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Rozprawy doktorskie na temat „Acute Leukaemia”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 25 lipca 2025

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1

Bomken, Simon Nicholas. "Investigating leukaemic propagation in childhood acute lymphoblastic leukaemia." Thesis, University of Newcastle Upon Tyne, 2013. http://hdl.handle.net/10443/1865.

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Childhood acute lymphoblastic leukaemia (ALL) does not possess a propagating cell hierarchy, at least as defined by B-cell precursor immunophenotype. Indeed, many, or even all, leukaemic blasts may have the potential to propagate the disease. This unusual characteristic mirrors the substantial capacity for clonal expansion demonstrated by fully differentiated normal lymphoid cells. This Fellowship aimed to investigate the genetic programmes underlying the propagation of acute lymphoblastic leukaemia. An initial candidate approach confirmed the expression of PIWIL2, a gene critical to the maint

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2

Bradbury, Dawn Ann. "Factors regulating the autocrine growth of leukaemic cells in acute myeloblastic leukaemia." Thesis, Nottingham Trent University, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.332817.

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Knapper, Steven. "FLT3 inhibitors in acute myeloid leukaemia." Thesis, University of Oxford, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.432548.

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4

Smith, 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.

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5

Quinn, M. F. "Homeobox gene expression in acute leukaemia." Thesis, Queen's University Belfast, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.398094.

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6

Abadir, Edward. "Novel Targets in Acute Myeloid Leukaemia." Thesis, University of Sydney, 2020. https://hdl.handle.net/2123/23677.

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Background: Antibody based immunotherapies have revolutionised the treatment of haematological malignancies. Despite recent advances in Acute Myeloid Leukaemia (AML) most patients still have poor outcomes. Current surface targets in AML are not ideal and ongoing work is required to examine new antigens for meaningful clinical outcomes. Hypothesis: CD302 and CD300f have inherent properties that make them promising potential targets in AML. Preclinical work will establish these antigens as suitable targets in AML for further study. Methods: We looked at the distribution of CD302 on AML and Haema

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7

Mannari, 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.

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Acute myeloid leukaemia is a clonal disorder characterised by recurrent chromosomal translocations. One of the commonest, is the t(8;21) which results in part of the AML1 gene being juxtaposed to most of the ETO gene with the resultant chimeric protein, AML1-ETO, acting predominantly as a transcriptional repressor. Despite the extensive literature available, the exact mechanism by which the chimeric protein results in AML has not been fully elucidated. By using exon arrays and high throughput sequencing as tools it was hoped to gain further insights into the molecular basis of this disease. Ge

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8

Swanepoel, Yolande. "A retrospective study of acute lymphoblastic leukaemia in Paediatric patients at Dr George Mukhari Hospital (2003-2007)." Thesis, University of Limpopo (Medunsa Campus), 2008. http://hdl.handle.net/10386/262.

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Thesis (M Med(Haematology))-- University of Limpopo (Medunsa Campus), 2008.<br>Introduction: ALL (Acute Lymphoblastic Leukaemia) is the most common leukaemia in childhood. The two most important features predictive of outcome are age and presenting WBC at diagnosis. NCI risk criteria are applied to all children with precursor B-ALL, dividing them into NCI “high risk” (age < 1 year and ≥ 10 yrs, WBC > 50 x 10 9/ ) and NCI “standard risk” (age ≥ 1 year and < 10 yrs, WBC < 50 x 10 9/ ). Gender, immunophenotyping and genetic studies are other features that have been shown to be associated with

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9

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.

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10

Cartwright, Cher Suzanne. "Thiopurine Metabolism in Childhood Acute Lymphoblastic Leukaemia." Thesis, University of Sheffield, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.500442.

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11

Olwill, Shane. "Annexin II expression in acute myeloid leukaemia." Thesis, University of Ulster, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.274092.

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12

Armenteros-Monterroso, Elena. "Investigating reptin function in acute myeloid leukaemia." Thesis, University College London (University of London), 2017. http://discovery.ucl.ac.uk/10038392/.

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Acute myeloid leukaemia (AML) is a disease characterized by the clonal expansion of immature white blood cells, which show increased proliferation, self-renewal and a block of differentiation. Despite recent advances in therapy, AML still causes over half of all leukaemia related paediatric deaths, as cytogenetically defined subgroups with poor prognosis are still prevalent. Chromosomal translocations, which encode abnormal fusion proteins, are common in patients with AML, and the MLL (Mixed Lineage Leukaemia) locus is the most frequently rearranged in paediatric AML. Previous studies in our l

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13

Stringaris, Katherine. "Natural killer cells and acute myeloid leukaemia." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/18014.

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Despite successful induction chemotherapy, most patients with acute myeloid leukemia (AML) will relapse. Immune surveillance by T cells or natural killer (NK) cells may play a role in preventing relapse. This thesis examines the potential of NK cells to control AML. Study 1 explored in 248 patients with haematological malignancies from the US National Institutes of Health, the genetic diversity of NK killer immunoglobulin receptor (KIR) genes in patients and their stem cell donors and their impact on outcome after stem cell transplantation (SCT) for haematological malignancy. Individuals with

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14

Dokal, Arran D. "Investigating the heterogeneity of leukaemia kinase networks and the impact of the microenvironment on leukaemic cell signalling." Thesis, Queen Mary, University of London, 2018. http://qmro.qmul.ac.uk/xmlui/handle/123456789/36218.

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The tumour microenvironment plays a key role in tumour progression. In this thesis acute myeloid leukaemia (AML) was used as a model system to investigate the interplay between stromal and cancer cells. AML is a heterogeneous clonal disorder of haematopoietic undifferentiated progenitor cells or 'blast cells', which accumulate in the bone marrow and lead to the reduced output of crucial haematopoietic elements. Due to its heterogeneity (at least in part), treatment of the disease has not witnessed great innovation in the past 30 years. The bone marrow microenvironment (BMM) has a key role in t

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15

Carapeti, Melina. "Identification of acquired genetic changes in acute leukaemia." Thesis, Imperial College London, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287882.

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16

Morgan, Rhys. "Role of γ-catenin in acute myeloid leukaemia". Thesis, Cardiff University, 2011. http://orca.cf.ac.uk/55145/.

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Acute myeloid leukaemia (AML) is a heterogeneous clonal disorder of haematopoietic cells that primarily affects the elderly. Previously, our laboratory identified y-catenin as significantly overexpressed in AML. y-Catenin shares close structural and functional homology with the more intensively studied /3-catenin. Both catenins have dual roles in cell adhesion complexes and in transcription. Their transcriptional role is regulated by Wnt signalling which is critical for normal development and is one of the most frequently dysregulated processes in AML. In spite of this, little is known regardi

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17

Elmantaser, Musab Elmabrouk M. "Bone health in children with acute lymphoblastic leukaemia." Thesis, University of Glasgow, 2013. http://theses.gla.ac.uk/4447/.

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In chapter 1, bone structure, bone growth and development, osteoporosis in children and skeletal morbidities in children with acute lymphoblastic leukaemia (ALL) are discussed. After that, the mechanostat and the effect of whole body vibration (WBV) on bone health are considered. Finally, I examine diagnostic approaches to assess the musculoskeletal system. In chapter 2, the incidence and risk factors for skeletal morbidity in ALL children are determined. The medical records of all (n,186, male,110) children presenting with ALL between 1997 and 2007 and treated on UKALL97, UKALL97/01 or UKALL2

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18

Wilson, Kerrie Lauren. "Malignant stem cells in childhood acute lymphoblastic leukaemia." Thesis, University of Newcastle Upon Tyne, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.525030.

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19

Brown, Nicola Jane Marie. "Inactivation of P21(WAF1/CIP1) in acute leukaemia." Thesis, University of Newcastle Upon Tyne, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.446232.

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20

Sorour, Amani Fouad Abdel Halim. "Chromosome 6q16-21 deletions in acute lymphoblastic leukaemia." Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.399158.

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21

Pyzer, 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.

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The tumour microenvironment consists of an immunosuppressive niche created by the complex interactions between cancer cells and surrounding stromal cells. A critical component of this environment are myeloid-derived suppressor cells (MDSCs), a heterogeneous group of immature myeloid cells arrested at different stages of differentiation and expanded in response to a variety of tumour factors. MDSCs exert diverse effects in modulating the interactions between immune effector cells and malignant cells. An increased presence of MDSCs is associated with tumour progression, poorer outcomes, and decr

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22

Green, C. L. "Studies on CEBPA mutations in acute myeloid leukaemia." Thesis, University College London (University of London), 2012. http://discovery.ucl.ac.uk/1379542/.

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Acute myeloid leukaemia (AML) is a highly heterogeneous disease with regard to clinical outcome, and molecular markers with prognostic impact can be used to stratify patients for risk-adapted therapy. CEBPA mutations have been associated with a favourable prognosis, however several questions remained, in particular whether one (CEBPA-single) or two (CEBPA-double) mutations were necessary for this benefit, and their interaction with other molecular markers. A method of detecting CEBPA mutations in patient samples using denaturing HPLC was developed and the CEBPA status of 1427 young adult AML p

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23

Putwain, 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.

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24

Mangolini, M. "Oncogenic signalling in t(12;21) Acute Lymphoblastic Leukaemia." Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1415780/.

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The t(12;21)(p13;q22) translocation is present in up to 25% of children with pre-B cell Acute Lymphoblastic Leukaemia (ALL). This translocation involves two transcription factors, TEL (ETV6) and AML (RUNX1), both of which have crucial roles in regulating haematopoiesis. Clinically, TEL-AML1 positive patients have good prognoses. However, late relapses, additional genetic lesions affecting prognosis, and long-term side-effects of chemotherapy remain a cause for concern. In light of recent studies showing genetic and functional heterogeneities in cells responsible for cancer clone maintenance an

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25

Jackson, Rosanna Katherine. "Personalisation of dexamethasone in childhood acute lymphoblastic leukaemia." Thesis, University of Newcastle upon Tyne, 2017. http://hdl.handle.net/10443/3940.

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Dexamethasone (dex) is a key treatment for childhood acute lymphoblastic leukaemia (ALL), but is associated with significant variability in terms of toxicity and efficacy. In this project, the following variables were assessed to better understand how dex personalisation may be achieved: pharmacokinetics, intracellular dex accumulation, glucocorticoid receptor (GR) posttranslational modifications and B-cell maturation state. For pharmacokinetic studies, samples were collected from 154 patients randomised to short (10mg/m2 x 14 days) or standard (6mg/m2 x 28 days) dex induction therapy, as part

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26

Vlachou, T. "FUNCTIONAL AND GENETIC HETEROGENEITY IN ACUTE MYELOID LEUKAEMIA." Doctoral thesis, Università degli Studi di Milano, 2017. http://hdl.handle.net/2434/471776.

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Acute myeloid leukaemia (AML) is the most frequent leukaemia in adults, and still represents a disease with an unmet medical need, with 50-60% of patients relapsing within 3 years after diagnosis. AMLs are characterised by a high degree of intra-tumour heterogeneity, both at the biological and the genetic level, which is critical for tumour maintenance and response to treatments. Biologically, AMLs are organised hierarchically, with rare stem-like cells (leukaemia stem cells, LSCs) endowed with the unique properties of self-renewal and differentiation. Genetically, AMLs harbour patient-specifi

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27

Austin, Stephen J. "The prognostic significance of the mixed lineage leukaemia partial tandem duplication in acute myeloid leukaemia." Thesis, Cardiff University, 2010. http://orca.cf.ac.uk/54154/.

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This study concerns a specific molecular genetic mutation, the mixed lineage leukaemia partial tandem duplication ( MLL PTD). MLL is a transcriptional regulator that known to be instrumental in both normal haematopoiesis and in leukaemogenesis. This study aimed to evaluate the prognostic importance of this abnormality through investigation of its influence on clinical outcome, its utility as a marker of minimal residual disease (MRD) and the downstream effects of its expression. A qualitative PCR assay was established and determined the frequency of MLL PTD to be 5.2% in <italic>de novo</itali

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28

Hussey, Damian J. "An investigation of the (4;11)(q21;p15) translocation in acute lymphocytic leukaemia /." Title page, contents and abstract only, 2000. http://web4.library.adelaide.edu.au/theses/09PH/09phh9725.pdf.

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Thesis (Ph.D.) -- University of Adelaide, Dept. of Medicine, 2000.<br>Copies of author's previously published articles inserted. Errata pasted onto verso of back end-paper. Bibliography: leaves 163-189.

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29

Chim, 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.

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30

Evans, Jane P. M. "Tyrosine protein kinases and their substrates in acute and chronic leukaemias and their leukaemia cell lines." Thesis, University of Oxford, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.235871.

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31

Grandage, 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/.

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Haematopoiesis is the result of tightly regulated signal transduction pathways mediated by cytokines and their receptors. Aberrations in these pathways are an underlying cause for diseases such as leukaemia and other myeloproliferative and lymphoproliferative disorders. The PI3-Kinase/Akt pathway is central to regulation of cell survival and proliferation. This study found that the PI3-Kinase pathway is activated in AML cells. This activation was reduced or abolished when the cells were incubated with the PI3-Kinase inhibitor, LY294002. Leukaemic cell survival appeared to be dependent on PI3-K

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32

Ivey, 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.

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Acute myeloid leukaemia (AML) is a highly heterogeneous disease in terms of genetics and at the clonal level. Despite improved understanding of the genetic landscape of AML, pathogenesis and cause of disease relapse remain poorly understood. To address these issues exome sequencing was carried out on 25 diagnostic and 12 relapse samples from 28 cytogenetic standard risk AML patients. More than 500 somatic mutations were identified, including recognised recurrent mutations, and novel variants with driver potential. Copy number variations were also investigated, identifying loss of heterozygosit

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33

Rehe, Klaus. "Diversity of cancer stem cells in acute lymphoblastic leukaemia." Thesis, University of Newcastle Upon Tyne, 2012. http://hdl.handle.net/10443/1777.

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For many cancers research led to controversial results regarding frequency and identity of cancer stem cells, cells that self-renew and are able to reconstitute the full phenotype of the original malignancy. In some malignancies such as acute myeloid leukaemia the hierarchical stem cell model that suggests that only rare and immunophenotypically immature blasts exhibit stem cell characteristics, resembling the normal physiological haematopoietic hierarchy, has been well established. In contrast to that, the stochastic model states that all or at least a substantial proportion of malignant cell

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34

Lim, 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.

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In this study 12 acute myeloid leukaemia (AML) patients (3 in 1<SUP>st</SUP> complete remission (CR), 3 in 2<SUP>nd</SUP> CR, 3 in early relapse or partial remission and 3 in frank relapse) were treated with continuous infusion of recombinant Interleukin-2 (rIL-2). Adverse reactions among these patients were common. In all patients, there were evidence of lymphocyte activation with subsequent upregulation of the cellular cytotoxic functions following the infusion of rIL-2. Despite this, clinical response among patients treated with active disease remains disappointing, with only 1 patient achi

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35

Aldhafiri, Fahad Khalid. "Weight status during and after childhood acute lymphoblastic leukaemia." Thesis, University of Glasgow, 2013. http://theses.gla.ac.uk/4500/.

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Background: This thesis sits within the arena of weight status during and after childhood acute lymphoblastic leukaemia (ALL), with a particular focus on the prevalence of unhealthy weight status amongst (ALL), Saudi and UK populations. Each chapter in the thesis explores different aspects of unhealthy weight status in ALL which had been highlighted as gaps in the literature at a conference in Puebla, Mexico, at the end of 2006. A summary of each study is given below. Study 1: Background: This study estimated prevalence of unhealthy weight status and metabolic syndrome (MS) amongst Saudi survi

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36

Chim, Chor-sang James, and 詹楚生. "Study of gene promoter methylation in acute promyelocytic leukaemia." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B25256725.

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卓大治 and Tai-chi Cheuk. "Childhood acute lymphoblastic leukaemia with TEL-AML1 gene fusion." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31969690.

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38

Kozlowski, Ryszard E. "Aspects of blast cell proliferation in acute myeloblastic leukaemia." Thesis, Nottingham Trent University, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.293853.

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39

Sulong, Sarina. "Determination of allelic imbalance in childhood acute lymphoblastic leukaemia." Thesis, University of Newcastle Upon Tyne, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.445581.

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40

Le, 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.

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Understanding the immune system in patients with cancer and how it interacts with malignant cells is critical for the development of successful immunotherapeutic strategies at a time when novel cancer treatment approaches are required. Acute myeloid leukaemia (AML) results in widespread interaction between the malignant cells and T cells and as such, offers an opportunity to study these interactions. A flow cytometric analysis of T cells in the peripheral blood of patients presenting with AML illustrated that the absolute number of T cells is increased in AML compared with healthy controls. Fu

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41

Sundaresh, A. "Aberrant transcriptional pathways in t(12;21) Acute Lymphoblastic Leukaemia." Thesis, University College London (University of London), 2016. http://discovery.ucl.ac.uk/1522624/.

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The single most frequent chromosomal translocation associated with childhood Acute Lymphoblastic Leukaemia is the t(12;21) rearrangement, that creates a fusion gene between TEL (ETV6) and AML1 (RUNX1). Although TELAML1+ patients have a very good prognosis, relapses occur in up to 20% of cases and many patients face long-term side effects of chemotherapy. Our laboratory has previously shown that TEL-AML1 regulates Signal Transducer and Activator of Transcription 3 (STAT3) activation, which is critical for survival of the leukaemic cells. In this study, inhibition of STAT3 in TEL-AML1+ cells res

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42

El-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/.

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Acute myeloid leukaemia (AML) is a heterogeneous disease with numerous recurrent cytogenetic and molecular abnormalities. This heterogeneity is reflected in the variation in clinical outcome seen in patients. This disparity in outcome is also seen within groups of patients who have the same mutation or no known molecular abnormalities. To investigate whether the DNA methylation profile of samples can provide prognostic information, the methylome of forty cytogenetically normal AML samples that were wild-type for NPM1 and FLT3 was analysed, 20 were from patients with chemosensitive disease and

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43

Shah, Niraj Mayank. "The role of NRF2 in acute myeloid leukaemia (AML)." Thesis, University of Liverpool, 2018. http://livrepository.liverpool.ac.uk/3022789/.

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Acute Myeloid Leukaemia refers to the excess proliferation of myeloid progenitor cells. Whilst the 5-year survival rate is 40% in younger patients, this falls to 5% in patients over 65 and resistance to front-line chemotherapy agents remain a problem. We previously identified NRF2, a regulator of anti-oxidant genes, to be constitutively activated in AML and this correlated with resistance to chemotherapy. Recent studies have also suggested NRF2 also plays a more oncogenic role. To further understand NRF2's role in both chemotherapy resistance and oncogenesis we looked at its ability to regulat

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44

Oram, Sarah Helen. "Cis-regulation of LM02 in T-acute lymphoblastic leukaemia." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609663.

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45

Mansour, M. R. "Role of the Notch signalling pathway in acute leukaemia." Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1420122/.

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The Notch signalling pathway is important in development and differentiation of a diverse range of both embryonic and adult tissues. There is now strong evidence implicating aberrant Notch signalling in the pathogenesis of T-cell acute lymphoblastic leukaemia (T-ALL), with over 50% of paediatric patients having activating mutations in NOTCH-1. This thesis aims to explore several aspects of the Notch pathway in both T-ALL and acute myeloid leukaemia (AML). Chapter one summarises the published data on the Notch signalling pathway itself, addressing the basic understanding of Notch activation thr

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46

Naiel, Abdulbasit. "Study of acute myeloid leukaemia with known chromosomal translocations." Thesis, Brunel University, 2014. http://bura.brunel.ac.uk/handle/2438/9303.

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Acute myeloid leukaemia (“AML”) is a clonal disease characterised by increased, uncontrolled abnormal white blood cells and the accumulation of leukaemia immature cells in the bone marrow and bloodstream. Chromosomal rearrangements have been detected in almost half of AML cases. It has been proven that the chromosomal rearrangements constitute a marker for the diagnosis and prognosis of AML and have therapeutic consequences. The discovery of these rearrangements has led to a new World Health Organization (“WHO”) classification system. However, small regions of cryptic chromosomal rearrangement

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47

Ede, Benjamin Christopher. "Improving therapies for childhood T cell acute lymphoblastic leukaemia." Thesis, University of Bristol, 2017. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.752757.

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48

RIBEIRO, 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.

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A Leucemia Mielóide Aguda (LMA) é o segundo tipo de leucemia mais diagnosticado e o mais comum entre adultos. É uma condição hematológica caracterizada pela infiltração da medula óssea e do sangue por populações clonais de células mielóides imaturas, anormalmente diferenciadas e altamente proliferativas. É uma doença muito heterogénea, originando-se a partir de uma grande variedade de linhagens hematopoiéticas, com perfis genéticos distintos.(2,3) Uma das apresentações menos comuns desta doença é a acidose láctica (acumulação de lactato no sangue), relacionada com um mau prognóstico de sob

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Yu, N. "Identifying and targeting dormant cells in acute myeloid leukaemia." Thesis, University of Nottingham, 2016. http://eprints.nottingham.ac.uk/33679/.

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Relapse in AML is thought to arise from dormant leukaemic cells that are characterised by low RNA synthesis activity, protected by the bone marrow (BM) niche, and may evade the effects of chemotherapeutic drugs. Our aim was to investigate agents which might be able to overcome chemoprotection by targeting the intrinsic apoptosis pathway. We developed in vitro assays to identify and characterise the dormant AML cells using combinations of markers, including the cell-division marker PKH26, leukaemia-associated phenotypes (LAPs), and dormancy markers. In a dormancy model based on 12-day AML/strom

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Robinson, Hazel M. "Acquired abnormalities of chromosome 21 in acute lymphoblastic leukaemia." Thesis, University of Southampton, 2008. https://eprints.soton.ac.uk/161483/.

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The intrachromosomal amplification of chromosome 21 (iAMP21) was identified as a novel and prognositically important acquired chromosomal abnormality in childhood acute lymphoblastic leukaemia (ALL). It is defined by multiple copies of the RUNX1 gene, as seen by fluorescence in situ hybridisation (FISH), localised to a single abnormal duplicated chromosome 21 [dup(21)]. The morphological form of this chromosome is highly variable between patients and currently the only reliable method of detection is FISH with probes to RUNX1. Studies of 48 iAMP21 patients using detailed FISH techniques and ar

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