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Relevant bibliographies by topics / Chronic myeloid leukaemia; Treatment / Dissertations / Theses

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Dissertations / Theses on the topic 'Chronic myeloid leukaemia; Treatment'

Author: Grafiati

Published: 4 June 2021

Last updated: 4 February 2022

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1

Chuah, Charles Thuan Heng. "Bisphosphonates in the treatment of Imatinib-resistant chronic myeloid leukaemia." Thesis, Imperial College London, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.429553.

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2

Van, Rhee Frits. "Detection and treatment of residual disease in Philadelphia positive leukaemias." Thesis, Imperial College London, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.285168.

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3

Deininger, Michael Werner Nikolaus. "STI571, a novel tyrosine kinase inhibitor : pre-clinical evaluation and application to identify downstream targets of BCR-ABL." Thesis, Imperial College London, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.325912.

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4

Rusakiewicz, Sylvie. "Development of epitope-based immunotherapy for the treatment of chronic myeloid leukaemia." Thesis, University College London (University of London), 2005. http://discovery.ucl.ac.uk/1446802/.

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Haematopoietic stem cell transplantation, one of the major treatments for Chronic Myeloid Leukaemia (CML), provides an allogeneic Graft-versus-Leukaemia (GvL) effect mediated by the donor T cells infused with the graft. The antigens recognized by these T cells are not yet identified. One candidate antigen is the CML specific BCR7ABL oncogene. The aim of this thesis is to investigate immunotherapeutic strategies for the treatment of CML targeted to BCR/ABL epitopes. We characterised BCR/ABL derived peptides that are naturally processed and presented on the surface of CML cells in the context of

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5

Mendes, Alexandrina Maria da Silva. "Evolution of treatment response to IMATINIB in patients diagnosed with chronic myeloid leukaemia." Dissertação, Instituto de Ciências Biomédicas Abel Salazar, 2008. http://hdl.handle.net/10216/20905.

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6

Mendes, Alexandrina Maria da Silva. "Evolution of treatment response to IMATINIB in patients diagnosed with chronic myeloid leukaemia." Master's thesis, Instituto de Ciências Biomédicas Abel Salazar, 2008. http://hdl.handle.net/10216/20905.

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7

Cheng, Man-ying, and 鄭文瑛. "Prescribing pattern of imatinib among chronic phase chronic myeloid leukaemia (CML) patients and its financial impact on Hong Kong." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/196548.

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Background: Chronic myeloid leukaemia (CML) is a haematological malignant disease involving haematopoietic stem cells. It is caused by a known reciprocal chromosomal t(9;22)(q34;q11) translocation, or known as Philadelphia chromosome. The translocation results in the formation of a chimeric BCR-ABL fusion gene. In the most recent guidelines published by NCCN and European LeukemiaNet in 2013, tyrosine kinase inhibitors (TKI) specifically inhibiting the Bcr-Abl tyrosine kinase, are the first-line therapy for patients with chronic phase CML. Imatinib is the oldest among the 3 TKI, and is the most

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8

Heaney, Nicholas Benjamin. "Proteasome inhibition in chronic myeloid leukaemia." Thesis, Connect to e-thesis, 2009. http://theses.gla.ac.uk/832/.

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Thesis (MD.) - University of Glasgow, 2009.<br>MD. thesis submitted to the Faculty of Medicine, Division of Cancer Sciences and Molecular Pathology, University of Glasgow, 2009. Includes bibliographical references. Print version also available.

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9

Cwynarski, Katherine Louise. "Targets for therapy of chronic myeloid leukaemia." Thesis, Imperial College London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.412517.

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10

Abu-Eisha, Hazem Mahmoud. "T-cell responses in chronic myeloid leukaemia." Thesis, University of Liverpool, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.421045.

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11

Khorashad, Sorouri. "New prognostic factors in chronic myeloid leukaemia." Thesis, Imperial College London, 2010. http://hdl.handle.net/10044/1/5626.

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The tyrosine kinase inhibitor imatinib mesylate (IM) has proved a major advance in the management of patients with chronic myeloid leukaemia (CML) but about 15% of patients do not achieve complete cytogenetic responses (CCyR) (primary resistance) and a further 15-20% of those who do achieve CCyR eventually lose their response (secondary resistance). The best characterised mechanism of resistance is the expansion of a Ph-positive clone bearing an amino-acid substitution in the BCR-ABL1 kinase domain (KD). We screened over 300 CML patients for KD mutations and demonstrated that detection of a mu

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12

Ibrahim, Amr Reda Ahmed El Bahy. "Prognostic factors in chronic myeloid leukaemia therapy." Thesis, Imperial College London, 2012. http://hdl.handle.net/10044/1/9509.

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Chronic myeloid leukaemia (CML) is a chronic myeloproliferative disease that is characterized by the presence of the BCR-ABL1 protein, with subsequent increased tyrosine kinase activity. The Introduction of imatinib and second generation tyrosine kinase inhibitors revolutionized CML therapy; however, prognostic factors that can predict disease outcome are still measured using scores that have been developed during the chemotherapy and IFN-α era. This raises the need for modern scores that match the current era. The EUTOS score that has been recently introduced by the ELN promised significant a

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13

O'Brien, Stephen Gerard. "Haemopoietic stem cell purging in chronic myeloid leukaemia." Thesis, Imperial College London, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300928.

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14

Butler, Paul Crispin. "Neutrophil function and adhesion in chronic myeloid leukaemia." Thesis, Nottingham Trent University, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.385309.

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15

Alabouh, Hanan A. "Targeting splice factor kinases in chronic myeloid leukaemia." Thesis, University of the West of England, Bristol, 2017. http://eprints.uwe.ac.uk/30825/.

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Alternative splicing of pre-mRNA is a ubiquitous and versatile mechanism controlling the expression of human genes. In humans, approximately 93% of multi-exonic genes are alternatively spliced, producing functionally distinct proteins. Dysregulation of alternative splicing results in the overexpression of the oncogene splice factor SRSF1, which has been implicated in various types of tumours. Initial research has shown that the alternatively spliced isoforms of vascular endothelial growth factor (VEGF) (pro- angiogenic) promotes tumorigenesis. VEGF is regulated through serine-arginine (SR)- sp

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16

Söderlund, Stina. "Clinical and Immunological Studies in Chronic Myeloid Leukaemia." Doctoral thesis, Uppsala universitet, Hematologi, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-324272.

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Chronic myeloid leukaemia (CML) is characterised by the constitutively active tyrosine kinase BCR-ABL. Standard treatment with tyrosine kinase inhibitors (TKI) in the chronic phase (CP) of CML conveys excellent long-term prognosis but is associated with side effects and costs. Treatment free remission (TFR) is possible in a proportion of patients discontinuing treatment after obtaining deep treatment responses but it is not fully known how to select the right patients for stopping attempts. Treatment of accelerated phase (AP) and blast crisis (BC) is more complicated and the prognosis more dis

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17

Gao, Ling Min. "Cytogenetic and molecular studies in chronic myeloid leukaemia." Thesis, Imperial College London, 1990. http://hdl.handle.net/10044/1/46311.

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18

Al-Jedai, Abdullah H. "Notch signalling in CD34+ cells in chronic myeloid leukaemia." Thesis, University of Manchester, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.495604.

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Notch signalling is critical for haemopoietic stem cell self-renewal and survival. Chronic Myeloid Leukaemia (CML) is a stem cell disease characterised by the presence of the Philadelphia (Ph) chromosome, and subsequent expression of the BCR-ABL oncogene. The well established role for Notch signalling in human T-cell acute lymphoblastic leukaemia (T-ALL) and the reported mteraction between Notch and ABL in different developmental contexts in DrosopMa raise the possibility that Notch signal ing may be dysregulated in CML. Therefore, this project aims to investigate whether Notch signalling is.a

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19

Wang, Lihui. "Molecular mechanisms of imatinib resistance in chronic myeloid leukaemia." Thesis, University of Liverpool, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.539518.

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20

Lucas, Claire Marie. "Biomarkers predictive of clinical outcome in chronic myeloid leukaemia." Thesis, University of Liverpool, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.569570.

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Imatinib has undoubtedly revolutionised the treatment of chronic myeloid leukaemia (CML) and hence has become first-line treatment. At the time of carrying out this work, the only data available on the efficacy of imatinib for newly diagnosed CML patients were from a single clinical trial, IRIS. In a complete population study in our geographical area, following two years of imatinib treatment, the complete cytogenetic response (CCR) rate w:£s only 51 %, which is considerably worse than IRIS. / Clinical decisions would be greatly facilitated if it was possible to accurately ! predict a patient'

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21

Drummond, Mark William. "Telomere dynamics and telomerase expression in chronic myeloid leukaemia." Thesis, University of Glasgow, 2003. http://theses.gla.ac.uk/41113/.

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INTRODUCTION: Chronic myeloid leukaemia (CML) is a clonal myeloproliferative disorder of the haemopoietic stem cell (HSC), with a variable clinical course. Chronic phase (CP) disease, typically of 4-5 years duration, progresses to accelerated (AP) and then blastic phase (BP), with the latter behaving as a particularly aggressive acute leukaemia of either myeloid (MBP) or lymphoid (LBP) lineage. Treatment is most successful when delivered in CP, and accurate prognostic indices are required to individualise treatment. Increased telomere shortening has been described during progression of CML, an

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22

Sears, Daniel. "Identification of PI3K/Akt targets in chronic myeloid leukaemia." Thesis, Imperial College London, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.505451.

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23

Essafi, Abdelkader. "Role of Fox03a in Chronic Myeloid Leukaemia (CML) Pathogenesis." Thesis, Imperial College London, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.487755.

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Chronic myeloid leukaemia (CML) is the neoplastic expansion of haematopoietic stem/progenitor cells caused by BCR-ABL, a constitutively active tyrosine kinase. CML progresses through three stages by the modulation of the proliferation, survival and differentiation of haematopoietic progenitor cells. This is reversed by the BCR-ABL specific inhibitor STI571 (Oleevec, Imatinib). BCR-ABL mediates its oncogenic activities through the activation of different pathways, most notably through the activation of the phosphoinositide 3-kinase (PI3K) / protein kinase B (PKB/AKT) pathway. The activation of

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24

Miller-Reynolds, Angela Rose-Marie. "Suicide gene therapy in murine models of chronic myeloid leukaemia." Thesis, Imperial College London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.412871.

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25

Chinswangwatanakul, Wimol. "Role of p16 in chronic myeloid leukaemia and normal haemopoiesis." Thesis, Imperial College London, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.313953.

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26

Lu, W. "Characterisation of CCN3 signalling pathway in Chronic Myeloid Leukaemia (CML)." Thesis, Queen's University Belfast, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.517404.

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27

Crossman, Lucy C. "Predictors of imatinib response in patients with chronic myeloid leukaemia." Thesis, University of Newcastle Upon Tyne, 2006. http://hdl.handle.net/10443/1012.

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The majority of patients with chronic myeloid leukaemia (CML) achieve a complete cytogenetic response (CCR) on imatinib. However, we cannot predict which patients will have a suboptimal response. We set out to investigate ways of predicting poor cytogenetic response to imatinib in patients with CML. We examined patients with CML for the possession of particular alleles of the rs2290573 and IL-I P +3953 polymorphisms because these polymorphisms had been linked with the rate of achievement of a major cytogenetic response (MCR). Following the discovery of a polymorphism (K247R) within the P-Ioop

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28

Watson, Fiona. "Neutrophil function and dysfunction in myelodysplasia and chronic myeloid leukaemia." Thesis, University of Liverpool, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240944.

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29

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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30

Grand, Frances Hector. "BCR-ABL positive and negative haemopoietic cells in chronic myeloid leukaemia." Thesis, Imperial College London, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.401488.

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31

Yong, Agnes Siew Mee. "Identification of genes responsible for the heterogeneity of chronic myeloid leukaemia." Thesis, Imperial College London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.413749.

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32

Lin, Feng. "Minimal residual disease after bone marrow transplantation for chronic myeloid leukaemia." Thesis, Imperial College London, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.285196.

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33

Zhou, Peixun. "Localisation, activity and targeting of Bcr-Abl in chronic myeloid leukaemia." Thesis, University of Glasgow, 2011. http://theses.gla.ac.uk/2749/.

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Chronic myeloid leukaemia (CML) is a myeloproliferative disease of stem cell origin. It is characterised by the Philadelphia chromosome and Bcr-Abl oncoprotein which is a constitutively activated tyrosine kinase that is causative in CML. Treatment of CML was revolutionized by tyrosine kinase inhibitors (TKIs) in the last decade. TKIs target Bcr-Abl and block its tyrosine kinase activity. Despite the success of TKI in eliminating differentiated CML cells, primitive quiescent CML stem cells still resist or persist with TKI treatment. In this study, several strategies have been investigated towar

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34

Karvela, Maria. "Investigation of autophagy as a survival factor for chronic myeloid leukaemia." Thesis, University of Glasgow, 2013. http://theses.gla.ac.uk/4271/.

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Tyrosine kinase inhibitors (TKIs) have revolutionised the treatment of chronic myeloid leukemia (CML), however, fail to cure the disease due to the persistence of a refractory fraction of stem/progenitor cells. Autophagy is a recycling mechanism utilised by the cell as a survival mechanism under stressful conditions, and its induction has been suggested to have a cytoprotective role in cancer cells. In this study we demonstrate that autophagy is triggered in CML upon TKI-mediated inhibition of BCR-ABL, and protects from cell death. In order to evaluate if specific autophagy inhibition enhances

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35

McDonald, E. "Cancerous inhibitor of protein phosphatase 2A (CIP2A) in chronic myeloid leukaemia." Thesis, University of Liverpool, 2015. http://livrepository.liverpool.ac.uk/3000532/.

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Chronic myeloid leukaemia (CML) is a myeloproliferative disorder arising in a haematopoietic stem cell (HSC) and defined by the presence of BCR-ABL1, a deregulated tyrosine kinase that drives numerous oncogenic signalling pathways. Current CML therapies are tyrosine kinase inhibitors (TKIs) that target the constitutive action of BCR-ABL1. However, resistance to TKIs remains a concern for a substantial proportion of CML patients and thus investigating the mechanisms underlying poor clinical response is of great importance. The tumour suppressor protein phosphatase 2A (PP2A) plays a crucial role

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36

de, Lavallade Hugues Francois. "Combined application of targeted therapy and immunotherapy in chronic myeloid leukaemia." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/14263.

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Combining vaccination against leukaemia-derived antigens and treatment with tyrosine kinase inhibitors (TKI) in chronic phase CML is potentially a promising strategy to eradicate a reservoir of TKI resistant leukaemic cells. Previous studies have documented conflicting effects of TKIs on the immune response. I aimed to determine the in vivo immunomodulatory effects of TKIs on T and B-cell immune responses to antigens in patients with CML on TKIs. I first demonstrated that that the B-cell response to H1N1 influenza vaccine was significantly better in patients with CML compared to patients with

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37

Patel, Hetal. "Investigation of multimolecular complexes and signalling in chronic myeloid leukaemia (CML)." Thesis, Imperial College London, 2008. http://hdl.handle.net/10044/1/7747.

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Chronic Myeloid Leukaemia (CML) arises as a consequence of the expression of a chimaeric fusion protein; p210BCR-ABL. Many publications report that p210BRR-ABL forms complexes with multiple cytoplasmic proteins which affect signalling pathways demonstrated in cell lines or transduced cells. This has been necessary because primary haemopoietic cell lysates contain a degradative activity which rapidly and permanently destroys p210BCR-ABL. We have identified that the degradative enzymes located in the cell lysosomes and have demonstrated substantial inhibition of the p210BCR-ABL-degradative activ

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38

Zhang, Ji Guang. "Molecular analysis of the BCR-ABL translocation in chronic myeloid leukaemia." Thesis, Imperial College London, 1997. http://hdl.handle.net/10044/1/11963.

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39

Chase, Andrew John. "Cytogenetic and molecular characterisation of chromosome 13 abnormalities in leukaemia." Thesis, Imperial College London, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.325910.

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40

Kabarowski, Janusz Henryk. "The mechanism of transformation by the BCR-ABL tyrosine kinase oncogene." Thesis, Institute of Cancer Research (University Of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.266577.

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41

Reid, Alistair Gordon. "Genomic heterogeneity in Philadelphia positive leukaemias." Thesis, Anglia Ruskin University, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.269108.

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42

Hui, Chung-Yee Rosaline. "Role and regulation of FOXO transcription factors in chronic myeloid leukaemia (CML)." Thesis, Imperial College London, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.444408.

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43

Daghistani, Mustafa. "Investigation of molecular heterogeneity and new prognostic biomarkers in chronic myeloid leukaemia." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/18677.

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In Chronic Myeloid Leukaemia (CML) tyrosine kinase inhibitor (TKI) therapy has greatly prolonged survival for patients in the chronic phase of CML and is effective also in patients in the accelerated blast phase. However, primary and secondary resistance to TKI remains a significant clinical challenge. Similarly, while a number of additional genetic lesions accompany transformation to the advanced phase, no change provides a method of prospectively distinguishing those patients who will progress rapidly to blast crisis from those whose disease pursues a relatively indolent course. The precise

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44

Roos, Cecilia. "Studies of leukotriene C4 synthase expression and regulation in chronic myeloid leukaemia /." Karlstad : Faculty of Technology and Science, Biomedical Science, Karlstads universitet, 2008. http://www.diva-portal.org/kau/abstract.xsql?dbid=1598.

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45

Roy, Swagata. "EVI1 isoform expression, knockdown and biological activity in chronic myeloid leukaemia (CML)." Thesis, Glasgow Caledonian University, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.547415.

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46

Mitchell, Rebecca. "Exploring BCR-ABL-independent mechanisms of TKI-resistance in chronic myeloid leukaemia." Thesis, University of Glasgow, 2017. http://theses.gla.ac.uk/7977/.

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As the prevalence of Chronic Myeloid Leukaemia (CML) grows, due to the therapeutic success of tyrosine kinase inhibitors (TKI), we are witnessing increased incidences of drug resistance. Some of these patients have failed all currently licensed TKIs and have no mutational changes in the kinase domain that may explain the cause of TKI resistance. This poses a major clinical challenge as there are currently no other drug treatment options available for these patients. Therefore, our aim was to identify and target alternative survival pathways against BCR-ABL in order to eradicate TKI-resistant c

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47

Francis, Sebastian. "Factors affecting the response to tyrosine kinase inhibitors in chronic myeloid leukaemia." Thesis, University of Liverpool, 2015. http://livrepository.liverpool.ac.uk/2050461/.

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Chronic myeloid leukaemia (CML) is a clonal stem cell disorder characterised by the Philadelphia chromosome. The treatment and outcomes of CML patients have improved with the introduction of tyrosine kinase inhibitors (TKI). Imatinib is associated with complete cytogenetic response (CCR) rate of 71% at 12 months, as documented by large phase 3 clinical trials. I carried out a large population study in the Merseyside, Cheshire and North Wales area, which showed a maximal CCR rate of 65% over 5 years of observation. This suggests there is a higher rate of imatinib failure in a general unselected

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48

Fowler, Rachael. "Studies of the Wnt/Beta-catenin signalling pathway in chronic myeloid leukaemia." Thesis, University of Liverpool, 2014. http://livrepository.liverpool.ac.uk/2007740/.

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The Wnt/β-catenin signalling pathway is involved in regulating cellular transcription of numerous target genes in chronic myeloid leukaemia (CML). A previous report using granulocyte-macrophage progenitors (GMPs) showed that elevated levels of unphosphorylated (active) β-catenin, alongside mis-splicing of glycogen synthase kinase 3β (GSK3β), correlated with disease progression. It was of interest to determine if using the more readily available peripheral blood mononuclear cells (MNCs) also showed any correlation with patient outcome when β-catenin and GSK3β were measured in this source materi

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49

Al-Mazedi, Maryam. "A therapeutic approach to chronic myeloid leukaemia using short hairpin RNA molecules." Thesis, King's College London (University of London), 2012. https://kclpure.kcl.ac.uk/portal/en/theses/a-therapeutic-approach-to-chronic-myeloid-leukaemia-using-short-hairpin-rna-molecules(185139fb-ed9b-46d7-a5a8-04532c44640b).html.

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Chronic myeloid leukaemia (CML) was one of the first cancers to be linked to a chromosomal abnormality, the Philadelphia chromosome. This chromosome results in a translocation between chromosomes 9 and 22, where the ABL gene on chromosome 9, a tyrosine kinase, is translocated to the BCR gene region on chromosome 22 giving rise to an abnormal BCR/ABL fusion gene. The resultant fusion gene has an abnormally upregulated tyrosine kinase activity that results in an increase in the proliferation of immature white blood cells, thus leading to the development of CML. There are several breakpoints that

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50

Johnson, Peter R. E. "The biology and treatment of acute myeloid leukaemia in elderly patients." Thesis, University of Aberdeen, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.306856.

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Acute myeloid leukaemia (AML) is predominantly a disease of the elderly; the median age is 64 years and almost 60% of cases are over 60 years old. Unfortunately however, the treatment of AML in elderly patients is generally unsatisfactory with significantly poorer remission rates and overall survival than in younger patients. We have designed a novel treatment regimen consisting of Mitozantrone and Cytosine Arabinoside specifically for elderly patients and have evaluated the regimen in 104 patients over 60 years old in the North West region. The complete remission rate was 58%, the median dura

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