Spelling suggestions: "subject:": leukemia"" "subject:": eukemia""
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Understanding the function of the Mll-een leukaemic fusion gene by embryonic stem cell approaches江卓庭, Kong, Cheuk-ting. January 2003 (has links)
published_or_final_version / Biochemistry / Doctoral / Doctor of Philosophy
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Studies of Mll-Een fusion gene in a conditional mouse model of human leukemia曾漢文, Tsang, Hon-man. January 2007 (has links)
published_or_final_version / abstract / Pathology / Master / Master of Philosophy
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Cellular and molecular mechanisms of dendritic cell differentiation from cells of leukaemic originSun, Qian, 孫倩 January 2007 (has links)
published_or_final_version / abstract / Pathology / Doctoral / Doctor of Philosophy
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The effect of microtubule targeting chemotherapeutic agents on bone marrow derived mesenchymal stromal cells and its interaction withacute lymphoblastic leukemia blastsFung, Kwong-lam., 馮廣林. January 2009 (has links)
published_or_final_version / Paediatrics and Adolescent Medicine / Master / Master of Philosophy
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AN EXPLORATION OF PERCEPTIONS OF PAIN IN CHILDREN WITH LEUKEMIA.Strosnider, Deborah Vivian, 1958- January 1986 (has links)
No description available.
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Mapping of murine radiation-induced acute myeloid leukaemia susceptibility lociDarkhshan, Fatemeh January 2001 (has links)
No description available.
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Genetic analyses of radiation-induced leukaemias/lymphomasCleary, Helen Julia January 2000 (has links)
No description available.
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The Role of ATM in Promoting Normal T cell Development and Preventing T Cell LeukemogenesisMatei, Irina 24 September 2009 (has links)
The immune system recognizes and eliminates an enormous array of pathogens due to the diverse antigen receptor repertoire of T and B lymphocytes. However, the development of lymphocytes bearing receptors with unique specificities requires the generation of programmed double strand breaks (DSB) coupled with bursts of proliferation, rendering lymphocytes susceptible to mutations and oncogenic transformation. Thus, mechanisms responsible for monitoring global genomic integrity, such as those coordinated by the ATM (ataxia-telangiectasia mutated) kinase, must be activated during lymphocyte development to limit the oncogenic potential of antigen receptor locus recombination. I show that ATM deficiency compromises TCRα recombination and the post-mitotic survival of T-cell receptor αβ (TCRαβ+) CD4+CD8+ (DP) thymocytes, providing a molecular and developmental basis for the immunodeficiency characteristic of ATM loss. Moreover, I show that in early thymocyte progenitors undergoing TCRβ recombination, ATM loss leads to cell cycle defects and developmental arrest, likely facilitating the acquisition of mutations that contribute to leukemogenesis. Using ATM deficiency as a murine model of T cell precursor acute lymphoblastic leukemia (T-ALL), I demonstrate that IL-7 signaling, a critical survival and proliferation signal during early stages of normal thymocyte development, is also required for leukemic maintenance. Moreover, we show for the first time that in normal and leukemic thymocyte precursors, interleukin 7 receptor (IL-7R) expression and function are controlled by Notch signaling, a key determinant of T cell fate. Collectively, these findings provide insight into the mechanisms by which ATM promotes normal lymphocyte development and protects from neoplastic transformation, while establishing the groundwork for assessing the molecular events that lead to the initiation and stepwise progression of T cell leukemogenesis.
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Characterization of Signal Transduction Abnormalities Revealed Spleen Tyrosine Kinase as a Therapeutic Target in High-risk Precursor B Cell Acute Lymphoblastic LeukemiaPerova, Tatiana 20 June 2014 (has links)
Currently, the intensive chemotherapy remains the first line treatment for B cell acute lymphoblastic leukemia (B-ALL). Although these regimens have significantly improved patient outcomes, their use is associated with debilitating morbidities and fatal relapses, highlighting the great need in new agents that target essential survival signals in leukemia. Thus, the overall goal of my project was to gain insights into the signaling abnormalities that regulate aberrant proliferation and survival of B-ALL cells in an effort to identify novel targets in this malignancy.
This study demonstrated that pre-B cell receptor (pre-BCR)-independent spleen tyrosine kinase (SYK) activity was required for the survival and proliferation of a p53-/-PrkdcSCID/SCID mouse model of B-ALL. I extended this discovery to human disease, demonstrating that SYK was activated in primary B-ALL, independent of the pre-BCR expression. The small molecule SYK inhibitor fostamatinib (fosta) significantly attenuated proliferation of 79 primary diagnostic B-ALL samples at clinically achievable concentrations. Importantly, fosta treatment reduced dissemination of engrafting B-ALL cells into the spleen, liver, kidney and central nervous system (CNS) in a NOD.Prkdcscid/scidIl2rgtm1Wjl/SzJ xenotransplant model of B-ALL. Analysis of signaling abnormalities using a high-throughput phospho-flow cytometry platform demonstrated that pediatric and adult B-ALL samples exhibit variable basal activation of BCR,
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PI3K/AKT/mTOR, MAPK and JAK/STAT pathways. Importantly, we identified that fosta-mediated inhibition of SYK, PLC2, CRKL and EIF4E phosphorylation in B-ALL was predictive of its anti-leukemic activity, and was distinct from the cellular actions of other small molecule inhibitors of key nodal signaling pathways. Examination of molecular mechanism of fosta action by gene expression profiling revealed transcriptional effects of fosta treatment that included, most notably, potent inhibition of pathways involved in lymphocyte activation and inflammation. In conclusion, this study demonstrates that SYK signaling is crucial for B-ALL survival and provides detailed characterization of cellular and molecular mechanisms of fosta action in B-ALL. These data argue in favor of testing small molecule SYK inhibitors in pediatric and adult B-ALL.
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The role of macrophage scavenger receptors in host defence : studies in normal and genetically deficient murine modelsHaworth, Richard Ian January 1997 (has links)
No description available.
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