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Dissertations / Theses on the topic 'Apoptosis. Acute myeloid leukemia'

Author: Grafiati

Published: 4 June 2021

Last updated: 13 February 2022

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1

Lo, Carfield. "Identified of novel splicing variants of livin in acute myeloid leukemia." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B41897031.

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2

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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3

Lo, Carfield, and 盧德心. "Identified of novel splicing variants of livin in acute myeloid leukemia." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B41897031.

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4

Nakatani, Kana. "Inhibition of CDK4/6 and autophagy synergistically induces apoptosis in t(8;21) acute myeloid leukemia cells." Doctoral thesis, Kyoto University, 2021. http://hdl.handle.net/2433/263584.

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5

Lainey, Elodie. "Evaluation préclinique de l’azacytidine et de l’erlotinib seuls ou en association dans le traitement des syndromes myélodysplasiques." Thesis, Paris 11, 2013. http://www.theses.fr/2013PA11T066.

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Les syndromes myélodysplasiques (SMD) sont un ensemble d’hémopathies clonales de la cellule souche. Ils touchent les sujets âgés et se caractérisent par une hématopoïèse inefficace, une différenciation anormale et une transformation fréquente en leucémie aiguë myéloblastique (LAM). La prise en charge thérapeutique a considérablement évolué ces dix dernières années, principalement avec l’arrivée de la 5-azacytidine (Aza) dans les SMD de haut risque. Malheureusement, il existe fréquemment un échec ou une perte de réponse rapide au traitement responsable d’une survie médiane globale de seulement

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6

Tailler, Maximilien. "Les dérégulations de l’apoptose dans les syndromes myélodysplasiques et les leucémies aigues myéloïdes." Thesis, Paris 11, 2011. http://www.theses.fr/2011PA11T059.

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Les syndromes myélodysplasiques (SMD) peuvent être conçus comme des conditions pré-leucémiques dans lesquelles l’apoptose avorte les produits de différenciation de cellules souches mutées, potentiellement malignes. Néanmoins, peut-être à cause d’une inhibition progressive de l’apoptose, les SMD se transforment fréquemment en leucémies aiguës myéloïdes (LAM). Nos données indiquent que les SMD à faible risque se caractérisent par l’absence d’activation de NF-κB au sein des cellules portant des altérations cytogénétiques typiques. Par contre, dans les SMD à haut risque de transformation en LAM (a

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7

Shah, Viral Virendra [Verfasser]. "Enhancing PARP inhibition mediated DNA Damage and leveraging inherent anti-apoptotic dependencies in acute myeloid leukemia / Viral Virendra Shah." Mainz : Universitätsbibliothek der Johannes Gutenberg-Universität Mainz, 2020. http://d-nb.info/1223205320/34.

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8

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

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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

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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12

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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13

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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14

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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15

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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16

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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17

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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18

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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19

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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20

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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21

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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22

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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23

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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24

Putwain, Sarah Lucy. "The role of Sox4 in acute myeloid leukaemia." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648624.

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25

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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26

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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27

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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28

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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29

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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30

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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31

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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32

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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33

Chandran, Priya. "Bone Marrow Microenvironment in Acute Myleoid Leukemia." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/24301.

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Acute myeloid leukemia (AML) often remains refractory to current chemotherapy and transplantation approaches despite many advances in our understanding of mechanisms in leukemogenesis. The bone marrow “niche” or microenvironment, however, may be permissive to leukemia development and studying interactions between the microenvironment and leukemia cells may provide new insight for therapeutic advances. Mesenchymal stem cells (MSCs) are central to the development and maintenance of the bone marrow niche and have been shown to have important functional alterations derived from patients with diffe

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34

Chim, Chor-sang James. "Study of gene promoter methylation in acute promyelocytic leukaemia." Hong Kong : University of Hong Kong, 2002. http://sunzi.lib.hku.hk/hkuto/record.jsp?B25256725.

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35

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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36

Möllgård, Lars. "Drug resistance in acute myeloid leukemia : pharmacokinetic and in vitro studies /." Stockholm, 2001. http://diss.kib.ki.se/2001/91-628-4661-2/.

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37

Benajiba, Lina. "Identification and Characterization of New Therapeutic Targets in Acute Myeloid Leukemia." Thesis, Université Paris-Saclay (ComUE), 2018. http://www.theses.fr/2018SACLS173.

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La leucémie aiguë myéloïde (LAM) est une pathologie hématologique dont le pronostic reste très défavorable, malgré les progrès réalisés dans la compréhension des mécanismes physiopathologiques sous-tendant son développement. Identifier de nouvelles stratégies anti-leucémiques représente donc une étape clé dans la concrétisation des avancées thérapeutiques. Grâce à la combinaison de plusieurs approches de criblage génétiques et pharmacologiques, l’objectif de ma thèse a été de définir et valider de nouvelles cibles thérapeutiques dans les LAM. La première partie de ma thèse a eu pour but de tra

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38

Mitchell, Shaneice Renee. "Preclinical evaluation of NAMPT inhibitor KPT-9274 in Acute Myeloid Leukemia." The Ohio State University, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=osu1546527486477125.

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39

Jeon, Jae Yoon. "Preclinical and clinical development of kinase inhibitors in acute myeloid leukemia." The Ohio State University, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=osu158699311567933.

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40

Ristic, Marko. "ROS/SUMO relationship in the chemotherapeutic treatment of Acute Myeloid Leukemia." Thesis, Montpellier, 2015. http://www.theses.fr/2015MONTT047.

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Les leucémies aiguë myéloïde (LAM) sont un groupe d’hémopathies malignes, dont le traitement est généralement composé de deux génotoxiques : la cytarabine (Ara-C) et la daunorubicine (DNR). Nous avons montré que l’Ara-C et la DNR induisent la déconjugaison rapide de SUMO (Small Ubiquitin-related Modifier) de ses protéines cibles. Cette deSUMOylation est dûe à l'inactivation des enzymes E1 et E2 de SUMOylation par les espèces réactives de l'oxygène (ROS) produites par l’Ara-C et la DNR et est impliquée dans l'activation de l'apoptose. En outre, cet axe ROS/SUMO est anergisé dans les LAM chimior

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41

Li, Hubo. "Genome-Wide RNAi Screens for Novel Regulators of Acute Myeloid Leukemia." Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:14226105.

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Acute myeloid leukemia (AML) is a heterogeneous disease with complex molecular mechanisms. Recent advent of genomic technologies, such as copy number profiling, whole genome sequencing, and gene expression profiling has accumulated a plethora of large-scale data in AML cell lines and patient samples. However, the functional relevance of most genes identified by these methods has yet to be determined. To systematically characterize the genetic requirement in AML, we conducted genome-wide shRNA screens in 17 AML cell lines in parallel with 199 cell lines of other cancer types. We identified over

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42

Mingay, Matthew. "Vitamin C induced epigenomic remodelling in IDH1 mutant acute myeloid leukemia." Thesis, University of British Columbia, 2017. http://hdl.handle.net/2429/61020.

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The genomes of myeloid malignancies are characterized by epigenomic abnormalities. Heterozygous, inactivating TET2 mutations and neomorphic IDH mutations are recurrent and mutually exclusive in acute myeloid leukemia genomes. Ascorbic Acid (vitamin C) has been shown to stimulate the catalytic activity of TET2 in vitro and thus we sought to explore its effect in a leukemic model expressing IDH1R132H. Vitamin C treatment induced a reduction in cell proliferation and an increase in the expression of genes involved in leukocyte differentiation in IDH1R132H expressing cells. Genome-wide assessment

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43

Askew, David Stephen. "Characterization of novel myeloid differentiation antigen associated with acute myelogenous leukemia." Thesis, University of British Columbia, 1985. http://hdl.handle.net/2429/26768.

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A monoclonal antibody has been developed that detects a unique cell surface antigen (NHL-30.5) with a molecular weight of 180,000 expressed on the human acute promyelocytic cell line HL-60. In addition to HL-60 and other AML cell lines, the antibody reacts with a significant proportion of hemopoietic cells from 40/48 patients with acute myeloid leukemia (AML), and on a variety of other hematologic disorders characterized by the presence of immature myeloid blast cells. In contrast it does not react with normal mature hemopoietic cells, including lymphocytes, monocytes, granulocytes, erythrocyt

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44

Conrad, David Paul. "Development of Vesiculovirus-based Therapeutics for Acute Leukemia." Thesis, Université d'Ottawa / University of Ottawa, 2014. http://hdl.handle.net/10393/31743.

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Outcomes for most patients with acute leukemia remain dismal. In-vitro, vesiculovirus members induced rapid apoptosis of acute leukemia cells. Intravenous injection of lymphoblastic leukemia cells infected ex-vivo with attenuated Vesicular Stomatitis Virus or Maraba Virus followed by gamma-irradiation, controlled leukemic progression in murine recipients. Essential properties of this autologous vaccine [immunotherapy by Leukemia-Oncotropic Virus (iLOV)] and the host’s immune system were characterized. iLOV durability was restricted to the leukemia used to manufacture the vaccine. At administra

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45

Willander, Kerstin. "Molecular genetic studies on Chronic Lymphocytic Leukemia and Acute Myeloid Leukemia - with focus on prognostic markers." Doctoral thesis, Linköpings universitet, Avdelningen för cellbiologi, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-104951.

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The present thesis is focused on the prognostic value of genetic variations and alterations in the initiation and development of chronic lymphocytic leukemia (CLL) and acute myeloid leukemia (AML) patients. Several prognostic markers based on genetic or chromosomal aberrations are today used in clinic in these heterogeneous diseases. Novel biomarkers have been identified through next generation sequencing techniques and some of them may be useful as prognostic markers in clinical diagnostic. In papers I-IV we have investigated some of this markers in CLL and AML tumor cells. In papers I and II

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46

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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47

Gudgin, Emma-Jane. "Integrated epigenetic and genetic analysis of transcriptional dysregulation in acute myeloid leukaemia." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608093.

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48

Mak, Wan-ling Justina Crystaline, and 麥允齡. "The effects of a methionine aminopepitdase inhibitor fumagillin on leukemia cell growth in-vitro." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/193534.

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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 in

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49

Xiao, Kang. "Investigating the functional roles of Mcl-1 in apoptosis in mammalian cells /." View abstract or full-text, 2009. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202009%20XIAO.

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50

Vangala, Rajani Kanth. "AML1/ETO Downregulates the Transcription Factor PU.1 in Acute Myeloid Leukemia." Diss., lmu, 2003. http://nbn-resolving.de/urn:nbn:de:bvb:19-10271.

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