Teses / dissertações sobre o tema "Myeloid leukemia"
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Veja os 50 melhores trabalhos (teses / dissertações) para estudos sobre o assunto "Myeloid leukemia".
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Cheung, Man-sze, e 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.
Texto completo da fonteCheung, 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.
Texto completo da fonteYaseen, Mumtaz. "Proteomics of Acute Myeloid Leukemia:". Diss., lmu, 2007. http://nbn-resolving.de/urn:nbn:de:bvb:19-69882.
Texto completo da fonteGunnarsson, Niklas. "Chronic myeloid leukemia and cancer". Doctoral thesis, Umeå universitet, Medicin, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-141144.
Texto completo da fonteVARINELLI, MARCO. "MODELLING CHRONIC MYELOID LEUKEMIA IN ZEBRAFISH". Doctoral thesis, Università degli studi di Brescia, 2021. http://hdl.handle.net/11379/544088.
Texto completo da fonteCornforth, 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.
Texto completo da fonteZhang, 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.
Texto completo da fonteGarcía, Montolío Marc 1991. "The Role of PHF19 in myeloid leukemia". Doctoral thesis, Universitat Pompeu Fabra, 2019. http://hdl.handle.net/10803/667911.
Texto completo da fonteEl complejo de proteínas Polycomb (PcG), es un grupo de reguladores epigenéticos altamente conservados que participan en distintas funciones biológicas como el desarrollo embrionario, la auto renovación de las células madre, la proliferación y están involucradas también en cáncer. La proteína PHD finger 19 (PHF19), es un factor asociado al complejo represor Polycomb 2 (PRC2). PHF19 ha sido propuesta como reguladora de la actividad de PRC2 en células madre embrionarias. También se ha visto que esta sobreexpressada en diferentes canceres y líneas celulares cancerígenas. Nosotros hemos demostrado que la eliminación de PHF19 disminuye la proliferación de las líneas celulares mieloides cancerígenas. Hemos demostrado que la depleción de PHF19 en las células de leucemia crónica mieloide las induce a diferenciarse hacia eritrocitos. Mecánicamente, hemos demostrado que PHF19 regula la proliferación de esta línea celular mediante su interacción con el regulador de ciclo celular p21. Además, hemos observado que MTF2, un homólogo de PHF19, se deposita en aquellos genes donde previamente estaba PHF19. En conjunto, nuestros resultados muestran que PHF19 es un factor transcripcional clave en líneas celulares mieloides y sugieren que la inhibición de PHF19 podría ser una potencial diana para ser explorada para el tratamiento de la leucemia mieloide.
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.
Texto completo da fonteDespite 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 %.
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.
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 profiles in order to better understand why treatment fails in some patients and how therapy may be improved.
Blood samples were analysed to study the pharmacokinetics of doxorubicin (n=41), etoposide (n=45) and 6-thioguanine (n=50). Doxorubicin plasma concentration and total body clearance were correlated to the effect of induction therapy, and doxorubicin plasma concentration was an independent factor for complete remission, both in univariate and multivariate analysis including sex, age, and white blood cell count at diagnosis. For etoposide and 6-thioguanine no correlation was found between pharmacokinetics and clinical effect. Children with Down syndrome (DS) tended to reach higher blood concentrations of etoposide and thioguanine nucleotides, indicating that dose reduction may be reasonable to reach the same drug exposure as in children without DS.
Leukemic cells from 201 children with newly diagnosed AML, 15 of whom had DS, were successfully analysed for in vitro drug sensitivity by the fluorometric microculture cytotoxicity assay (FMCA). We found that samples from children with DS were highly sensitive to most drugs used in AML treatment. In non-DS children, the t(9;11) samples were significantly more sensitive to cytarabine (p=0.03) and doxorubicin (p=0.035) than other samples. The findings might explain the very favorable outcome reported in children with DS and t(9;11)-positive AML. A specific drug resistance profile was found for several other genetic subgroups as well. A detailed study of MLL-rearranged leukemia showed that cellular drug sensitivity is correlated both to partner genes and cell lineage, findings that support the strategy of contemporary protocols to include high-dose cytarabine in the treatment of patients with MLL-rearrangement, both in AML and acute lymphoblastic leukemia (ALL).
Our results indicate that drug resistance and pharmacokinetic studies may yield important information regarding drug response in different sub-groups of childhood AML, helping us to optimize future chemotherapy in childhood AML.
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.
Texto completo da fonteAbubakar, Aminu Abdussalam. "Chemotherapeutic responses of marine myeloid leukemias". Thesis, University of St Andrews, 1990. http://hdl.handle.net/10023/13522.
Texto completo da fonteDerolf, 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/.
Texto completo da fonteXue, 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.
Texto completo da fonteXue, 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.
Texto completo da fonteDemajo, Meseguer Santiago 1985. "ZRF1-mediated transcriptional regulation in acute myeloid leukemia". Doctoral thesis, Universitat Pompeu Fabra, 2014. http://hdl.handle.net/10803/283478.
Texto completo da fonteLa leucèmia mieloide aguda (LMA) està relacionada freqüentment amb anomalies epigenètiques i desregulació de la transcripció gènica, que provoquen una proliferació cel·lular aberrant i l'acumulació de precursors indiferenciats. ZRF1, un factor epigenètic caracteritzat recentment i implicat en la regulació transcripcional, es troba altament sobreexpressat en la LMA humana, però es desconeix si juga cap paper en la progressió de la malaltia. En aquesta tesi, s'ha investigat la funció de ZRF1 en la regulació transcripcional en la LMA. Es demostra que el silenciament de ZRF1 provoca una disminució de la proliferació, un increment de l'apoptosi i una inducció de la diferenciació en cèl·lules de LMA humana. El tractament amb àcid retinoic (AR), un inductor de la diferenciació que es fa servir actualment per a tractar determinades LMAs, produeix un canvi funcional en ZRF1, que passa de repressor a activador de la diferenciació. A nivell molecular, ZRF1 controla la xarxa de gens regulada per l’AR a través de la seva interacció amb el receptor de l'AR α (RARα) i la seva unió als gens diana de l'AR. El nostre estudi d'expressió a nivell de tot el genoma revela que ZRF1 regula la transcripció de gairebé la meitat dels gens diana de l'AR. En concordança amb les nostres observacions in vitro que mostren que ZRF1 regula la proliferació, l'apoptosi i la diferenciació, el silenciament de ZRF1 provoca una forta inhibició en la progressió de la leucèmia en models de xenotrasplantament en ratolí. Finalment, el silenciament de ZRF1 coopera amb el tractament amb AR en la supressió de la leucèmia in vivo. Conjuntament, aquests resultats mostren que ZRF1 és un regulador transcripcional clau en la progressió de la leucèmia i suggereixen que la inhibició de ZRF1 podria ser una nova estratègia a explorar en al tractament de la LMA.
Belt, Alex J. "Zebrafish Model of MLL-Rearranged Acute Myeloid Leukemia". VCU Scholars Compass, 2018. https://scholarscompass.vcu.edu/etd/5600.
Texto completo da fonteBodini, M. "Genomics of treatment response in Acute Myeloid Leukemia". Doctoral thesis, Università degli Studi di Milano, 2017. http://hdl.handle.net/2434/469570.
Texto completo da fonteVALLETTA, SIMONA. "Recurrent SETBP1 mutations in atypical chronic myeloid leukemia". Doctoral thesis, Università degli Studi di Milano-Bicocca, 2014. http://hdl.handle.net/10281/50227.
Texto completo da fonteNamasu, 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.
Texto completo da fonteShipman, 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.
Texto completo da fonteScience, Faculty of
Microbiology and Immunology, Department of
Graduate
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.
Texto completo da fonteScience, Faculty of
Microbiology and Immunology, Department of
Graduate
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.
Texto completo da fonteDoepfner, Kathrin T. "Targeting receptor tyrosine kinase signaling in acute myeloid leukemia /". Zürich, 2008. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000253043.
Texto completo da fontePrenkert, 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.
Texto completo da fonteRothe, Katharina. "Characterization of novel therapeutic targets in chronic myeloid leukemia". Thesis, University of British Columbia, 2015. http://hdl.handle.net/2429/56175.
Texto completo da fonteMedicine, Faculty of
Medical Genetics, Department of
Graduate
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.
Texto completo da fonteVo, Thanh-Trang. "Mitochondrial Priming Determines Chemotherapeutic Response in Acute Myeloid Leukemia". Thesis, Harvard University, 2012. http://dissertations.umi.com/gsas.harvard:10384.
Texto completo da fonteMa, Leyuan. "Targeting Drug Resistance in Chronic Myeloid Leukemia: A Dissertation". eScholarship@UMMS, 2016. https://escholarship.umassmed.edu/gsbs_diss/870.
Texto completo da fonteVarchol, Karen. "Parental occupational exposures and acute myeloid leukemia in offspring /". The Ohio State University, 2000. http://rave.ohiolink.edu/etdc/view?acc_num=osu1488203857250743.
Texto completo da fonteValia, 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.
Texto completo da fonteMa, Leyuan. "Targeting Drug Resistance in Chronic Myeloid Leukemia: A Dissertation". eScholarship@UMMS, 2011. http://escholarship.umassmed.edu/gsbs_diss/870.
Texto completo da fonteTeleanu, Maria-Veronica [Verfasser]. "RUNX1 mutations in acute myeloid leukemia / Maria-Veronica Teleanu". Ulm : Universität Ulm, 2017. http://d-nb.info/1135665141/34.
Texto completo da fonteMILOVANOVIC, SARA. "NON-GENETIC MECHANISMS OF CHEMORESISTANCE IN ACUTE MYELOID LEUKEMIA". Doctoral thesis, Università degli Studi di Milano, 2022. https://hdl.handle.net/2434/946408.
Texto completo da fonteCorlazzoli, F. "REGENERATION-ASSOCIATED WNT SIGNALING ACTIVATION IN ACUTE MYELOID LEUKEMIA". Doctoral thesis, Università degli Studi di Milano, 2012. http://hdl.handle.net/2434/169569.
Texto completo da fonteRESTELLI, CECILIA. "THE ROLE OF QUIESCENCE IN ACUTE MYELOID LEUKEMIA GROWTH". Doctoral thesis, Università degli Studi di Milano, 2022. http://hdl.handle.net/2434/909748.
Texto completo da fonteMAREGA, 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.
Texto completo da fonteHeaney, Nicholas Benjamin. "Proteasome inhibition in chronic myeloid leukaemia". Thesis, Connect to e-thesis, 2009. http://theses.gla.ac.uk/832/.
Texto completo da fonteMD. 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.
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.
Texto completo da fonte關子祺 e 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.
Texto completo da fonteKwan, 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.
Texto completo da fonteMhadgut, Hemendra M. D., Chandana M. D. Kamireddy, Alok M. D. Sinha, Sakshi M. D. Singal e 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.
Texto completo da fonteDorrance, 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.
Texto completo da fonteDeshpande, 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.
Texto completo da fonteMansurov, Alay, Sakshi Singal Singal, Sara Masood e Devapiran Jaishankar. "Myeloid Sarcoma". Digital Commons @ East Tennessee State University, 2019. https://dc.etsu.edu/asrf/2019/schedule/14.
Texto completo da fonteNagura, Eiichi, Saburo Minami, Koichiro Nagata, Yoshihisa Morishita, Hideo Takeyama, Hiroshi Sao, Hisamitsu/ Suzuki et al. "Acute myeloid leukemia in the elderly : 159 Nagoya case studies". Nagoya University School of Medicine, 1999. http://hdl.handle.net/2237/5348.
Texto completo da fonteEriksson, 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.
Texto completo da fonteHo, Siu-ki, e 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.
Texto completo da fontepublished_or_final_version
Pathology
Master
Master of Philosophy
Han, Ho-chun, e 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.
Texto completo da fontepublished_or_final_version
Medicine
Master
Master of Philosophy
Man, Cheuk-him, e 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.
Texto completo da fontepublished_or_final_version
Medicine
Doctoral
Doctor of Philosophy
Fontana, Maria Chiara <1990>. "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.
Texto completo da fonte