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Dissertations / Theses on the topic 'Proteine bcr-abl'

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Published: 4 June 2021

Last updated: 12 February 2022

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1

Cotteret, Sophie. "Induction de la résistance à l'apoptose par Bcr-Abl : amplification génique, inhibition des voies dépendante et -indépendante de l'activation des caspases." Bordeaux 2, 2000. http://www.theses.fr/2000BOR28733.

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2

Hess, Patricia M. "Role of c-Jun NH-terminal Kinase in Bcr/Abl Induced Cell Transformation: a dissertation." eScholarship@UMMS, 2003. https://escholarship.umassmed.edu/gsbs_diss/88.

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The c-Jun NH2-terminal kinase (JNK) group of kinases include ten members that are created by alternative splicing of transcripts derived from Jnk1, Jnk2 and Jnk3 genes. The JNK1 and JNK2 protein kinases are ubiquitously expressed while JNK3 is expressed in a limited number of tissues. The JNK signaling pathway is implicated in multiple physiological processes including cell transformation. There is growing evidence that JNK signaling is involved in oncogenesis. Nevertheless, the role that JNK plays in malignant transformation is still unclear. The aim of this thesis is to examine the role of J

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3

Silva, Ana Elisa Barreiros Bueno da. "Aspectos moleculares da transformação celular induzida por Bcr-Abl." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/42/42133/tde-03062008-153936/.

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As leucemias cromossomo Ph-positivas estão intimamente associadas à expressão da tirosina-quinase Bcr-Abl. Esta oncoproteína promove independência de fatores de crescimento, alterações na adesão e inibição da apoptose por mecanismos ainda não totalmente elucidados. O objetivo desse estudo foi avaliar a contribuição da atividade quinase de Bcr-Abl para seu potencial anti-apoptótico e identificar alterações moleculares envolvidas na transformação celular induzida por essa proteína. Nossos resultados sugerem que a resistência à apoptose não depende da manutenção constante da atividade tirosina-qu

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4

Marusyk, Andriy. "Decreased cellular fitness as a tumor promoter /." Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2006.

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Thesis (Ph.D. in Molecular Biology) -- University of Colorado at Denver and Health Sciences Center, 2006.<br>Typescript. Includes bibliographical references (leaves 124-145). Free to UCD Anschutz Medical Campus. Online version available via ProQuest Digital Dissertations;

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5

Petrola, Maria Juracy Solon. "Perfil do estresse oxidativo em pacientes portadores de Leucemia MielÃide CrÃnica." Universidade Federal do CearÃ, 2011. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=10856.

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Chronic myeloid leukemia (CML) is characterized by clonal expansion of hematopoietic progenitor cells, result from the translocation (9:22). The oncogene BCR-ABL, in the Ph chromosome, is transcribed and translated into a fusion protein BCR / ABL. The ABL tyrosine kinase (TK) in the fusion protein is constitutively activated and is needed for the initial leukemogenic event of CML and its activity induces production of reactive oxygen species (ROS). Of particular relevance to CML is the fact that an increase of ROS can have consequences, facilitating genomic instability may contribute to diseas

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6

Gurjar, Purujit. "Design and Synthesis of Anti Cancer Agents that Inhibit Cysteine Proteases, Limit Oxidative Stress or Terminate Proliferation of BCR-ABL Expressing Cells." University of Cincinnati / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1535635261401718.

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7

Coppo, Paul. "Mise au point d'un modèle de cellules souches transformées par l'oncogène BCR-ABL : conséquences sur la différenciation et l''autorenouvellement." Paris 7, 2006. http://www.theses.fr/2006PA077224.

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La leucémie myéloïde chronique (LMC) est une affection maligne clonale de la cellule souche hématopoïétique caractérisée par la présence du chromosome Philadelphie (ou Phi), issu de la translocation entre les chromosomes 9 et 22. Celui-ci génère l'oncoprotéine BCR-ABL ayant une activité tyrosine kinase constitutive. Actuellement, les mécanismes précis de l'expansion myéloïde, de l'autorenouvellement du clone leucémique, et du blocage de la différenciation lors de la crise blastique observés dans la LMC restent inconnus. Afin d'étudier les mécanismes par lesquels BCR-ABL pourrait orienter la de

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8

Eiring, Anna Marie. "Altered mRNA Metabolism in Chronic Myelogenous Leukemia: Loss of MicroRNA-328 Decoy Activity is Important for Blastic Transformation of Leukemic Progenitors." The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1250701551.

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9

Katsoulas, Athanasia. "Design and mechanism of action of novel agents termed "combi-molecules" engineered for tandem targeting for Bcr-abl expressing leukemia cells." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111884.

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Bcr-abl expression being associated with anti-apoptotic signaling and expression of DNA repair enzymes, we surmised that single molecules capable of blocking abl tyrosine kinase (TK) function and damaging DNA should lead to compounds with potency superior to that of GleevecRTM. To this end, we designed novel agents termed "combi-molecules" programmed to not only behave as bcr-abl inhibitors on their own, but also to further degrade to another inhibitor and a DNA damaging species. The released inhibitor was designed to sustain bcr-abl inhibition following degradation of the combi-molecule and t

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10

Bewry, Nadine N. "STAT3 Contributes to Resistance Towards BCR-ABL Inhibitors in a Bone Marrow Microenvironment Model of Drug Resistance in Chronic Myeloid Leukemia Cells." [Tampa, Fla] : University of South Florida, 2009. http://purl.fcla.edu/usf/dc/et/SFE0002892.

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11

Ress, Angelika. "Proteininteraktionspartner von Beta-Catenin Identifikation von Protein-Proteininteraktionen, Charakterisierung von Modulatoren des Wnt-Signaltransduktionsweges, Wege zu einem neuen Verständnis des Onkoproteins Bcr-Abl /." [S.l. : s.n.], 2004. http://www.diss.fu-berlin.de/2004/334/index.html.

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12

Peng, Cong. "Novel Therapeutic Targets for Ph+ Chromosome Leukemia and Its Leukemia Stem Cells: A Dissertation." eScholarship@UMMS, 2010. https://escholarship.umassmed.edu/gsbs_diss/473.

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The human Philadelphia chromosome (Ph) arises from a translocation between chromosomes 9 and 22 [t(9;22)(q34;q11)]. The resulting chimeric BCR-ABLoncogene encodes a constitutively activated, oncogenic tyrosine kinase that induces chronic myeloid leukemia (CML) and B-cell acute lymphoblastic leukemia (B-ALL). The BCR-ABL tyrosine kinase inhibitor (TKI), imatinib mesylate, induces a complete hematologic and cytogenetic response in the majority of CML patients, but is unable to completely eradicate BCR-ABL–expressing leukemic cells, suggesting that leukemia stem cells are not eliminated. Over tim

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13

Okada, Masayuki. "A novel mechanism for imatinib mesylate-induced cell death of BCR-ABL positive human leukemic cells : caspase-independent, necrosis-like programmed cell death mediated by serine protease activity." Kyoto University, 2005. http://hdl.handle.net/2433/145297.

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14

Griaud, François. "Proteomic analysis of leukaemogenic protein tyrosine kinase action." Thesis, University of Manchester, 2012. https://www.research.manchester.ac.uk/portal/en/theses/proteomic-analysis-of-leukaemogenic-protein-tyrosine-kinase-action(ff9d490b-5a94-45fc-a857-4f0826e4a11a).html.

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Introduction: Chronic myeloid leukaemia is a blood cancer which progresses from a chronic phase to an acute blast crisis if untreated. Disease progression and treatment resistance may be precipitated by the mutator action of BCR/ABL protein tyrosine kinase (PTK), but only few protein phosphosites involved in the DNA damage response have been investigated with respect to BCR/ABL action. Aim: The aim of this PhD project was to demonstrate that BCR/ABL PTK expression can affect the response to genotoxic stress signalling at the protein phosphorylation level. Methodology: Etoposide-induced DNA dam

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15

Liu, Xiaohu. "Functional and structural study of the AHI-1 SH3 domain, characterization of the BCR-ABL-AHI-1-Dynamin-2 protein complex and investigation of oncogenic roles of dynamin-2 in chronic myeloid leukemia." Thesis, University of British Columbia, 2016. http://hdl.handle.net/2429/60191.

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Tyrosine kinase inhibitor (TKI) therapies have been introduced into clinical practice with remarkable effects on chronic myeloid leukemia (CML). However, early relapse, acquired drug resistance and persistence of leukemic stem cells (LSCs) remain problematic. Improved treatments specifically targeting key molecular elements active in CML LSCs are needed. One candidate is the oncoprotein AHI-1 (Abelson helper integration site-1), which is highly deregulated in LSCs. It harbors two key domains, SH3 and WD40-repeat, which are known important mediators of protein-protein interactions. An AHI-1-med

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16

Chen, Yaoyu. "Critical Molecular Pathways in Cancer Stem Cells of Chronic Myeloid Leukemia: A Dissertation." eScholarship@UMMS, 2011. https://escholarship.umassmed.edu/gsbs_diss/536.

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Chronic myeloid leukemia (CML) is a disease characterized by the expansion of granulocytic cells. The BCR-ABL tyrosine kinase inhibitor imatinib, the frontline treatment for Ph+ leukemias, can induce complete hematologic and cytogenetic response in most chronic phase CML patients. Despite the remarkable initial clinic effects, it is now recognized that imatinib will unlikely cure patients because a small cell population containing leukemic stem cells (LSCs) with self-renewal capacity is insensitive to tyrosine kinase inhibitors. In Chapter I, I briefly review the BCR-ABL kinase and its related

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17

Nardinelli, Luciana. "Acompanhamento molecular de pacientes com leucemia mielóide crônica tratados com mesilato de imatinibe e avaliação dos mecanismos de resistência ao tratamento: mutação do gene BCR-ABL e expressão dos genes MDR1 e BCRP." Universidade de São Paulo, 2009. http://www.teses.usp.br/teses/disponiveis/5/5136/tde-02062009-092027/.

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A leucemia mielóide crônica (LMC) é caracterizada pela translocação (9;22) que dá origem ao gene quimérico BCR-ABL. Este gene codifica uma proteína com atividade tirosina quinase, p210, constitutivamente ativa. O três mecanismos envolvidos na patogênese da LMC são o aumento da proliferação celular, alteração da adesão celular ao estroma e matriz medular e inibição da apoptose. A introdução do mesilato de imatinibe (MI), um inibidor de tirosina quinase, revolucionou o tratamento da LMC levando pacientes em fase crônica a remissões duráveis, porém uma parcela destes não responde ou perde a respo

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18

Götz, Alexander. "Beeinflussung des Mdm2/p53-Systems durch Bcr-Abl und physiologische Wachstumssignale /." 2001. http://www.gbv.de/dms/bs/toc/335125913.pdf.

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19

Lee, Jie-Ling, and 李婕綾. "Investigation of the andrographolide-induced downregulation of Hsp90 client protein, Bcr-Abl." Thesis, 2017. http://ndltd.ncl.edu.tw/handle/z26342.

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碩士<br>國立陽明大學<br>生物藥學研究所<br>105<br>Andrographolide (ANDRO) is a natural product of diterpenoid lactone, which is isolated from the leaves of Andrographis paniculata. Professor Shu-Ling Fu (NYMU) previously reported that a cleaved fragment of Hsp90 was identified in ANDRO-treated cells by a proteomics approach. In addition, Fu’s lab also reported that ANDRO induced Hsp90 cleavage and decreased levels of Bcr-Abl in K562 cell, a cell line derived from patients with chronic myelogenous leukemia. A previous proteomics research previously reported that Hsp90 was a targeting protein of ANDRO. We specu

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20

Jarvis, Jordan. "Role of the Adapter Protein 3BP2 in BCR-ABL-mediated Signal Transduction and Leukemogenesis." Thesis, 2012. http://hdl.handle.net/1807/33254.

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3BP2 was originally identified through its interaction with the ABL kinase. Fusion of ABL with the BCR gene forms the BCR-ABL onco-protein, which is causative in Chronic Myeloid Leukemia (CML) and acute lymphoid leukemia (ALL). Due to the ability of 3BP2 to regulate ABL activity in osteoblasts, we hypothesize that 3BP2 modulates BCR-ABL signalling. Overexpression of 3BP2 in the CML-T1 cell line produced a marked decrease in global tyrosine phosphorylation. 3BP2 overexpression also resulted in a significant increase in CML-T1 cell growth, accompanied by altered ERK1/2, AKT, SYK, LYN, HCK, and C

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21

Babiarová, Katarína. "Rekombinantní vakcíny proti solidním a hematologickým nádorům: vývoj a stanovení jejich účinnosti." Doctoral thesis, 2013. http://www.nusl.cz/ntk/nusl-327445.

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K. Babiarová Ph.D. Thesis ABSTRACT Cancer immunotherapy is concerned generally with the activation of cancer immunity specific for tumor antigens (TA) produced by cancer cells. My PhD thesis focused on the development of different types of cancer vaccines expressing various TA and predominantly on the determination of the efficacy of these vaccines. For studying TA-specific cancer cellular immunity in mice immunized with these vaccines, I used mainly the ELISPOT-IFNγ assay. First, DNA, recombinant vaccinia virus (rVACV) and peptide vaccines against WT1 positive tumors were prepared. They consi

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22

Mirakaj, Valbona [Verfasser]. "Analyse des BCR-ABL-Proteins als Antigen zur Induktion von antigenspezifischen zytotoxischen T-Zellen / vorgelegt von Valbona Mirakaj." 2007. http://d-nb.info/983724032/34.

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23

Pavan, Kumar Reddy N. G. [Verfasser]. "Role of SOCS proteins in FLT3-ITD and BCR-ABL mediated leukemogenesis / by Pavan Kumar Reddy, N. G." 2010. http://d-nb.info/1009446452/34.

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24

Santos, Diogo Pires dos. "The potential therapeutic effect of heat shock protein 90 inhibition in chronic myeloid leukemia." Master's thesis, 2018. http://hdl.handle.net/10316/82142.

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Trabalho Final do Mestrado Integrado em Medicina apresentado à Faculdade de Medicina<br>A Proteína de Choque Térmico 90 (HSP90) facilita a maturação, estabilidade, atividade e enrolamento intracelular de mais de 200 proteínas, designadas “proteínas clientes”. Nas células cancerígenas, a HSP90 ajuda a superar múltiplos stresses ambientais, incluindo instabilidade genómica/aneuploidia, stress proteotóxico, necessidades nutricionais aumentadas, níveis de oxigénio reduzidos, e ajudam na evasão ao sistema imune. Uma das proteínas clientes da HSP90 é a proteína BCR-ABL, uma oncoproteína responsável

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25

Cheng, Hao-Yuan, and 鄭皓遠. "Combination of protein tyrosine kinase inhibitor AG1024 with paclitaxel enhances cell program death in BCR-ABL-mediated resistance of K562 cell line." Thesis, 2005. http://ndltd.ncl.edu.tw/handle/30227831001776366712.

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碩士<br>國立陽明大學<br>醫學生物技術研究所<br>93<br>Chronic myelogenous leukaemia (CML) is a clonal malignancy of the pluripotent haematopoietic stem cell, characterised by an uncontrolled proliferation and expansion of myeloid progenitors expressing a fusion oncogene, BCR-ABL, the molecular counterpart of the Ph1 chromosome. Many evidences showed that the tyrosine kinase activity of BCR-ABL is able to activate several major signalling pathways in malignant cells, including Ras, JAK/STAT and PI3K/Akt and also prevent cells apoptosis under some antineoplastic agents such as paclitaxel. Targeting these abnormali

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26

Reß, Angelika [Verfasser]. "Proteininteraktionspartner von Beta-Catenin : Identifikation von Protein-Proteininteraktionen, Charakterisierung von Modulatoren des Wnt-Signaltransduktionsweges, Wege zu einem neuen Verständnis des Onkoproteins Bcr-Abl / vorgelegt von Angelika Reß." 2004. http://d-nb.info/973889896/34.

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