Thematische Bibliographien / Motility of leukemia cells / Dissertationen
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Dissertationen zum Thema „Motility of leukemia cells“

Autor: Grafiati
Veröffentlicht am 28. Juni 2021
Zuletzt aktualisiert am 1. Februar 2022

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1

Renaudin, Xavier. „Rôle de FANCA dans la régulation de la neddylation de protéines membranaires“. Thesis, Paris 11, 2014. http://www.theses.fr/2014PA112187.

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Le but de cette thèse était d’identifier de nouveaux substrats au complexe FANC Core,déficient dans l’Anémie de Fanconi, une pathologie génétique rare. Cette maladie estcaractérisée par un phénotype hétérogène associant une pancytopénie à des malformationscongénitales et une prédisposition accrues aux leucémies myéloïdes aigues.L’anémie de Fanconi est causée par la mutation biallélique dans un des seize gènesFANC. Les protéines produites par ces gènes participent à une même voie moléculaireimpliquée dans la signalisation des dommages de l’ADN. Huit de ces protéines forment lecomplexe FANC Core, une E3 ubiquitine ligase, dont les seuls substrats à ce jour sontFANCD2 et FANCI.Dans le but d’identifier de nouveaux substrats du complexe FANC Core, j’ai réalisé uneanalyse protéomique après immunoprécipitation des peptides modifiés par l’ubiquitine ou parles ubiquitin-like NEDD8 et ISG15. Cette expérience a été faite dans des cellules déficientespour la voie FANC, mutées sur les gène FANCA ou FANCC et comparée à des cellulescorrigées par l’expression de ces gènes.Cette analyse révèle que FANCD2 et FANCI sont les seules cibles du complexe FANCCore en réponse à des dommages de l’ADN.Néanmoins, je montre l’existence d’autres protéines qui sont modifiées d’une manièreFANCA dépendante. Ces protéines sont pour la grande majorité des protéines membranairesou associées aux membranes cytoplasmiques. Parmi celles-ci, j’ai pu déterminer que lerécepteur aux chimiokines, CXCR5, était modifié d’une manière FANCA dépendante parl’ubiquitin-like NEDD8. Cette modification impacte sur la localisation de la protéine à lamembrane et à des conséquences sur la migration des cellules.J’ai aussi montré que FANCA participe d’une manière similaire à la régulation de lalocalisation membranaire d’autres protéines comme APLP2.Ainsi, il est proposé par ce travail un rôle de la protéine FANCA en dehors du complexeFANC Core et en dehors de la réparation des dommages à l’ADN. Comment la protéineFANCA participe à la régulation du trafic des protéines membranaires reste un point nonrésolu à ce jour
The aim of this thesis was to find new substrates of the E3-ubiquitin ligase activity of theFANC Core complex, mutated in the rare genetic disorder Fanconi Anemia. This disease ischaracterized by bone marrow failure, developmental abnormalities and predisposition tocancer. Eight of the 16 known FANC proteins participate in the FANCcore nuclear complex,which has E3 ubiquitin-ligase activity and monoubiquitinates FANCD2 and FANCI inresponse to replication stress.In this thesis, I used mass spectrometry to compare cellular extracts from FANC Corecomplex deficient FA-A and FA-C cells to their ectopically corrected counterparts after agenotoxic stress.FANCD2 and FANCI appear to be the only true direct targets of the FANCcore complex.However, I also identified other proteins that undergo post-translational modifications throughFANCA- or FANCC-specific direct or indirect mechanisms that are independent of theFANCcore complex. The majority of these potential FANCA or FANCC target proteinslocalize to the cell membrane.Finally, I demonstrated that (a) the chemokine receptor CXCR5 is a neddylated protein; (b)FANCA, surprisingly, appears to modulate CXCR5 neddylation through a currently unknownmechanism; (c) CXCR5 neddylation is involved in the targeting of this receptor to the cellmembrane; and (d) CXCR5 neddylation stimulates cell migration/motility.I also confirmed that the role of FANCA in neddylation is not restrict to CXCR5 but also to,at least, one other protein, APLP2.My work has uncovered a new signaling pathway that is potentially involved in the rarehuman syndrome Fanconi Anemia and in cell motility and has highlighted a potential newfunction for the FANCA protein independant of the FANC Core complex and of a genotoxicstress
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2

Smrčková, Zuzana. „Motilita leukemických buněk analyzovaná nekoherentním holografickým kvantitativním zobrazováním fáze“. Master's thesis, Vysoké učení technické v Brně. Fakulta strojního inženýrství, 2021. http://www.nusl.cz/ntk/nusl-444984.

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This diploma thesis deals with the issue of motility analysis in leukemia cells. An accurate description of the cell movement and the detection of differences in motility under experimental conditions can be obtained by quantitative analysis of cell motility using time-lapse recording. The first part of this work describes various types of tumor cell migraton. The second part focuses on methods of analysis of cell motility in tissue culture using time-lapse recording, which include image acquisition and processing. Part of this chapter describes a coherence-controlled holographic microscope, which was used in the practical part and for which an insert was designed to ensure the exact and stable position of the individual chambers. The last part is focused on the research of leukemic cell motility, which is concluded by a discussion of the obtained results. The appendix contains a published study included acknowledgement to the author of this diploma thesis for participation in the project.
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3

Zhang, Lu [Verfasser]. „Immunogenicity of leukemia stem cells in acute myeloid leukemia / Lu Zhang“. Ulm : Universität Ulm. Medizinische Fakultät, 2012. http://d-nb.info/1020022574/34.

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4

Bai, Limiao, und 白利苗. „In silico simulation of actin-based motility“. Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B46429116.

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5

Suck, Garnet, Yeh Ching Linn und Torsten Tonn. „Natural Killer Cells for Therapy of Leukemia“. Karger, 2016. https://tud.qucosa.de/id/qucosa%3A71644.

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Clinical application of natural killer (NK) cells against leukemia is an area of intense investigation. In human leukocyte antigen-mismatched allogeneic hematopoietic stem cell transplantations (HSCT), alloreactive NK cells exert powerful anti-leukemic activity in preventing relapse in the absence of graft-versus-host disease, particularly in acute myeloid leukemia patients. Adoptive transfer of donor NK cells post-HSCT or in non-transplant scenarios may be superior to the currently widely used unmanipulated donor lymphocyte infusion. This concept could be further improved through transfusion of activated NK cells. Significant progress has been made in good manufacturing practice (GMP)-compliant large-scale production of stimulated effectors. However, inherent limitations remain. These include differing yields and compositions of the end-product due to donor variability and inefficient means for cryopreservation. Moreover, the impact of the various novel activation strategies on NK cell biology and in vivo behavior are barely understood. In contrast, reproduction of the thirdparty NK-92 drug from a cryostored GMP-compliant master cell bank is straightforward and efficient. Safety for the application of this highly cytotoxic cell line was demonstrated in first clinical trials. This novel ‘off-theshelf’ product could become a treatment option for a broad patient population. For specific tumor targeting chimeric-antigen-receptor-engineered NK-92 cells have been designed.
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6

Birkenmeier, Gerd, Nasr Y. A. Hemdan, Susanne Kurz, Marina Bigl, Philipp Pieroh, Tewodros Debebe, Martin Buchold, Rene Thieme, Gunnar Wichmann und Faramarz Dehghani. „Ethyl pyruvate combats human leukemia cells but spares normal blood cells“. Universitätsbibliothek Leipzig, 2016. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-213853.

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Ethyl pyruvate, a known ROS scavenger and anti-inflammatory drug was found to combat leukemia cells. Tumor cell killing was achieved by concerted action of necrosis/apoptosis induction, ATP depletion, and inhibition of glycolytic and para-glycolytic enzymes. Ethyl lactate was less harmful to leukemia cells but was found to arrest cell cycle in the G0/G1 phase. Both, ethyl pyruvate and ethyl lactate were identified as new inhibitors of GSK-3β. Despite the strong effect of ethyl pyruvate on leukemia cells, human cognate blood cells were only marginally affected. The data were compiled by immune blotting, flow cytometry, enzyme activity assay and gene array analysis. Our results inform new mechanisms of ethyl pyruvate-induced cell death, offering thereby a new treatment regime with a high therapeutic window for leukemic tumors.
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7

Choi, Mi-Yon. „P53 mediated cell motility in H1299 lung cancer cells“. VCU Scholars Compass, 2010. http://scholarscompass.vcu.edu/etd/109.

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Studies have shown that gain-of- function mutant p53, AKT, and NFκB promote invasion and metastasis in tumor cells. Signals transduced by AKT and p53 are integrated via negative feedback between the two pathways. Tumor derived p53 was also indicated to induce NFκB gene expression. Due to the close relationship between p53/AKT and p53/NFκB, we hypothesized that AKT and NFκB can enhance motility in cells expressing mutant p53. Effects on cell motility were determined by scratch assays. CXCL5- chemokine is also known to induce cell motility. We hypothesized that enhanced cell motility by AKT and NFκB is mediated, in part, by CXCL5. CXCL5 expression levels in the presence and absence of inhibitors were determined by qRT-PCR. We also hypothesized that gain-of-function mutant p53 contributes to the activation of AKT. The effect of mutant p53 on AKT phosphorylation was investigated with a Ponasterone A- inducible mutant cell line (H1299/R175H) and vector control. These results indicated that AKT and NFκB enhance motility in cells expressing mutant p53 and this enhanced motility is, in part, mediated by CXCL5. However, AKT phosphorylation was independent of mutant p53.
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8

Peng, Cong. „Novel Therapeutic Targets for Ph+ Chromosome Leukemia and Its Leukemia Stem Cells: A Dissertation“. eScholarship@UMMS, 2010. https://escholarship.umassmed.edu/gsbs_diss/473.

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The human Philadelphia chromosome (Ph) arises from a translocation between chromosomes 9 and 22 [t(9;22)(q34;q11)]. The resulting chimeric BCR-ABLoncogene encodes a constitutively activated, oncogenic tyrosine kinase that induces chronic myeloid leukemia (CML) and B-cell acute lymphoblastic leukemia (B-ALL). The BCR-ABL tyrosine kinase inhibitor (TKI), imatinib mesylate, induces a complete hematologic and cytogenetic response in the majority of CML patients, but is unable to completely eradicate BCR-ABL–expressing leukemic cells, suggesting that leukemia stem cells are not eliminated. Over time, patients frequently become drug resistant and develop progressive disease despite continued treatment. Two major reasons cause the imatinib resistance. The first one is the BCR-ABL kinase domain mutations which inhibit the interaction of BCR-ABL kinase domain with imatinib; the second one is the residual leukemia stem cells (LSCs) in the patients who are administrated with imatinib. To overcome these two major obstacles in CML treatment, new strategies need further investigation. As detailed in Chapter II, we evaluated the therapeutic effect of Hsp90 inhibition by using a novel water-soluble Hsp90 inhibitor, IPI-504, in our BCR-ABL retroviral transplantation mouse model. We found that BCR-ABL mutants relied more on the HSP90 function than WT BCR-ABL in CML. More interestingly, inhibition of HSP90 in CML leukemia stem cells with IPI-504 significantly decreases the survival and proliferation of CML leukemia stem cells in vitro and in vivo. Consistent with these findings, IPI-504 treatment achieved significant prolonged survival of CML and B-ALL mice. IPI-504 represents a novel therapeutic approach whereby inhibition of Hsp90 in CML patients and Ph+ ALL may significantly advance efforts to develop a cure for these diseases. The rationale underlying the use of IPI-504 for kinase inhibitor–resistant CML has implications for other cancers that display oncogene addiction to kinases that are Hsp90 client proteins. Although we proved that inhibition of Hsp90 could restrain LSCs in vitro and in vivo, it is still unclear how to define specific targets in LSCs and eradicate LSCs. In Chapter III, we took advantage of our CML mouse model and compared the global gene expression signature between normal HSCs and LSCs to identify the downregulation of Pten in CML LSCs. CML develops faster when Pten is deleted in Ptenfl/fl mice. On the other hand, Pten overexpression significantly delays the CML development and impairs leukemia stem cell function. mTOR is a major downstream of Pten-Akt pathway and it is always activated or overepxressed when Pten is mutated or deleted in human cancers. In our study, we found that inhibition of mTOR by rapamycin inhibited proliferation and induced apoptosis of LSCs. Notably, our study also confirmed a recent clinical report that Pten has been downregulated in human CML patient LSCs. In summary, our results proved the tumor suppressor role of Pten in CML mouse model. Although the mechanisms of Pten in leukemia stem cells still need further study, Pten and its downstream, such as Akt and mTOR, should be more attractive in LSCs study.
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9

Chu, Peter P. „Immune-mediated apoptosis of chronic lymphocytic leukemia cells /“. Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2001. http://wwwlib.umi.com/cr/ucsd/fullcit?p3031939.

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10

Sawai, Hirofumi. „Role for ceramide in apoptosis of leukemia cells“. Kyoto University, 1997. http://hdl.handle.net/2433/202164.

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11

Thurston, Gavin O. „Studies on the effect of radiation on 3T3 cell motility“. Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/29441.

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The ability of mammalian cells to locomote is important in a variety of normal and pathological processes. Previous work has suggested that low doses of x-irradiation may perturb cell motility, a finding that may have important consequences in embryogenesis, cancer metastasis, and immune response. This thesis has sought to study in more detail the effect of radiation on mammalian cell motility. Work performed in other laboratories used the colloidal gold assay and time lapse cinemicroscopy to study x-irradiation induced changes to 3T3 fibroblast motility in tissue culture. These studies were repeated here, with qualitative results similar to those reported earlier. However, these methods were not amenable to a detailed quantitative analysis. For this, spatial and temporal information on the motility and dynamic morphology of a large number of cells is required. Such a task would be impossible to perform manually, thus an automated microscope system was developed that used a computer-driven precision stage and a solid state optical sensor to track individual cells in tissue culture. Information on motility and morphology was concurrently extracted from many cells. As part of the thesis, several techniques were developed to analyze and display these data, and to correlate motility and morphology observations. These techniques were directed at preserving the actual process of 3T3 cell motility, and parameters were measured to quantify the short term persistence of cell movement (on a time scale of 0.5 to 2 hours), and the long term persistence of cells in maintaining certain characteristic behaviour (on a time scale of 3 to 12 hours). The response of 3T3 fibroblasts to x-irradiation was characterized by a number of parameters. The population average cell speed was measured following treatment, and a dose response and time response was determined in the range of 1.5 Gy. Other motility parameters indicate that the normal process of cell motility, evidenced by a series of motile segments, was disrupted by x-rays. This was thought to reflect perturbation to the control mechanisms of cell motility. The morphology of 3T3 cells stained with Coomassie blue was examined in an effort to correlate the observed motility changes with changes in the fixed cell morphology. This stain is a general structural protein stain with higher affinity toward microfilaments. High doses of x-rays were required to produce significant perturbation to cell morphology, and in the dose regime of interest, the morphology of irradiated cells was not identifiably different from control. Of note is that it was the well spread, quiescent cells that seemed least perturbed by large doses of irradiation. In summary, x-rays apparently disrupt the normal process of cell motility. Several lines of evidence suggest that actively migrating cells are the most perturbed by irradiation. This work has developed techniques to quantify cell motility in a meaningful way, and to characterize the x-ray induced perturbations.
Science, Faculty of
Physics and Astronomy, Department of
Graduate
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12

Garg, Ayush A. „Electromagnetic Fields Alter the Motility of Metastatic Breast Cancer Cells“. The Ohio State University, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=osu1563816767104018.

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13

Shalapour, Shabnam [Verfasser]. „Leukemia-associated genetic aberrations in mesenchymal stem cells of children with acute lymphoblastic leukemia / Shabnam Shalapour“. Berlin : Freie Universität Berlin, 2010. http://d-nb.info/1024054853/34.

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14

Cheung, Man-sze, und 張敏思. „Characterization of Leukemic stem cells in acute myeloid Leukemia“. Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B40687582.

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15

Puram, Rishi Venkata. „Defining and Targeting Transcriptional Pathways in Leukemia Stem Cells“. Thesis, Harvard University, 2014. http://nrs.harvard.edu/urn-3:HUL.InstRepos:13070042.

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Acute myeloid leukemia (AML) is a clonal neoplastic disorder organized as a cellular hierarchy, with the self-renewing leukemia stem cell (LSC) at the apex. Recurrent mutations in transcription factors (TF) and epigenetic regulators suggest that AML is driven by aberrant transcriptional circuits, but these circuits have not been fully defined in an LSC model. To study transcriptional mechanisms relevant to leukemogenesis in vivo, we generated a murine serial transplantation model of MLL-AF9-driven, myelomonocytic leukemia with genetically- and phenotypically-defined LSCs. Using this model, we pursued two related lines of investigation. First, we performed an in vivo RNA interference (RNAi) screen to identify transcription factors required for LSC function. This screen highlighted the circadian rhythm TFs, Clock and Bmal1, as genes essential for the survival of murine leukemia cells, and we validated this finding with CRISPR/Cas-based genome editing and knockdown studies in AML cell lines. Utilizing luciferase reporter mice to track expression of the circadian target gene Per2, we demonstrated that both leukemic and normal hematopoietic cells have the capacity for oscillating, circadian-dependent gene expression. Importantly, using murine knockout models, we found that normal hematopoietic stem and progenitor cells (HSPC), in contrast to leukemia cells, do not depend on Bmal1. We further demonstrated that selective depletion of LSCs following circadian perturbation is mediated through enhanced myeloid differentiation. ChIP-Seq studies revealed that the circadian rhythm network is integrally connected to the LSC self-renewal circuitry and highlighted putative Clock/Bmal1 targets in leukemia, providing a mechanistic basis for our findings. Second, we performed a functional and genomic characterization of our MLL-AF9 serial transplantation model to explore mechanisms of disease evolution and clonal selection in AML. Limiting dilution studies demonstrated that serial transplantation results in a reduction in disease latency, dramatic enrichment of leukemia-initiating cells (LIC), and reconfiguration of the LSC hierarchy. While mutations in known AML-associated genes were not linked to disease progression, RNA-sequencing (RNA-Seq) demonstrated that the increase in LIC frequency in serially transplanted leukemias is driven by changes in cell cycle and differentiation. In aggregate, these studies offer insights into the biological mechanisms regulating LSC self-renewal and disease evolution in AML.
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Cheung, Man-sze. „Characterization of Leukemic stem cells in acute myeloid Leukemia“. Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B40687582.

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17

Liu, Chenli, und 刘陈立. „Formation of novel biological patterns by controlling cell motility“. Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B46541913.

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The Best PhD Thesis in the Faculties of Dentistry, Engineering, Medicine and Science (University of Hong Kong), Li Ka Shing Prize,2010-11
published_or_final_version
Biochemistry
Doctoral
Doctor of Philosophy
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18

Lane, Alison Briana. „Campylobacter jejuni motility is regulated by co-culture with epithelial cells“. Online access for everyone, 2007. http://www.dissertations.wsu.edu/Thesis/Spring2007/a_lane_1050207.pdf.

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19

Ramsden, Amy Elizabeth. „Spatial Distribution and Motility of Salmonella- Containing Vacuoles within Host Cells“. Thesis, Imperial College London, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.506440.

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20

Yu, Xiao. „Study of the Motility of Biological Cells by Digital Holographic Microscopy“. Scholar Commons, 2014. https://scholarcommons.usf.edu/etd/5159.

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In this dissertation, I utilize digital holographic microscopy (DHM) to study the motility of biological cells. As an important feature of DHM, quantitative phase microscopy by digital holography (DH-QPM) is applied to study the cell-substrate interactions and migratory behavior of adhesive cells. The traction force exerted by biological cells is visualized as distortions in flexible substrata. Motile fibroblasts produce wrinkles when attached to a silicone rubber film. For the non-wrinkling elastic substrate polyacrylamide (PAA), surface deformation due to fibroblast adhesion and motility is visualized as tangential and vertical displacement. This surface deformation and the associated cellular traction forces are measured from phase profiles based on the degree of distortion. Intracellular fluctuations in amoeba cells are also analyzed statistically by DH-QPM. With the capacity of yielding quantitative measures directly, DH-QPM provides efficient and versatile means for quantitative analysis of cellular or intracellular motility. Three-dimensional profiling and tracking by DHM enable label-free and quantitative analysis of the characteristics and dynamic processes of objects, since DHM can record real-time data for micro-scale objects and produce a single hologram containing all the information about their three-dimensional structure. Here, I utilize DHM to visualize suspended microspheres and microfibers in three dimensions, and record the four-dimensional trajectories of free-swimming cells in the absence of mechanical focus adjustment. The displacement of microfibers due to interactions with cells in three spatial dimensions is measured as a function of time at sub-second and micrometer levels in a direct and straightforward manner. It has thus been shown that DHM is a highly efficient and versatile means for quantitative tracking and analysis of cell motility.
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21

Haylock, David Norman. „Ex vivo expansion of human haemopoietic progenitor cells“. Title page, abstract and contents only, 2001. http://web4.library.adelaide.edu.au/theses/09PH/09phh4181.pdf.

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"December 2001." Includes bibliographical references (leaves 178-225) Focuses on the ex vivo growth of human haemopoietic progenitor cells with the objective of defining culture conditions for generating myeloid post-progenitor cells for therapy
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22

Wang, Qiao. „Analysis of the role of invariant V[alpha]24+NKT cells in the pathogenesis of chronic lymphocytic leukaemia /“. [St. Lucia, Qld.], 2001. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe16185.pdf.

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23

Reed, Reiss. „Investigating the role of T-cells in chronic lymphocytic leukemia“. Thesis, Cardiff University, 2015. http://orca.cf.ac.uk/73613/.

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T-cells appear to have multiple conflicting roles in CLL. On the one hand tumour-specific T-cells could be used to deliver effective immunotherapy; on the other hand, certain T-cell populations may enhance CLL survival and disease progression. The aim of this thesis was to address these contradictory aspects and to provide a deeper understanding of the role of T-cells in CLL. Firstly, candidate peptides from the pro-apoptotic protein Bax were used to activate potential CLL specific T-cells from HLA-A2+ patients. A CD8+ T-cell clone (6C5) was isolated and it’s specificity was initially mapped to (Bax161-170; LLSYFGTPT) and(Bax160–170; GLLSYFGTPT). However, 6C5 failed to recognise HLA-A2+ CLL cells in vitro, and failed to recognise highly purified forms of the peptides. Further characterisation, involving mass spectrometry and HPLC, mapped T-cell specificity to a modified peptide (LLSY(3-tBu)FGTPT). A second strand of this project involved detailed phenotypic analysis of T-cells from CLL patients (n=97) in order to investigate the basis for immune dysfunction. This analysis indicated that patients with an inverted CD4:CD8 ratio (CLLIR), displayed a skewing towards a highly differentiated T-cell phenotype, as well as expression of markers associated with replicative senescence (CD57+, CD27-) within CD4+ and CD8+ T-cell compartments. In addition, CD4+ T-cells expressing markers associated with immunosuppression (PD-1+, TIM-3+) were also increased in CLLIR. Importantly, the inversion of the CD4:CD8 ratio was associated with shorter progression-free survival. Furthermore, the frequencies of distinct T-cell populations were also shown to haveprognostic impact in both univariate analysis (CD4+PD-1+, CD4+CD57+, CD8+CD57+ and CD8+CD27-) and multivariate analysis (CD4+CD27-PD-1+LAG-3+ and CD8+CD27- CD57+PD-1+). To further evaluate the differences between CLLIR and CLLNR patients, preliminary transcriptional analysis was performed, focusing on genes associated with T-cell function. By contrast, transcriptional analysis suggested that genes associated with activation rather than suppression were enriched in CLLIR.
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24

Matsubara, Yasushi. „Delineation of immunoregulatory properties of adult T cell leukemia cells“. Kyoto University, 2007. http://hdl.handle.net/2433/135653.

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25

Ansprenger, Christian [Verfasser], und Hannah-Mari [Akademischer Betreuer] Baldauf. „Studies on dendritic cells and "leukemia derived dendritic cells" in the treatment of acute myeloid leukemia and myelodysplastic syndrome / Christian Ansprenger ; Betreuer: Hannah-Mari Baldauf“. München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2021. http://d-nb.info/1238518605/34.

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26

Batista, José Miguel Sebastiao Fernandes. „FAM49 : a novel regulator of the protrusive behaviour and motility of cells“. Thesis, University of Glasgow, 2016. http://theses.gla.ac.uk/7690/.

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Most eukaryotic cell motility relies on plasma membrane protrusions, which depend on the actin cytoskeleton and its tight regulation. The SCAR/WAVE complex, a pentameric assembly comprising SCAR/WAVE, Nap1, CYFIP/Pir121, Abi and HSPC300, is a key driver of actin-based protrusions such as pseudopods. SCAR/WAVE is thought to activate the Arp2/3 complex, a crucial actin nucleator, after being itself activated by upstream signals such as active Rac1. Despite recent progress on the study of the SCAR/WAVE complex, its regulation is still incompletely understood, with Nap1’s role being particularly enigmatic. Upon screening for potential Nap1 binding partners in the social amoeba Dictyostelium discoideum – a well established model organism in the study of the actin cytoskeleton and cell motility – we found FAM49, a ~36 kDa protein of unknown function which is highly conserved in Metazoa (animals) and evolutionarily closer species such as D. discoideum. Interestingly, D. discoideum’s FAM49 and its homologs contain a DUF1394 domain, which is also predicted in CYFIP/Pir121 proteins and most likely involved in their direct binding to active Rac1, which in turn contributes to SCAR/WAVE’s activation. FAM49’s unknown role, apparent high degree of conservation and potential connections to SCAR/WAVE and Rac1 persuaded us to start investigating its function and biological relevance in D. discoideum, leading to the work presented in this thesis. Several pieces of our data collectively support a function for FAM49 in modulating the protrusive behaviour, and ultimately motility, of D. discoideum cells, as well as a regulatory link between FAM49 and Rac1. FAM49’s involvement in protrusion regulation was first hinted at by our observation that GFP-tagged FAM49 is enriched in pseudopods. The possibility of a link with Rac1 was then strengthened by two additional observations: first, pseudopodial GFP-FAM49 is substantially co-enriched with active Rac, both showing fairly comparable spatio-temporal accumulation dynamics; second, when dominant-active (G12V) Rac1 is expressed in cells, it triggers the recruitment and persistent accumulation of GFP-FAM49 at the plasma membrane, where both become highly co-enriched. We subsequently determined that fam49 KO cells differ from wild-type cells in the way they protrude and move, as assessed in under-agarose chemotaxis assays. In particular, our data indicate that fam49 KO cells tend to display a lower degree of global protrusive activity, their protrusions extend more slowly and are less discrete, and the cells end up moving at lower speeds and with higher directional persistence. This phenotype was substantially rescued by FAM49 re-expression. While re-expressing FAM49 in fam49 KO cells we generated putative FAM49 overexpressor cells; compared to wild-type cells, they displayed atypically thin pseudopods and what seemed to be an excessively dynamic, and perhaps less coordinated, protrusive behaviour. Additional data in our study suggest that pseudopods made by fam49 KO cells are still driven by SCAR/WAVE, which is clearly not being replaced by WASP (as is now known to be the case in D. discoideum cells lacking a functional SCAR/WAVE complex). Nonetheless, the peculiar dynamics of those pseudopods imply that SCAR/WAVE’s activity is regulated differently when FAM49 is lost, though it remains to be determined how. This thesis is the first report of a dedicated study on FAM49 and lays the foundation for future research on it.
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Tian, Jing. „Inhibition of melanoma cell motility by the snake venom disintegrin eristostatin“. Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 61 p, 2007. http://proquest.umi.com/pqdweb?did=1397900451&sid=10&Fmt=2&clientId=8331&RQT=309&VName=PQD.

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28

Chandran, Priya. „Bone Marrow Microenvironment in Acute Myleoid Leukemia“. Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/24301.

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Acute myeloid leukemia (AML) often remains refractory to current chemotherapy and transplantation approaches despite many advances in our understanding of mechanisms in leukemogenesis. The bone marrow “niche” or microenvironment, however, may be permissive to leukemia development and studying interactions between the microenvironment and leukemia cells may provide new insight for therapeutic advances. Mesenchymal stem cells (MSCs) are central to the development and maintenance of the bone marrow niche and have been shown to have important functional alterations derived from patients with different hematological disorders. The extent to which MSCs derived from AML patients are altered remains unclear. The aim of this study was to detect changes occurring in MSCs obtained from human bone marrow in patients with AML by comparing their function and gene expression pattern with normal age-matched controls. MSCs expanded from patients diagnosed with acute leukemia were observed to have heterogeneous morphological characteristics compared to the healthy controls. Immunohistochemistry and flow data confirmed the typical cell surface immunophenotype of CD90+ CD105+ CD73+ CD34- CD45-, although MSCs from two patients with AML revealed reduced surface expression of CD105 and CD90 antigens respectively. Differentiation assays demonstrated the potential of MSCs from AML patients and healthy donors to differentiate into bone, fat and cartilage. However, the ability of MSCs from AML samples to support hematopoietic function of CD34+ progenitors was found to be impaired while the key hematopoietic genes were found to be differentially expressed on AML-MSCs compared to nMSCs. These studies indicate that there exist differences in the biologic profile of MSCs from AML patients compared to MSCs derived from healthy donors. The results described in the thesis provide a formulation for additional studies that may allow us to identify new targets for improved treatment of AML.
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Imam, Hasan. „Effects of protein kinase inhibitors on chronic lymphocytic leukemia (CLL) cells“. Thesis, Linköpings universitet, Institutionen för klinisk och experimentell medicin, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-73883.

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B cell Chronic lymphocytic leukemia (B-CLL) is a neoplastic disorder characterized by accumulation of B lymphocytes due to uncontrolled growth and resistance to apoptosis. Src family kinases (SFKs) are non receptor tyrosine kinases present in the cytosol, which couple with downstream B cell receptor signaling and thus mediate growth, survival, proliferation and antiapoptosis. In CLL cells SFKs are remarkably overexpressed, especially Lyn kinase. This gives the rational to use SFKs inhibitor to treat CLL. Addition of the specific pharmacological inhibitors of SFKs, bosutinib and saracatinib, inhibited the global tyrosine phosphorylation as well as the basal auto-phosphorylation of SFKs. Mechanistically, inhibition of SFKs is coupled to apoptosis induction via decreased protein levels of the anti-apoptotic proteins Bcl-2, Mcl-1 and survivin, which were demonstrated by Western blotting. To assess apoptosis induction, annexin V binding to freshly isolated CLL cells with or without treatment with kinase inhibitors was measured flow cytometrically. Using the inhibitors at a concentration of 10 μM the average percentages of annexin V-positive, apoptotic cells in 11 CLL samples increased from 24 % in untreated controls to 55 %, 45 % and 37 % after treatment with bosutinib, saracatinib and dasatinib, respectively. The response to each of the inhibitors showed a high but comparable degree of variation among the investigated CLL samples. On the average bosutinib induced apoptosis with significantly higher efficiency than dasatinib, which calls for further investigation of its pre-clinical potential for treatment of CLL.
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Bento, Rui Pedro Garcia de Oliveira. „CAR-modified T cells targeted to CD19 antigen for lymphocytic leukemia“. Master's thesis, Universidade de Aveiro, 2014. http://hdl.handle.net/10773/13445.

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Mestrado em Biomedicina Farmacêutica
Cellular immunotherapies, or Advanced Therapy Medicinal Products (ATMPs), are emerging as novel and specific therapeutic approaches to treat diseases, such as certain types of leukemias, which are difficult or impossible to treat with today’s biopharmaceutical products. Breakthroughs in basic, preclinical, and clinical science spanning cellular immunology, and cellprocessing technologies has allowed clinical applications of chimeric antigen receptor–based therapies. A recent example is CTL019, a lentivirus-based gene therapy for autologous T cells, acquired by Novartis in 2012 through a global alliance with the University of Pennsylvania. Although this technology is still in its infancy, clinical trials have already shown clinically significant antitumor activity in chronic lymphocytic leukemia and acute lymphocytic leukemia. Trials targeting a variety of other adult and pediatric malignancies are under way. The potential to target essentially any tumor-associated cell-surface antigen for which a monoclonal antibody can be made opens up an entirely new arena for targeted therapy of cancer. The regulatory environment for these Advanced Therapies Medicinal Products is complex and in constant evolution. Many challenges lie ahead in terms of manufacturing process, non-conventional supply chain logistics, business models, intellectual property, funding and patient access.
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31

Merchand, Reyes Giovanna. „Targeting myeloid cells as a potential Chronic Lymphocytic Leukemia therapeutic strategy“. The Ohio State University, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=osu1595259890785332.

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32

Fortier, Hélène. „AFM Indentation Measurements and Viability Tests on Drug Treated Leukemia Cells“. Thesis, Université d'Ottawa / University of Ottawa, 2016. http://hdl.handle.net/10393/34345.

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A significant body of literature has reported strategies and techniques to assess the mechanical properties of biological samples such as proteins, cellular and tissue systems. Atomic force microscopy has been used to detect elasticity changes of cancer cells. However, only a few studies have provided a detailed and complete protocol of the experimental procedures and data analysis methods for non-adherent blood cancer cells. In this work, the elasticity of NB4 cells derived from acute promyelocytic leukemia (APL) was probed by AFM indentation measurements to investigate the effects of the disease on cellular biomechanics. Understanding how leukemia influences the nanomechanical properties of cells is expected to provide a better understanding of the cellular mechanisms associated to cancer, and promises to become a valuable new tool for cancer detection and staging. In this context, the quantification of the mechanical properties of APL cells requires a systematic and optimized approach for data collection and analysis, in order to generate reproducible and comparative data. This Thesis elucidates the automated data analysis process that integrates programming, force curve collection and analysis optimization to assess variations of cell elasticity in response to processing criteria. A processing algorithm was developed by using the IGOR Pro software to automatically analyze large numbers of AFM data sets in an efficient and accurate manner. In fact, since the analysis involves multiple steps that must be repeated for many individual cells, an automated and un-biased processing approach is essential to precisely determine cell elasticity. Different fitting models for extracting the Young’s modulus have been systematically applied to validate the process, and the best fitting criteria, such as the contact point location and indentation length, have been determined in order to obtain consistent results. The designed automated processing code described in this Thesis was used to correlate alterations in cellular biomechanics of cancer cells as they undergo drug treatments. In order to fully assess drug effects on NB4 cells, viability assays were first performed using Trypan Blue staining for primary insights before initiating thorough microplate fluorescence intensity readings using a LIVE/DEAD viability kit involving ethidium and calcein AM labelling components. From 0 to 24 h after treatment using 30 µM arsenic trioxide, relative live cell populations increased until 36 h. From 0 to 12 h post-treatment, relative populations of dead cells increased until 24 h post-treatment. Furthermore, a drastic drop in dead cell count has been observed between 12 and 24 h. Additionally, arsenic trioxide drug induced alterations in elasticity of NB4 cells can be correlated to the cell viability tests. With respect to cell mechanics, trapping of the non-adherent NB4 cells within fabricated SU8-10 microwell arrays, allowed consistent AFM indentation measurements up to 48 h after treatment. Results revealed an increase in cell elasticity up to 12 h post-treatment and a drastic decrease between 12 and 24 h. Furthermore, arsenic trioxide drug induced alterations in elasticity of NB4 cells can be correlated to the cell viability tests. In addition to these indentation and viability testing approaches, morphological appearances were monitored, in order to track the apoptosis process of the affected cells. Relationships found between viability and elasticity assays in conjunction with morphology alterations revealed distinguish stages of apoptosis throughout treatment. 24 h after initial treatment, most cells were observed to have burst or displayed obvious blebbing. These relations between different measurement methods may reveal a potential drug screening approach, for understanding specific physical and biological of drug effects on the cancer cells.
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Steward, W. P. „The structure of proteoglycans associated with normal and malignant cells“. Thesis, University of Manchester, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.234215.

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34

Fu, Xiongfei, und 傅雄飞. „Quantitative study of pattern formation on a density-dependent motility biological system“. Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B48199424.

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Quantitative biology is an emerging field that attracts intensive research interests. Pattern formation is a widely studied topic both in biology and physics. Scientists have been trying to figure out the basic principles behind the fascinating patterns in the nature. It’s still difficult to lift the complex veil on the underling mechanisms, especially in biology, although lots of the achievements have been achieved. The new developments in synthetic biology provide a different approach to study the natural systems, test the theories, and develop new ones. Biological systems have many unique features different from physics and chemistry, such as growth and active movement. In this project, a link between cell density and cell motility is established through cell-cell signaling. The genetic engineered Escherichia coli cell regulates its motility by sensing the local cell density. The regulation of cell motility by cell density leads to sequential and periodical stripe patterns when the cells grow and expand on a semi-solid agar plate. This synthetic stripe pattern formation system is quantitative studied by quantitative measurements, mathematical modeling and theoretical analysis. To characterize the stripe pattern, two novel methods have been developed to quantify the key parameters, including cell growth, spatiotemporal cell density profile and cell density-dependent motility, besides the standard molecular biological measurements. To better understand the underlying principle of the stripe pattern formation, a quantitative model is developed based on the experiments. The detailed dynamic process is studied by computer simulation. Besides, the model predicts that the number of stripes can be tuned by varying the parameters in the system. This has been tested by quantitatively modulation of the basal expression level of a single gene in the genetic circuit. Moreover, theoretical analysis of a simplified model provides us a clear picture of the stripe formation process. The steady state traveling wave solution is obtained, which leads to an analytic ansatz that can determine the phase boundary between the stripe and the no-stripe phases. This study does not only provide a quantitative understanding about the novel mechanism of stripe pattern formation, but also sets an good example of quantitative studies in biology. The techniques, methods and knowledge gleaned here may be applied in various interdisciplinary fields.
published_or_final_version
Physics
Doctoral
Doctor of Philosophy
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35

Lok, Chun-nam, und 陸振南. „Regulation of transferrin receptor expression in human leukemic HL-60 cells: gene expression and cellular signaling“. Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1996. http://hub.hku.hk/bib/B31235141.

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36

Lok, Chun-nam. „Regulation of transferrin receptor expression in human leukemic HL-60 cells : gene expression and cellular signaling /“. Hong Kong : University of Hong Kong, 1996. http://sunzi.lib.hku.hk/hkuto/record.jsp?B17310659.

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37

Seller, Zerrin. „Role of #alpha#4#beta#1-mediated signalling in malignant melanoma adhesion and motility“. Thesis, King's College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.266520.

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38

Chen, Helen Hong. „Finite element-based computer simulation of motility, sorting, and deformation in biological cells“. Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape17/PQDD_0012/NQ30595.pdf.

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39

Lewis, Ian D. „Characterisation of normal and leukaemic stem cells in chronic myeloid leukaemia /“. Title page, contents and abstract only, 1998. http://web4.library.adelaide.edu.au/theses/09PH/09phl6745.pdf.

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40

Chan, Shing, und 陳誠. „Generation and functional characterization of dendritic cells from bone marrow of patients with leukaemia diseases and various haemato-oncological conditions“. Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B31970394.

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41

Chan, Shing. „Generation and functional characterization of dendritic cells from bone marrow of patients with leukaemia diseases and various haemato-oncological conditions“. Hong Kong : University of Hong Kong, 2002. http://sunzi.lib.hku.hk/hkuto/record.jsp?B25176511.

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42

Zhu, Wen-hui, und 朱文輝. „Regulation of apotosis in human leukemic HL-60 cells: roles of caluium, protein kinase C and intacellular pH“. Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1995. http://hub.hku.hk/bib/B31235499.

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43

Zhu, Wen-hui. „Regulation of apotosis in human leukemic HL-60 cells : roles of caluium, protein kinase C and intacellular pH /“. Hong Kong : University of Hong Kong, 1995. http://sunzi.lib.hku.hk/hkuto/record.jsp?B16553226.

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44

Ehinger, Mats. „On the role of the tumor suppressor gene p53 in leukemic cell differentiation“. Lund : Lund University, 1997. http://catalog.hathitrust.org/api/volumes/oclc/68945098.html.

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45

Thompson, Bridget. „Murine acute myeloid leukemia cells expressing the cytosine deaminase gene induce protective immunity to parental leukemic cells“. Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape4/PQDD_0020/MQ54149.pdf.

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46

Emmanuelle, Sara Anouchka Supper. „Modification of Gene Expression, Proliferation, and Function of OP9 Stroma Cells by Bcr-Abl-Expressing Leukemia Cells“. Kyoto University, 2015. http://hdl.handle.net/2433/202804.

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47

Baran, Yusuf. „Multiple Drug Resistance Mechanisms In Imatinib Resistat Human Chronic Myeloid Leukemia Cells“. Phd thesis, METU, 2006. http://etd.lib.metu.edu.tr/upload/12607612/index.pdf.

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In this study, mechanisms of resistance to Imatinib-induced apoptosis in human K562 and Meg-1 chronic myeloid leukemia (CML) cells were examined. Continuous exposure of cells to step-wise increasing concentrations of Imatinib resulted in the selection of 0.2 and 1 &
#956
M imatinib resistant cells. Measurement of endogenous ceramide levels showed that treatment with Imatinib increased the generation of C18-ceramide significantly, which is mainly synthesized by the human longevity assurance gene 1 (hLASS1), in sensitive, but not in resistant cells. Mechanistically, analysis of mRNA and enzyme activity levels of hLASS1 in the absence or presence of Imatinib did not show any significant differences in the resistant cells when compared to its sensitive counterparts, suggesting that accumulation and/or metabolism, but not the synthesis of ceramide, might be altered in resistant cells. iv Indeed, further studies demonstrated that expression levels, and enzyme activity of sphingosine kinase-1 (SK-1), increased significantly in resistant K562 or Meg-1 cells. The expression levels of glucosyl ceramide synthase (GCS) also increased in resistant cells, comparing to the sensitive counterparts, which indicates conversion of pro-apoptotic ceramide to glucosyl ceramide. Expression analyses of BCR-ABL gene demonstrated that expression levels of BCR-ABL gene increased gradually as the cells acquired the resistance. However, Nucleotide sequence analyses of ABL kinase gene revealed that there was no mutation in Imatinib binding region of the gene in resistant cells. There was also an increase in expression levels of MDR1 gene in resistant cells, which transport the toxic substances outside of cells. In conclusion, these data show, for the first time, a role for endogenous ceramide synthesis via hLASS1 in Imatinib-induced apoptosis, and those alterations of the balance between the levels of ceramide and S1P. Mainly the overexpression of SK-1 seems to result in resistance to Imatinib in K562 cells. The cellular resistance may also result from conversion of ceramide to glucosyl ceramide, from overexpression of BCR-ABL and MDR1 genes but not due to mutations in Imatinib binding site of ABL kinase.
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Christiansson, Lisa. „Myeloid-Derived Suppressor Cells and Other Immune Escape Mechanisms in Chronic Leukemia“. Doctoral thesis, Uppsala universitet, Klinisk immunologi, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-197604.

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Chronic myeloid leukemia (CML) is characterized by the Philadelphia chromosome, a minute chromosome that leads to the creation of the fusion gene BCR/ABL and the transcription of the fusion protein BCR/ABL in transformed cells. The constitutively active tyrosine kinase BCR/ABL confers enhanced proliferation and survival on leukemic cells. CML has in only a few decades gone from being a disease with very bad prognosis to being a disease that can be effectively treated with oral tyrosine kinase inhibitors (TKIs). TKIs are drugs inhibiting BCR/ABL as well as other tyrosine kinases. In this thesis, the focus has been on the immune system of CML patients, on immune escape mechanisms present in untreated patients and on how these are affected by TKI therapy. We have found that newly diagnosed, untreated CML patients exert different kinds of immune escape mechanisms. Patients belonging to the Sokal high-risk group had higher levels of myeloid-derived suppressor cells (MDSCs) as well as high levels of the programmed death receptor 1 (PD-1)-expressing cytotoxic T cells compared to control subjects. Moreover, CML patients had higher levels of myeloid cells expressing the ligand for PD-1, PD-L1. CML patients as well as patients with B cell malignacies had high levels of soluble CD25 in blood plasma. In B cell malignacies, sCD25 was found to be released from T regulatory cells (Tregs). Treatment with the TKIs imatinib or dasatinib decreased the levels of MDSCs in peripheral blood. Tregs on the other hand increased during TKI therapy. The immunostimulatory molecule CD40 as well as NK cells increased during therapy, indicating an immunostimulatory effect of TKIs. When evaluating immune responses, multiplex techniques for quantification of proteins such as cytokines and chemokines are becoming increasingly popular. With these techniques a lot of information can be gained from a small sample volume and complex networks can be more easily studied than when using for example the singleplex ELISA. When comparing different multiplex platforms we found that the absolute protein concentration measured by one platform rarely correlated with the absolute concentration measured by another platform. However, relative quantification was better correlated.
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Ailles, Laurie Elizabeth. „Detection, characterization, and genetic modification of acute myeloid leukemia (AML) stem cells“. Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ38845.pdf.

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50

Cornforth, Terri Victoria. „Characterising the cell biology of leukemic stem cells in acute myeloid leukemia“. Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:654b2176-fd50-427e-86f2-74e928054bef.

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Acute Myeloid leukemia (AML) is an aggressive haematological malignancy that mainly affects the elderly. Relapse is common and is thought to be due to the presence of chemotherapy resistant leukemic stem cells (LSC). Within the CD34+ disease (>5% of the blast cells expressing CD34) , two subtypes have been identified; an LMPP/GMPlike expanded type and a MPP/CMP-like expanded type, the former is the most common, accounting for around 80% of CD34+ AML. Both the GMP-like and LMPPlike expanded populations show LSC activity. To improve our understanding of the disease and gain better insight in to how to develop treatments, the molecular basis of the disease needs to be investigated. I investigated miRNAs in the GMP/LMPP-like expanded AML. miRNAs are small non-coding RNAs involved in the regulation of mRNA. In recent years miRNAs have been shown to be implicated in many different diseases. To investigate the role miRNAs play in AML, miRNA expression was profiled in leukemic and normal bone marrow. Bioinformatic analysis was then used to examine the different miRNA expression profiles between normal and leukemic marrow. Our study showed that miRNAs are dysregulated in AML. miRNAs from the miR-17-92 and its paralogous cluster miR-106b-92 were amongst the miRNAs to be found down regulated in AML As had been seen previously at an mRNA level, on an miRNA level the LSC populations more closely resembled more mature progenitor populations than HSC and MPP populations, however the LSC populations did display an aberrant stem cell-like miRNA signature.
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