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Dissertations / Theses on the topic 'Myeloid leukemia'

Author: Grafiati
Published: 4 June 2021
Last updated: 25 July 2025

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1

Cheung, Man-sze, and 張敏思. "Characterization of Leukemic stem cells in acute myeloid Leukemia." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B40687582.

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2

Cheung, Man-sze. "Characterization of Leukemic stem cells in acute myeloid Leukemia." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B40687582.

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3

Yaseen, Mumtaz. "Proteomics of Acute Myeloid Leukemia:." Diss., lmu, 2007. http://nbn-resolving.de/urn:nbn:de:bvb:19-69882.

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4

Gunnarsson, Niklas. "Chronic myeloid leukemia and cancer." Doctoral thesis, Umeå universitet, Medicin, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-141144.

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Background Chronic myeloid leukemia (CML) is a relatively rare hematological malignancy with a constant incidence of approximately 90 new cases each year in Sweden (0.9 cases/100 000 inhabitants). The etiology is largely unknown but high doses of ionizing radiation are a known but rare risk factor. The treatment options were for a long time limited to chemotherapies i.e. hydroxyurea and busulfan, interferon’s and allogeneic hematopoietic stem cell transplantation and the median survival were only about four years. Since the beginning of the 21st century a new way of treating CML has been intr
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5

VARINELLI, MARCO. "MODELLING CHRONIC MYELOID LEUKEMIA IN ZEBRAFISH." Doctoral thesis, Università degli studi di Brescia, 2021. http://hdl.handle.net/11379/544088.

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6

Cornforth, Terri Victoria. "Characterising the cell biology of leukemic stem cells in acute myeloid leukemia." Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:654b2176-fd50-427e-86f2-74e928054bef.

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Acute Myeloid leukemia (AML) is an aggressive haematological malignancy that mainly affects the elderly. Relapse is common and is thought to be due to the presence of chemotherapy resistant leukemic stem cells (LSC). Within the CD34+ disease (>5% of the blast cells expressing CD34) , two subtypes have been identified; an LMPP/GMPlike expanded type and a MPP/CMP-like expanded type, the former is the most common, accounting for around 80% of CD34+ AML. Both the GMP-like and LMPPlike expanded populations show LSC activity. To improve our understanding of the disease and gain better insight in to
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7

Zhang, Lu [Verfasser]. "Immunogenicity of leukemia stem cells in acute myeloid leukemia / Lu Zhang." Ulm : Universität Ulm. Medizinische Fakultät, 2012. http://d-nb.info/1020022574/34.

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8

García, Montolío Marc 1991. "The Role of PHF19 in myeloid leukemia." Doctoral thesis, Universitat Pompeu Fabra, 2019. http://hdl.handle.net/10803/667911.

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Polycomb group (PcG) of proteins are a group of highly conserved epigenetic regulators involved in many biological functions such as embryonic development, stem cell self-renewal, cell proliferation, and cancer. PHD finger protein 19 (PHF19) is an associated factor of Polycomb Repressor Complex 2 (PRC2) that has been proposed to regulated its activity in embryonic stem cells. PHF19 has been shown to be up-regulated in different human cancers as well as cancer cell lines. In particular, myeloid leukemia cell lines show increased levels of PHF19, yet little is known about its function. Here, we
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9

Palle, Josefine. "Optimizing Chemotherapy in Childhood Acute Myeloid Leukemia." Doctoral thesis, Uppsala University, Department of Women's and Children's Health, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-9189.

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<p>Despite major advances in our understanding of the biology of childhood acute myeloid leukemia (AML) and the development of new cytotoxic drugs, the prognosis of long-term survival is still only 60-65 %.</p><p>In the present research, we studied the pharmacokinetics of drugs used in the induction therapy of childhood AML and performed in vitro drug sensitivity testing of leukemic cells from children with AML.</p><p>The aims of the studies were to correlate the results of the analysis to biological and clinical parameters and to identify subgroups of AML with specific drug sensitivity profil
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10

Watson, Alexander Scarth. "Autophagy in hematopoiesis and acute myeloid leukemia." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:2e66c5c3-4774-44d1-8345-d0dc827da16d.

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Acute myeloid leukemia (AML) develops following oncogenic alterations to hematopoietic stem (HSC) and progenitor cells (HSPCs) in the bone marrow, resulting in dysregulated proliferation of immature myeloid progenitors that interferes with normal hematopoiesis. Understanding the mechanisms of HSPC protection against damage and excessive division, and how these pathways are altered during leukemic progression, is vital for establishing effective therapies. Here, we show that autophagy, a lysosomal degradation pathway, is increased in HSPCs using a novel imaging flow cytometry autophagy assay. L
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11

Abubakar, Aminu Abdussalam. "Chemotherapeutic responses of marine myeloid leukemias." Thesis, University of St Andrews, 1990. http://hdl.handle.net/10023/13522.

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The murine myeloid leukaemias employed in this study were induced in male CBA/H mice following irradiation with sublethal doses of X-ray. The responses of these leukaemic cell lines and normal (murine) bone marrow cells to cytosine arabinoside and mitoxantrone treatment in vitro were monitored. Both clonogenic, and nonclonogenic chemotherapeutic assays such as radioactive precursor uptake, dye-exclusion assay and autoradiography were employed to determine drug-induced cell lethality. In addition, the in vitro proliferative responses of the leukaemic cell lines and normal bone marrow cells to g
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12

Derolf, Åsa Rangert. "Predictors of prognosis in acute myeloid leukemia a clinical and epidemiological study /." Stockholm, 2010. http://diss.kib.ki.se/2010/978-91-7409-788-7/.

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13

Xue, Liting. "Oncogene Function in Pre-Leukemia Stage of INV(16) Acute Myeloid Leukemia: A Dissertation." eScholarship@UMMS, 2014. https://escholarship.umassmed.edu/gsbs_diss/740.

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The CBFbeta-SMMHC fusion protein is expressed in acute myeloid leukemia (AML) samples with the chromosome inversion inv(16)(p13;q22). This fusion protein binds the transcription factor RUNX with higher affinity than its physiological partner CBFbeta and disrupts the core binding factor (CBF) activity in hematopoietic stem and progenitor cells. Studies in the Castilla laboratory have shown that CBFbeta-SMMHC expression blocks differentiation of hematopoietic progenitors, creating a pre-leukemic progenitor that progresses to AML in cooperation with other mutations. However, the combined function
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14

Xue, Liting. "Oncogene Function in Pre-Leukemia Stage of INV(16) Acute Myeloid Leukemia: A Dissertation." eScholarship@UMMS, 2010. http://escholarship.umassmed.edu/gsbs_diss/740.

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The CBFbeta-SMMHC fusion protein is expressed in acute myeloid leukemia (AML) samples with the chromosome inversion inv(16)(p13;q22). This fusion protein binds the transcription factor RUNX with higher affinity than its physiological partner CBFbeta and disrupts the core binding factor (CBF) activity in hematopoietic stem and progenitor cells. Studies in the Castilla laboratory have shown that CBFbeta-SMMHC expression blocks differentiation of hematopoietic progenitors, creating a pre-leukemic progenitor that progresses to AML in cooperation with other mutations. However, the combined function
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15

Demajo, Meseguer Santiago 1985. "ZRF1-mediated transcriptional regulation in acute myeloid leukemia." Doctoral thesis, Universitat Pompeu Fabra, 2014. http://hdl.handle.net/10803/283478.

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Acute myeloid leukemia (AML) is frequently linked to epigenetic abnormalities and deregulation of gene transcription, which lead to aberrant cell proliferation and accumulation of undifferentiated precursors. ZRF1, a recently characterized epigenetic factor involved in transcriptional regulation, is highly overexpressed in human AML, but it is not known whether it plays a role in leukemia progression. In this thesis, we have investigated the function of ZRF1-mediated transcriptional regulation in AML. We demonstrate that ZRF1 depletion decreases cell proliferation, increases apoptosis an
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16

Belt, Alex J. "Zebrafish Model of MLL-Rearranged Acute Myeloid Leukemia." VCU Scholars Compass, 2018. https://scholarscompass.vcu.edu/etd/5600.

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Acute myeloid leukemia (AML) is the second most common type of leukemia and accounts for 80% of adult acute leukemia cases and is characterized by the accumulation of poorly or undifferentiated myeloid blast cells. Standard treatment includes chemotherapy, which if unsuccessful, is followed by more rigorous chemotherapy as well as stem cell transplantation. Considering most patients are over the age of 45, these more rigorous therapies are not always possible, and as such, new therapies must be developed. Furthermore, AML patients harboring a chromosomal rearrangement involving Multiple Lineag
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17

Bodini, M. "Genomics of treatment response in Acute Myeloid Leukemia." Doctoral thesis, Università degli Studi di Milano, 2017. http://hdl.handle.net/2434/469570.

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Acute Myeloid Leukaemia (AML) is a cancer of the myeloid lineage of blood cells characterised by rapid growth of undifferentiated myeloid precursors that accumulate in the bone marrow and suppress normal haematopoiesis. It is the most common adult leukaemia with an estimated number of more than 60’000 new cases for the US in 2016. Despite the high rates of complete remissions achieved after treatment (60-80% in young adults), the number of patient that will result cured after induction and consolidation therapy is very low (~12%). The molecular basis of relapsing disease is still unclear and t
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18

VALLETTA, SIMONA. "Recurrent SETBP1 mutations in atypical chronic myeloid leukemia." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2014. http://hdl.handle.net/10281/50227.

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Atypical chronic myeloid leukemia (aCML) is a heterogeneous disorder belonging to the group of myelodysplastic/myeloproliferative (MDS/MPN) syndromes. aCML shares clinical and laboratory features with Chronic Myeloid Leukemia (CML), but it lacks the Philadelphia chromosome and the resulting BCR-ABL fusion gene. This crucial difference with CML points to a different pathogenetic process. Because no specific recurrent genomic or karyotypic abnormalities have been identified in aCML, and the molecular pathogenesis of this disease has remained elusive with a dismal outcome, we performed exome-sequ
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19

Namasu, Carolina Yaeko [Verfasser]. "The role of ABR in myeloid differentiation and acute myeloid leukemia / Carolina Yaeko Namasu." Halle, 2017. http://d-nb.info/116614061X/34.

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20

Shipman, Robert Charles. "The molecular characterization of a common human myelogenous leukemia-associated antigen (CAMAL)." Thesis, University of British Columbia, 1987. http://hdl.handle.net/2429/27530.

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Previous studies had demonstrated the presence of the p70 (CAMAL) molecule in human myeloid leukemia cells and the promyelocytic leukemia cell line HL60, but not in equivalent preparations of normal cells (Malcolm et al., 1982, 1984; Shipman et al., 1983; Logan et al., 1984). Subsequent studies demonstrated that the p70 (CAMAL) protein was detectable and expressed in human myeloid leukemia cells and the leukemic cell lines HL60, KG1, K562 and U937. The association of p70 (CAMAL) expression with human myeloid leukemia cells prompted its consideration as a candidate leukemia-associated antigen.
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21

Logan, Patricia Marie. "Detection and possible significance of a common leukemia-associated antigen, CAMAL, in human myeloid leukemia." Thesis, University of British Columbia, 1987. http://hdl.handle.net/2429/28860.

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Human acute nonlymphoblastic or myelogenous leukemia (ANLL or AML) is a malignant disease of the bone marrow involving hemopoietic (blood-forming) cells of the myeloid lineage. ANLL is a complex neoplastic disease, whose fundamental nature is only partially understood despite intensive research. The disease is complicated by its apparent heterogeneity in terms of the degree of differentiation of hemopoietic stem cell involvement in different patients and the cellular expression of immunologically defined surface markers. The presence of a common antigen in myelogenous leukemia (CAMAL) has been
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22

Slape, Christopher Ian. "Molecular characterisation of translocations involving chromosome band 1p36 in acute myeloid leukaemia." Title page, table of contents and abstract only, 2002. http://web4.library.adelaide.edu.au/theses/09PH/09phs6313.pdf.

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"October 2002" Bibliography: leaves 159-198. This thesis describes the mapping of the breakpoints of three different chromosome rearrangements, all involving 1p36, in acute myeloid leukaemia (AML) patients, and an investigation into the molecular outcomes of these rearrangements.
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23

Doepfner, Kathrin T. "Targeting receptor tyrosine kinase signaling in acute myeloid leukemia /." Zürich, 2008. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000253043.

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24

Prenkert, Malin. "On mechanisms of drug resistance in acute myeloid leukemia." Doctoral thesis, Örebro universitet, Hälsoakademin, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-10603.

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In this thesis focus has been to increase the knowledge and understanding of some of the mechanisms responsible for drug resistance in acute myeloid leukemia, as well as identify possibilities to predict drug resistance at diagnosis. We have studied the intracellular behavior of cytostatic drugs and their main metabolites (paper I) and the cellular response to cytostatic drugs (paper III). A new flow cytometry in vitro chemosensitivity assay was developed, to enable identification of viable myeloid cells and determination of drug sensitivity (paper II). Finally, possible new markers involved i
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25

Rothe, Katharina. "Characterization of novel therapeutic targets in chronic myeloid leukemia." Thesis, University of British Columbia, 2015. http://hdl.handle.net/2429/56175.

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The identification of BCR-ABL1 as the key molecular event in chronic myeloid leukemia (CML) has revolutionized treatment opportunities for early phase patients. Imatinib mesylate (IM) and other ABL1 tyrosine kinase inhibitors (TKIs) have been introduced into the clinic with remarkable effects. However, initial and acquired resistance, relapse and in particular, the persistence of CML stem cells upon TKI therapy represent critical challenges and warrant the identification of predictive biomarkers and novel, distinct targets for improved treatment strategies. In this work, I investigated how C
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26

Holt, Bronno van der. "Translational studies in elderly patients with acute myeloid leukemia." [S.l.] : Rotterdam : [The Author] ; Erasmus University [Host], 2007. http://hdl.handle.net/1765/10514.

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27

Vo, Thanh-Trang. "Mitochondrial Priming Determines Chemotherapeutic Response in Acute Myeloid Leukemia." Thesis, Harvard University, 2012. http://dissertations.umi.com/gsas.harvard:10384.

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Gain- and loss-of-function studies of the BCL-2 family of proteins have shown that they can impact chemotherapeutic sensitivity. However, cells contain myriad anti-apoptotic and pro-apoptotic BCL-2 family members making it difficult to predict cell fate decisions based on the initial conditions of these proteins. BH3 profiling is a tool that measures mitochondrial priming, the readiness of a cell to die through the intrinsic (or mitochondrial) apoptotic pathway. Priming is due to the cumulative effect of the BCL-2 family of proteins that act as the gate keepers of the mitochondrial apoptoti
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28

Ma, Leyuan. "Targeting Drug Resistance in Chronic Myeloid Leukemia: A Dissertation." eScholarship@UMMS, 2016. https://escholarship.umassmed.edu/gsbs_diss/870.

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Inhibiting BCR-ABL kinase activity with tyrosine kinase inhibitors (TKIs) has been the frontline therapy for CML. Resistance to TKIs frequently occurs, but the mechanisms remain elusive. First, to uncover survival pathways involved in TKI resistance in CML, I conducted a genome-wide RNAi screen in human CML cells to identify genes governing cellular sensitivity to the first generation TKI called IM (Gleevec). I identified genes converging on and activating the MEK/ERK pathway through transcriptional up-regulation of PRKCH. Combining IM with a MEK inhibitor synergistically kills TKI-resistant C
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29

Varchol, Karen. "Parental occupational exposures and acute myeloid leukemia in offspring /." The Ohio State University, 2000. http://rave.ohiolink.edu/etdc/view?acc_num=osu1488203857250743.

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30

Valia, Dhvani. "EMERGING NATURAL KILLER CELL IMMUNOTHERAPY FOR ACUTE MYELOID LEUKEMIA." Case Western Reserve University School of Graduate Studies / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=case1561938259242716.

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31

Ma, Leyuan. "Targeting Drug Resistance in Chronic Myeloid Leukemia: A Dissertation." eScholarship@UMMS, 2011. http://escholarship.umassmed.edu/gsbs_diss/870.

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Inhibiting BCR-ABL kinase activity with tyrosine kinase inhibitors (TKIs) has been the frontline therapy for CML. Resistance to TKIs frequently occurs, but the mechanisms remain elusive. First, to uncover survival pathways involved in TKI resistance in CML, I conducted a genome-wide RNAi screen in human CML cells to identify genes governing cellular sensitivity to the first generation TKI called IM (Gleevec). I identified genes converging on and activating the MEK/ERK pathway through transcriptional up-regulation of PRKCH. Combining IM with a MEK inhibitor synergistically kills TKI-resistant C
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32

Teleanu, Maria-Veronica [Verfasser]. "RUNX1 mutations in acute myeloid leukemia / Maria-Veronica Teleanu." Ulm : Universität Ulm, 2017. http://d-nb.info/1135665141/34.

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33

MILOVANOVIC, SARA. "NON-GENETIC MECHANISMS OF CHEMORESISTANCE IN ACUTE MYELOID LEUKEMIA." Doctoral thesis, Università degli Studi di Milano, 2022. https://hdl.handle.net/2434/946408.

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Acute Myeloid Leukemia (AML) is the most common type of acute hematological malignancy in adults. 40–60% of patients relapse due to the emergence of cellular resistance to anti- leukemic drugs. Drug resistance in leukemic cells has been associated with intratumoral heterogeneity, among which quiescence, specifically, is considered a key factor for cell survival. Experimental evidence collected both from patients and model systems suggests that relapse is due to rare persistent AML cells which survive chemotherapy. Chemotherapy persistent cells are not yet biologically and molecularly defined.
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34

Corlazzoli, F. "REGENERATION-ASSOCIATED WNT SIGNALING ACTIVATION IN ACUTE MYELOID LEUKEMIA." Doctoral thesis, Università degli Studi di Milano, 2012. http://hdl.handle.net/2434/169569.

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Ample evidence exists in mouse models that acute myeloid leukemia (AML) develops through stepwise acquisition of collaborating genetic and epigenetic changes in self-renewing leukemia-initiating cells (LICs) that exhibit a committed myeloid immunophenotype. Recently, critical questions emerged regarding the characterization of LICs in the CD34+CD38- fraction and the AC133 antigen (a glycosylation-dependent epitope of CD133) seems to be one of the markers more appropriate to enrich for the LICs-containing fraction. The requirement of the Wnt/β-catenin pathway in the pathogenesis of acute
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35

RESTELLI, CECILIA. "THE ROLE OF QUIESCENCE IN ACUTE MYELOID LEUKEMIA GROWTH." Doctoral thesis, Università degli Studi di Milano, 2022. http://hdl.handle.net/2434/909748.

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Acute myeloid leukemia (AML) is the most common leukemia in adults and its prognosis is usually poor. The main culprit of therapy failure and leukemia relapse is the genomic and biological heterogeneity of the tumor. At biological level, AML is hierarchical organized with leukemia stem cells (LSCs) at the apex. LSCs are a rare cell population able to initiate and sustain leukemia growth and share many features with hematopoietic stem cells (HSCs), including self-renewal capacity and quiescence. Traditional therapies have limited effects on LSCs, mainly due to their quiescent state. Preliminar
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36

MAREGA, MANUELA. "Molecular mechanisms for the progression of chronic myeloid leukemia." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2010. http://hdl.handle.net/10281/17737.

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Chronic myeloid leukaemia (CML) is caused by the BCR-ABL hybrid gene. The molecular mechanisms leading from chronic phase (CP) to blast crisis (BC) are not understood. However, both the presence and the levels of BCR-ABL seem to be important for CML progression. BCR-ABL is under the transcriptional control of BCR promoter. Here we focused on the gene expression control of BCR and BCR-ABL upon myeloid differentiation in healthy donors (HDs), CP and BC patients. As previously reported, BCR-ABL is downregulated during myeloid maturation in CP patients. A similar pattern was detected for BCR (but
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37

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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38

Ihme, Erika Ruth Susann [Verfasser]. "Characterization of the Leukemia Initiating Cell in Human Acute Myeloid Leukemia / Erika Ruth Susann Ihme." Ulm : Universität Ulm, 2016. http://d-nb.info/1126036323/34.

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39

關子祺 and Tsz-ki Kwan. "The detection of BCR-ABL kinase domain mutation in the management of chronic myeloid leukemia." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B40738358.

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40

Kwan, Tsz-ki. "The detection of BCR-ABL kinase domain mutation in the management of chronic myeloid leukemia." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B40738358.

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41

Mhadgut, Hemendra M. D., Chandana M. D. Kamireddy, Alok M. D. Sinha, Sakshi M. D. Singal, and Devapiran M. D. Jaishankar. "Innumerable bone lesions: An atypical presentation of Acute Myeloid Leukemia." Digital Commons @ East Tennessee State University, 2021. https://dc.etsu.edu/asrf/2021/presentations/19.

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Acute myeloid leukemia(AML) is the most common acute leukemia among adults in the United states with approximately 19,940 people being diagnosed of this disease in 2020 and 11,180 deaths. It is a heterogenous group of malignancy characterized by clonal expansion of blast with myeloid lineage in the bone marrow, peripheral blood and/or other tissues. Our patient is a 79-year-old male who presented to the hospital with reports of sharp, throbbing low back pain for one month, moderately controlled with pain medications. He reported 5 lb. weight loss with decreased appetite over one month but deni
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42

Dorrance, Adrienne M. "The role of the partial tandem duplication of the MLL (MLL PTD) in leukemogenesis." Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1203712889.

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43

Deshpande, Aniruddha. "Characterisation of the Leukemic Stem Cell in a Murine Model of CALM/AF10 Positive Myeloid Leukemia." Diss., lmu, 2006. http://nbn-resolving.de/urn:nbn:de:bvb:19-57555.

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Mansurov, Alay, Sakshi Singal Singal, Sara Masood, and Devapiran Jaishankar. "Myeloid Sarcoma." Digital Commons @ East Tennessee State University, 2019. https://dc.etsu.edu/asrf/2019/schedule/14.

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Acute Myeloid Leukemia (AML) is a potentially fatal disease, more common in an elderly population. The American Cancer Society estimates 21,450 new cases of AML and 10,920 deaths from AML in the United States in 2019. This malignancy originating in the Bone Marrow (BM), usually presents with peripheral blood (PB) abnormalities. Rarely, AML, particularly monoblastic variants can present with extramedullary disease. Here we describe a case of AML presenting with diffuse lymphadenopathy and a biopsy revealing myeloid sarcoma. A 53 years old male developed diffuse lymphadenopathy. Failure of outpa
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45

Nagura, Eiichi, Saburo Minami, Koichiro Nagata, et al. "Acute myeloid leukemia in the elderly : 159 Nagoya case studies." Nagoya University School of Medicine, 1999. http://hdl.handle.net/2237/5348.

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46

Eriksson, Anna. "Studies of New Signal Transduction Modulators in Acute Myeloid Leukemia." Doctoral thesis, Uppsala universitet, Cancerfarmakologi och beräkningsmedicin, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-182440.

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Acute myeloid leukemia (AML) is a life-threatening malignant disorder with dismal prognosis. AML is characterized by frequent genetic changes involving tyrosine kinases, normally acting as important mediators in many basic cellular processes. Due to the overexpression and frequent mutations of the FMS-like receptor tyrosine kinase 3 (FLT3) in AML, this tyrosine kinase receptor has become one of the most sought after targets in AML drug development. In this thesis, we have used a combination of high-throughput screens, direct target interaction assays and sequential cellular screens, including
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47

Ho, Siu-ki, and 何肇騏. "DNA methylation patterns in t(8;21) acute myeloid leukemia patients." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B47151389.

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Acute myeloid leukemia (AML) is a heterogeneous disease both clinically and biologically. Approximately 55% of AML harbour karyotypic changes, and one of the most common chromosomal aberrations is the t(8;21)(q22;q22), which leads to the AML1-ETO fusion protein. Previous studies have found that this fusion protein recruits the N-CoR/mSin3A/HDAC complex, thereby acts as a transcriptional repressor. Recently, DNA methylation array studies have shown that DNA methylation patterns can stratify AML cases into different subgroups, and some of these correspond to certain chromosomal abnormalities,
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Han, Ho-chun, and 韓浩俊. "JAK-STAT pathway as potential target of acute myeloid leukemia." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B50534208.

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 Acute myeloid leukemia (AML) is a group of heterogeneous diseases characterized by an abnormal increase in myeloblasts. Despite intensive chemotherapy and allogeneic bone marrow transplantation, the treatment outcome of AML remains unsatisfactory, with a cure rate of only about 30%. Therefore, novel therapeutic strategies targeting the pathogenetic pathways of leukemia initiation and progression are needed. Using intracellular phospho-flow analysis with normal bone marrow as reference, we detected an increase in phosphorylated-STAT5 (pSTAT5) in three leukemic cell lines (K562, KG-1 and ML-
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49

Man, Cheuk-him, and 文卓謙. "Mechanism of sorafenib resistance in FLT3-ITD⁺ acute myeloid leukemia." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/193461.

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Acute myeloid leukemia (AML) is a group of heterogeneous diseases characterized by an abnormal increase in myeloblasts in circulation and/or bone marrow. Internal tandem duplication (ITD) of the fms-like tyrosine kinase 3 (FLT3) gene occurs in about 30% of AML and is associated with an inferior prognosis. Tyrosine kinase domain (TKD) mutations occur in about 5% with uncertain prognostic significance. Intensive chemotherapy and allogeneic hematopoietic stem cell transplantation (HSCT) are the mainstays of treatment. However these approaches have reached a deadlock with a cure rate of 30-40%. Ta
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Fontana, Maria Chiara <1990&gt. "Exploiting genomic instability in Acute Myeloid Leukemia: when TP53 fails." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2019. http://amsdottorato.unibo.it/9071/1/PhDTHESIS_Fontana_final.pdf.

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Abstract:
Acute myeloid leukemia (AML) is a myeloid neoplasm with a heterogenic genomic background and a poor prognosis. The main aims of this thesis are to deepen the pathogenic mechanism of genomic instability (1) and drug-resistance (2) p53-related, in order to identify new targets and biomarker of response through genomic and in vitro approaches. (1) A peculiar mechanism of genomic instability is chromothripsis, a one-step genome-shattering catastrophe resulting from disruption of one or few chromosomes in multiple fragments and consequent random rejoining and repair. Chromothripsis was detected
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