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Leukemia incidence and benzene air pollution in Portland, Oregon /Voss, Robert W. January 1900 (has links)
Thesis (M.S.)--Oregon State University, 2008. / Printout. Includes bibliographical references (leaves 89-99). Also available on the World Wide Web.
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The effects of a methionine aminopepitdase inhibitor fumagillin on leukemia cell growth in-vitroMak, Wan-ling, Justina Crystaline, 麥允齡 January 2013 (has links)
Acute Myeloid Leukaemia (AML) is a disease normally found in elderly patients, with the median age of presentation at about 68 years. At this age, many of the patients are frail and unlikely to respond well to intensive chemotherapy treatments. Conventional chemotherapy eradicates the proliferating leukaemic progenitors while leaving the quiescent leukaemic stem cells undisturbed. These quiescent LSCs are able to then bring about leukaemic relapse. Fumagillin is a natural metabolite from Asperigillus fumigatus that is generally used as an anti-microbial agent but it is also known to bind to intracellular MetAP-II and inhibit endothelial cell growth. Many cancers are found to have an over expression of MetAP-II.
In the past, MetAP-II inhibitors have been tested and shown success in angiogenesis inhibition and tumor reduction. The aim of this study is to observe whether methionine aminopeptidase-2 inhibitors can be used in the treatment of acute myeloid leukemia. The investigation included a dose response comparison of various AML cell lines to fumagillin treatment, cell proliferation assay, a colony forming unit assay, and cell cycle analysis of KG-1 cells following three days of fumagillin treatment. I have determined that fumagillin does indeed decrease the cellular proliferation of KG-1 in vivo and at 10μM, prevents colony formation in methylcellulose plating. There is an increase in cells found in the sub-G1 phase with fumagillin treatment, as analyzed by flow cytometry. It is interpolated that fumagillin treatment increases AML cell apoptosis, in addition to hindering its ability to grow in culture. / published_or_final_version / Medicine / Master / Master of Medical Sciences
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Integrated epigenetic and genetic analysis of transcriptional dysregulation in acute myeloid leukaemiaGudgin, Emma-Jane January 2013 (has links)
No description available.
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Study of gene promoter methylation in acute promyelocytic leukaemiaChim, Chor-sang, James. January 2002 (has links)
Thesis (M.D.)--University of Hong Kong, 2002. / Title from title frame. Includes bibliographical references (leaves 186-223).
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Identified of novel splicing variants of livin in acute myeloid leukemiaLo, Carfield. January 2009 (has links)
Thesis (M. Phil.)--University of Hong Kong, 2009. / Includes bibliographical references (leaves 99-111) Also available in print.
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Calpain and Calpastatin in a Mouse Model of Acute Myeloid LeukemiaFarr, Christina 07 December 2011 (has links)
I have studied the calpain system in acute myeloid leukemia using the 32D and 32Dkit cell lines. Specifically, I characterized the calpain system in the cell lines, and performed calpastatin overexpression and knockdown studies. I found that calpain activity is elevated in the 32D and 32Dkit cells, and calpain inhibition causes apoptosis. Both μ- and m-calpain contribute to the calpain activity in these cell lines. The 32Dkit cells have higher calpain activity than the 32D cells, which I have shown is partially attributed to basal ckit activation. Calpastatin was present in both cell lines, but exists mainly in a degraded form. Calpastatin overexpression lowered calpain activity and provided a growth disadvantage to the 32Dkit cells, but had no effect on 32D cells. Calpastatin knockdown caused a significant increase in calpain activity in the 32D cells, which changed the cell cycle distribution but had no other major effects.
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The expression, regulation and functional role of SOX7 gene in acute myeloid leukemiaFan, Kin-pong., 范健邦. January 2010 (has links)
published_or_final_version / Medicine / Master / Master of Philosophy
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Calpain and Calpastatin in a Mouse Model of Acute Myeloid LeukemiaFarr, Christina 07 December 2011 (has links)
I have studied the calpain system in acute myeloid leukemia using the 32D and 32Dkit cell lines. Specifically, I characterized the calpain system in the cell lines, and performed calpastatin overexpression and knockdown studies. I found that calpain activity is elevated in the 32D and 32Dkit cells, and calpain inhibition causes apoptosis. Both μ- and m-calpain contribute to the calpain activity in these cell lines. The 32Dkit cells have higher calpain activity than the 32D cells, which I have shown is partially attributed to basal ckit activation. Calpastatin was present in both cell lines, but exists mainly in a degraded form. Calpastatin overexpression lowered calpain activity and provided a growth disadvantage to the 32Dkit cells, but had no effect on 32D cells. Calpastatin knockdown caused a significant increase in calpain activity in the 32D cells, which changed the cell cycle distribution but had no other major effects.
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The role of Sox4 in acute myeloid leukaemiaPutwain, Sarah Lucy January 2014 (has links)
No description available.
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Identified of novel splicing variants of livin in acute myeloid leukemiaLo, Carfield., 盧德心. January 2009 (has links)
published_or_final_version / Medicine / Master / Master of Philosophy
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