Dissertations / Theses on the topic 'AML acute myeloid leukaemia'
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Shah, Niraj Mayank. "The role of NRF2 in acute myeloid leukaemia (AML)." Thesis, University of Liverpool, 2018. http://livrepository.liverpool.ac.uk/3022789/.
Full textBajuaifer, Nada A. "Translational regulation of ABCB1 gene in acute myeloid leukaemia (AML)." Thesis, University of Nottingham, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.594594.
Full textJawad, Mays Safa Hadi. "Genetic susceptibility to radiation-induced acute myeloid leukaemia (r-AML)." Thesis, University of Leicester, 2006. http://hdl.handle.net/2381/30366.
Full textVlachou, T. "FUNCTIONAL AND GENETIC HETEROGENEITY IN ACUTE MYELOID LEUKAEMIA." Doctoral thesis, Università degli Studi di Milano, 2017. http://hdl.handle.net/2434/471776.
Full textGasiorowski, Robin. "CD300f As A Novel Therapeutic Antibody Target For Acute Myeloid Leukaemia." Thesis, The University of Sydney, 2017. http://hdl.handle.net/2123/17190.
Full textMarsico, Paolo. "The effects of targeted therapy on cell viability and apoptosis on CML and AML cell lines." Thesis, University of Chester, 2019. http://hdl.handle.net/10034/621798.
Full textBodini, M. "Genomics of treatment response in Acute Myeloid Leukemia." Doctoral thesis, Università degli Studi di Milano, 2017. http://hdl.handle.net/2434/469570.
Full textMALLARDO, MARIA. "DISSECTING THE ROLE OF THE CYTOPLASMIC MUTANT NUCLEOPHOSMIN IN ACUTE MYELOID LEUKAEMIA DEVELOPMENT." Doctoral thesis, Università degli Studi di Milano, 2014. http://hdl.handle.net/2434/234152.
Full textGILIOLI, DIEGO. "Dissecting the role of cellular senescence in acute myeloid leukaemia immune-surveillance and response to therapy." Doctoral thesis, Università Vita-Salute San Raffaele, 2022. http://hdl.handle.net/20.500.11768/133076.
Full textTzelepis, Konstantinos. "Identification of novel genetic vulnerabilities and therapeutic targets in acute myeloid leukaemia using CRISPR dropout screens." Thesis, University of Cambridge, 2017. https://www.repository.cam.ac.uk/handle/1810/271130.
Full textMortera, Blanco Teresa. "Development of an ex vivo three dimensional (3-D) model of acute myeloid leukaemia (AML)." Thesis, Imperial College London, 2008. http://hdl.handle.net/10044/1/4390.
Full textTraikov, Sofia. "Loss of heterozygosity in acute myeloid leukaemia with normal karyotype." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2009. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-25082.
Full textSaia, M. "GENOME-WIDE ANALYSIS OF TRANSCRIPTION FACTOR NETWORKS IN MYELOID DIFFERENTIATION AND ACUTE MYELOID LEUKAEMIA." Doctoral thesis, Università degli Studi di Milano, 2013. http://hdl.handle.net/2434/219072.
Full textWoodward, Eleanor. "The use of gene expression profiling to identify novel minimal residual disease markers (MRD) in acute myeloid leukaemia (AML)." Thesis, Cardiff University, 2010. http://orca.cf.ac.uk/55179/.
Full textForster, Victoria Jane. "AML1/ETO promotes a mutator phenotype in t(8;21) acute myeloid leukaemia." Thesis, University of Newcastle Upon Tyne, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.606731.
Full textMICHELOZZI, ILARIA MARINA. "The role of the bone marrow microenvironment in aplastic anaemia and acute myeloid leukaemia: from pathogenesis to chemoresistance." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2019. http://hdl.handle.net/10281/241079.
Full textThe haematopoietic stem cell (HSC) niche is formed by several cell types which contribute to the regulation of the haematopoiesis within the bone marrow (BM). In pathological conditions, alterations of the BM microenvironment have been reported, but it is still debated whether they are cause or consequence of the disease. Support to leukaemic cells, especially to leukaemic stem cells (LSC), at the expense of normal HSC and protection against chemotherapeutic agents characterise the malignant BM niche. Thus, in order to eradicate LSC, promising therapeutic strategies may consider the chemoprotection exerted by the BM microenvironment in addition to LSC intrinsic features of refractoriness to conventional therapies. In the first part of this PhD project, we investigated the role of mesenchymal stromal cells (MSC) in the pathogenesis of aplastic anaemia (AA). Patient-derived MSC (AA-MSC) were characterised in vitro and, especially, in vivo taking advantage of our recently described in vivo BM niche model, based on the subcutaneous implantation of cartilaginous pellets generated from MSC (Serafini et al., Stem Cell Research, 2014). AA-MSC did not exhibit morphological, phenotypical, proliferative and differentiation defects in vitro. Only a reduced clonogenic potential was observed. Most importantly, they were able to recreate a functional and complete BM niche in vivo, proving their unaltered ability to support haematopoiesis and excluding their involvement in AA pathogenesis. In the second part of this PhD project, we analysed the effects of L-asparaginase (ASNase) on acute myeloid leukaemia (AML) cells, especially on LSC, and the contribution of the microenvironment to chemoresistance. ASNase was equally effective against unfractionated AML cells and against CD34+CD38- and CD34+CD38+ LSC, while slightly affecting healthy haematopoietic cells. The action of the drug against AML primitive cells was confirmed by clonogenic assays and by experiments performed in LSC supportive culture conditions. However, the anti-leukaemic potential of ASNase could be in part counteracted by MSC, expressing asparagine synthetase, and by monocytes/macrophages and blasts themselves, expressing cathepsin B, generating a protective niche. Lastly, we tested a new conditioning regimen based on the addition of fludarabine to irradiation in SCID-beige mice, a poorly permissive strain for human engraftment. The administration of fludarabine after irradiation increased the levels of engraftment of a AML cell line, KG-1, as compared to irradiation only, and it allowed the engraftment in 50% of primary AML blasts transplanted, reproducing human leukaemic infiltration. Thus, we generated a novel AML xenograft model in which we would like to test promising therapeutic agents, as ASNase, and to study different features of the malignant BM niche.
Thomas, Karla Mari. "Interim analysis of Acute Myeloid Leukaemia treated on the Red Cross Children's Hospital Rx 2071 (adapted from the MRC AML 15 protocol)." Master's thesis, University of Cape Town, 2017. http://hdl.handle.net/11427/27378.
Full textThomas, Karla Mari. "Interim analysis of Acute Myeloid Leukaemia treated on the Red Cross Children's Hospital Rx 2071 (adapted from the MRC AML 15 protocol)." Master's thesis, University of Cape Town, 2002. http://hdl.handle.net/11427/27378.
Full textTinsley, S. P. "To establish the role of mutations in c-KIT tyrosine kinase in the pathogenesis and therapy of core-binding factor-related acute myeloid leukaemia (AML)." Thesis, University College London (University of London), 2014. http://discovery.ucl.ac.uk/1433249/.
Full textPyzer, Athalia Rachel. "Myeloid-derived suppressor cells in acute myeloid leukaemia." Thesis, Queen Mary, University of London, 2017. http://qmro.qmul.ac.uk/xmlui/handle/123456789/36704.
Full textKnapper, Steven. "FLT3 inhibitors in acute myeloid leukaemia." Thesis, University of Oxford, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.432548.
Full textSmith, Matthew Liam Walker. "Mutation profiling in acute myeloid leukaemia." Thesis, Queen Mary, University of London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.416112.
Full textAbadir, Edward. "Novel Targets in Acute Myeloid Leukaemia." Thesis, University of Sydney, 2020. https://hdl.handle.net/2123/23677.
Full textDakik, Hassan. "Caractérisation des NADPH oxydases et effet de leur inhibition dans les leucémies aigues myéloïdes." Thesis, Tours, 2017. http://www.theses.fr/2017TOUR3309.
Full text350,000 leukaemia are diagnosed each year worldwide. In acute myeloid leukaemia (AML), relapse remains a major problem and the oxidative metabolism might play a crucial role in the therapeutic response. Low level of reactive oxygen species (ROS) is associated with properties of leukemic stem cells and quiescence whereas higher level promotes leukoblasts proliferation. ROS homeostasis relies on a tightly regulated balance between the oxidant and antioxidant systems. Although the antioxidant system is extensively studied in AML, the oxidant system remains poorly documented. In this work we aimed to study the seven NADPH oxidases (NOX) complexes in 25 AML human cell lines and primary samples. NOX transcriptional and protein profiles are variable with a higher expression of NOX2 in cell lines belonging to mature differentiation stages. An equivalent level of enzymatic activity was observed across all the cell lines. To reveal the contribution of NOX to global ROS production in the cells, two NOX inhibitors, DPI and VAS3947, were then used. Although both inhibitors efficiently blocked NOX activity they unexpectedly triggered strong oxidative stress leading to reduced cell proliferation and strong apoptosis, DPI by increasing mitochondrial ROS while VAS3947 by increasing cytoplasmic ROS production. To highlight which of the subunits were involved and to understand the mechanisms, NOX2 and p22phox subunits were inhibited using shRNA strategy. These did not affect cell proliferation but revealed a compensation effect. Our data suggest that NOX inhibition might be potential therapeutic strategy by increasing oxidative stress in leukemic cells
Taussig, David. "Characterisation of acute myeloid leukaemia stem cells." Thesis, Queen Mary, University of London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.424766.
Full textOlwill, Shane. "Annexin II expression in acute myeloid leukaemia." Thesis, University of Ulster, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.274092.
Full textArmenteros-Monterroso, Elena. "Investigating reptin function in acute myeloid leukaemia." Thesis, University College London (University of London), 2017. http://discovery.ucl.ac.uk/10038392/.
Full textStringaris, Katherine. "Natural killer cells and acute myeloid leukaemia." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/18014.
Full textMannari, Deepak. "The genomics of acute myeloid leukaemia : an investigation into the molecular pathogenesis of acute myeloid leukaemia with t(8;21)." Thesis, Queen Mary, University of London, 2012. http://qmro.qmul.ac.uk/xmlui/handle/123456789/8822.
Full textNagura, Eiichi, Saburo Minami, Koichiro Nagata, Yoshihisa Morishita, Hideo Takeyama, Hiroshi Sao, Hisamitsu/ Suzuki, et al. "Acute myeloid leukemia in the elderly : 159 Nagoya case studies." Nagoya University School of Medicine, 1999. http://hdl.handle.net/2237/5348.
Full textMorgan, Rhys. "Role of γ-catenin in acute myeloid leukaemia." Thesis, Cardiff University, 2011. http://orca.cf.ac.uk/55145/.
Full textGreen, C. L. "Studies on CEBPA mutations in acute myeloid leukaemia." Thesis, University College London (University of London), 2012. http://discovery.ucl.ac.uk/1379542/.
Full textPutwain, Sarah Lucy. "The role of Sox4 in acute myeloid leukaemia." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648624.
Full textGrandage, V. L. "Investigation of aberrant signal transduction in acute myeloid leukaemia." Thesis, University College London (University of London), 2007. http://discovery.ucl.ac.uk/1445527/.
Full textIvey, Adam Stuart. "Molecular characterisation and tracking disease in acute myeloid leukaemia." Thesis, King's College London (University of London), 2016. https://kclpure.kcl.ac.uk/portal/en/theses/molecular-characterisation-and-tracking-disease-in-acute-myeloid-leukaemia(a3aac920-4bbe-4360-afbd-2bd1dbe5e738).html.
Full textLim, Seah-Hooi. "Immunotherapy and recombinant interleukin-2 in acute myeloid leukaemia." Thesis, University of Aberdeen, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.484307.
Full textLe, Dieu Helen Rifca. "Characterisation of T cell defects in acute myeloid leukaemia." Thesis, Queen Mary, University of London, 2009. http://qmro.qmul.ac.uk/xmlui/handle/123456789/561.
Full textEl-Sharkawi, D. "Studies to investigate epigenetic factors in acute myeloid leukaemia." Thesis, University College London (University of London), 2016. http://discovery.ucl.ac.uk/1528735/.
Full textNaiel, Abdulbasit. "Study of acute myeloid leukaemia with known chromosomal translocations." Thesis, Brunel University, 2014. http://bura.brunel.ac.uk/handle/2438/9303.
Full textRIBEIRO, Ana Rita Matias Rosa de Almeida. "Insights into Acute Myeloid Leukaemia metabolism using NMR Spectroscopy." Master's thesis, Instituto de Higiene e Medicina Tropical, 2017. http://hdl.handle.net/10362/22443.
Full textAcute Myeloid Leukemia (AML) is the second most diagnosed type of leukemia and the most common in adults. It is a haematological disorder characterized by the bone marrow and peripheral blood infiltration of clonal populations of abnormally differentiated and highly proliferative blasts. It is a very heterogenous disease, originating from a wide variety of haematopoietic lineages with a diverse genetic landscape.(2,3) One of the less typical presentations of AML involves lactic acidosis (the accumulation of lactate in the blood) which has been correlated with poor survival prognosis. (4) This condition is correlated with high rates of aerobic glycolysis, the “Warburg effect”, resulting in the production of lactate that is excreted to the microenvironment. Several studies have found that some cancer cells have can take up lactate and utilize it as a source for oxidative metabolism.(5,6) We studied the glucose and lactate metabolism of three different AML lineages (HL60, THP1 and HEL) through NMR spectroscopy. We also investigated the influence of VEGF (another key player in tumour microenvironment, known to be involved in tumour-related angiogenesis in AML) in these cell lines.(7) Our results showed that the promyelocytic and monocytic lines can rely on lactate to sustain their energy and biomass demands, utilizing it as substrate for the TCA cycle and oxidative phosphorylation. On the monocytic line we confirmed that glucose is mainly metabolized through glycolysis and pentose phosphate pathway. The erythroleukemic line was unable to sustain its metabolism on lactate consumption, being dependent on glucose to sustain the cells’ metabolism. VEGF seem to have a positive effect on the HL60 and THP1 lines, increasing glycolytic rates and promoting nucleotide production, which suggest that it may have a role in supporting the alternative metabolism exhibited by these cells. So, the three lineages of AML display very different metabolic plasticity, with some having adapted to take advantage of their environment, while others seeming unable to adjust. We also investigated how exposure to different microenvironments influences AML cell metabolism. The normal environment of AML is the bone marrow (BM), but the cells can spread and accumulate in other organs of the body, where they are required to adapt to a completely different environment. In some cases, AML can involve infiltration of the Central Nervous System, usually in the form of leptomeningeal disease.(1) We inoculated HEL cells into the brain and BM of mice and, through multivariate analysis of NMR data, were able to distinguish between the metabolic profiles of the cells exposed to the two environments. Our results showed that the HEL cell line is much better suited to survive in the BM microenvironment than in the brain microenvironment. In both microenvironments, there were gradual metabolic modifications as the result of increased exposure, indicating that cell metabolism is not static and is influenced by the characteristics of the surrounding microenvironment. In conclusion, we showed that understanding leukaemia metabolism and its interaction with the microenvironment is indispensable for disease characterization and can provide valuable insights into the biologic mechanisms that govern AML progression and survival.
Yu, N. "Identifying and targeting dormant cells in acute myeloid leukaemia." Thesis, University of Nottingham, 2016. http://eprints.nottingham.ac.uk/33679/.
Full textKrishnamurthy, Pramila. "Cellular and vaccination-based immunotherapy of acute myeloid leukaemia." Thesis, King's College London (University of London), 2014. http://kclpure.kcl.ac.uk/portal/en/theses/cellular-and-vaccinationbased-immunotherapy-of-acute-myeloid-leukaemia(ea5188b6-c807-4a99-8473-e99f55f19559).html.
Full textGilby, Daniel C. "Analysis of myeloid tumour suppressor genes in acute myeloid leukaemia and idiopathic myelofibrosis." Thesis, University of Sheffield, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.505559.
Full textChim, Chor-sang James. "Study of gene promoter methylation in acute promyelocytic leukaemia." Hong Kong : University of Hong Kong, 2002. http://sunzi.lib.hku.hk/hkuto/record.jsp?B25256725.
Full textWalsby, Elisabeth Jane. "Role of FUS (TLS) in differentiation in acute myeloid leukaemia." Thesis, Cardiff University, 2004. http://orca.cf.ac.uk/55540/.
Full textOwen, Carolyn Jane. "The Molecular Basis of Familial Myelodysplasia and Acute Myeloid Leukaemia." Thesis, University of London, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.517976.
Full textDarkhshan, Fatemeh. "Mapping of murine radiation-induced acute myeloid leukaemia susceptibility loci." Thesis, University of Reading, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367693.
Full textZhao, L. "Identify critical signalling pathways in MLL-rearranged acute myeloid leukaemia." Thesis, University College London (University of London), 2014. http://discovery.ucl.ac.uk/1432505/.
Full textMILOVANOVIC, SARA. "NON-GENETIC MECHANISMS OF CHEMORESISTANCE IN ACUTE MYELOID LEUKEMIA." Doctoral thesis, Università degli Studi di Milano, 2022. https://hdl.handle.net/2434/946408.
Full textMaher, John. "The role of ras in myeloid leukaemogenesis." Thesis, Imperial College London, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.283668.
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