  
Myeloid Cell Line ◽  
Multicolour Fish ◽  
Chromosome Segments

Abstract Background The U937 cell line is widely employed as a research tool. It has a complex karyotype. A PICALM-MLLT10 fusion gene formed by the recurrent t(10;11) translocation is present, and the myeloid common deleted region at 20q12 has been lost from its near-triploid karyotype. We carried out a detailed investigation of U937 genome reorganisation including the chromosome 20 rearrangements and other complex rearrangements. Results SNP array, G-banding and Multicolour FISH identified chromosome segments resulting from unbalanced and balanced rearrangements. The organisation of the abnormal chromosomes containing these segments was then reconstructed with the strategic use of targeted metaphase FISH. This provided more accurate karyotype information for the evolving karyotype. Rearrangements involving the homologues of a chromosome pair could be differentiated in most instances. Centromere capture was demonstrated in an abnormal chromosome containing parts of chromosomes 16 and 20 which were stabilised by joining to a short section of chromosome containing an 11 centromere. This adds to the growing number of examples of centromere capture, which to date have a high incidence in complex karyotypes where the centromeres of the rearranged chromosomes are identified. There were two normal copies of one chromosome 20 homologue, and complex rearrangement of the other homologue including loss of the 20q12 common deleted region. This confirmed the previously reported loss of heterozygosity of this region in U937, and defined the rearrangements giving rise to this loss. Conclusions Centromere capture, stabilising chromosomes pieced together from multiple segments, may be a common feature of complex karyotypes. However, it has only recently been recognised, as this requires deliberate identification of the centromeres of abnormal chromosomes. The approach presented here is invaluable for studying complex reorganised genomes such as those produced by chromothripsis, and provides a more complete picture than can be obtained by microarray, karyotyping or FISH studies alone. One major advantage of SNP arrays for this process is that the two homologues can usually be distinguished when there is more than one rearrangement of a chromosome pair. Tracking the fate of each homologue and of highly repetitive DNA regions such as centromeres helps build a picture of genome evolution. Centromere- and telomere-containing elements are important to deducing chromosome structure. This study confirms and highlights ongoing evolution in cultured cell lines.

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