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Dissertations / Theses on the topic 'C-Myc'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

Evans, Joanne R. "The investigation of internal ribosome entry in the c-myc and c-myb genes." Thesis, University of Leicester, 2003. http://hdl.handle.net/2381/29681.

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The c-myc gene contains an internal ribosome entry site (IRES) within its 5' untranslated region. The IRES was shown to have different activities between cell lines suggesting a requirement for protein trans-acting factors that are present in these cell lines in varying amounts. In addition a number of proteins have been shown to interact with the IRES by north-western and UV cross-linking analysis. Investigation of the protein factors involved in c-myc IRES translation identified PCBP1 (Poly (rC) binding protein 1), PCBP2, HnRNPK (heterogeneous nuclear ribonucleoprotein K), UNR (upstream of N

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2

Beaudoin, Nicolas. "L’inhibition de c-MYC : l’approche MAX*." Mémoire, Université de Sherbrooke, 2015. http://hdl.handle.net/11143/6739.

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c-MYC est un facteur de transcription oncogénique dont l’expression est dérégulée dans 78% des gliomes. On observe d’ailleurs une corrélation positive entre sa surexpression et le grade des gliomes. De plus, cette surexpression serait essentielle à la survie des cellules souches tumorales, cellules qui seraient davantage résistantes à la chimiothérapie et à la radiothérapie en plus d’avoir un caractère plus invasif. Il a aussi été démontré que l’inhibition de c-MYC par ARN interférents peut sensibiliser les cellules cancéreuses à l’apoptose et réduire leur prolifération. S

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3

Hotti, Anneli. "Caspases in c-Myc-induced apoptosis." Helsinki : University of Helsinki, 2000. http://ethesis.helsinki.fi/julkaisut/laa/haart/vk/hotti/.

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4

Vervoorts, Jörg. "Molekulare Mechanismen der c-Myc-Transaktivierung Identifikation von hASH2, Nucleolin und CBP als neue c-Myc-Koaktivatoren /." [S.l. : s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=97123163X.

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5

Le, Quesne John P. C. "The c-myc IRES : structure and mechanism." Thesis, University of Leicester, 2000. http://hdl.handle.net/2381/29652.

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The proto-oncogene c-myc is central to the process whereby the cell commits itself to quiescence, differentiation, proliferation of apoptosis, and the expression of Myc protein is controlled at several levels, including translation. The 5' UTR of c-myc has been shown to contain an internal ribosome entry segment (IRES), allowing translation to proceed via an internally initiated mechanism. To determine the secondary structure of the IRES, structural data were obtained by chemical probing of 5' UTR RNA in vitro. These data were used as constraints upon the "mFold" RNA secondary structure predic

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6

Cannell, Ian G. "Regulation of c-Myc by miR-34c." Thesis, University of Nottingham, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.523121.

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7

Straaten, J. P. van. "Studies on the human c-myc gene product." Thesis, University of Cambridge, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.377708.

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8

Fleser, Angelica. "Resténose et expression des proto-oncogènes, c-myc, c-fos et c-jun." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/NQ35590.pdf.

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9

GIOVANNINI, VALENTINA, and VALENTINA GIOVANNINI. "NUOVE STRATEGIE ANTITUMORALI: PEPTIDI RETROINVERSI CHE MIMANO DOMINI FUNZIONALI SPECIFICI DI REGIONI DI C-MYC, COME INIBITORI COMPETITIVI DELLA PROTEINA C-MYC NATIVA." Doctoral thesis, La Sapienza, 2005. http://hdl.handle.net/11573/916799.

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10

Marhin, Wilson. "Characterization of c-myc as a transcriptional repressor." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq41469.pdf.

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11

Heath, Victoria J. "Inhibition of adipogenesis by the c-myc oncoprotein." Thesis, University of Glasgow, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.360306.

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12

Robinson, Helen. "Interaction between the proteins c-MYC and MLH1." Thesis, University of Glasgow, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.402010.

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13

Beer, Abigail J. "Development of an Inducible c-MYC Murine Model." The Ohio State University, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=osu1602754882137456.

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14

Dalgleish, Gillian Denise. "Localisation signals within the c-myc and c-fos 3'untranslated regions." Thesis, University of Aberdeen, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.481826.

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15

Marfil, Vives Vanessa. "Characterization of novel Hhex partners: SOX13 and c-Myc. New mechanism for the regulation of Wnt/TCF and c-Myc pathways." Doctoral thesis, Universitat Pompeu Fabra, 2010. http://hdl.handle.net/10803/22701.

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Hhex transcription factor is expressed in multiple endoderm-derived tissues, like the liver, where it is essential for proper development. The pleiotropic effect of Hhex in the embryo and its dual role as a transcriptional repressor/activator suggest the presence of different interaction partners capable of modulating its activity and function. In the current study we identified two new Hhex protein interactors: SOX13 and c-Myc. We show that Hhex interacts directly with SOX13. By doing so, Hhex sequesters SOX13 from the SOX13•TCF1 complex, overturning SOX13-dependent repression of the Wnt pa

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16

Gonzalez, Veronica. "Defining the Role of Nucleolin on the Transcriptional Regulation of c-MYC through Modulation of the c-MYC NHE III1 Element." Diss., The University of Arizona, 2010. http://hdl.handle.net/10150/195898.

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The activated product of the c-MYC proto-oncogene is one of the strongest known activators of carcinogenesis. It has been estimated that as many as one-seventh of all cancer deaths are associated with alterations in the c-MYC gene or its expression [1]. Therefore, understanding the regulation of c-MYC expression is a key factor in understanding carcinogenesis in many histologic classes of malignancy. The nuclease hypersensitive element (NHE) III₁ region of the c-MYC promoter has been shown to be particularly important in regulating c-MYC expression. Specifically, the formation of a G-quadruple

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17

Liu, Qingyuan. "Epigenetic Regulation of hTERT in Human Acute Promyelocytic Leukemia Cell Line NB4 and Role of c-Myc." Thesis, Paris 11, 2014. http://www.theses.fr/2014PA11T103.

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La régulation de la télomérase s’effectue à de nombreux niveaux dont la transcription de la sous-Unité catalytique (hTERT). Les travaux du laboratoire effectués sur les cellules NB4, modèle de Leucémie Aiguë Promyélocytaire (LAP), ont montré que l'acide rétinoïque tout-Trans (ATRA) réprime la transcription de hTERT. Cette répression peut être associée à la différenciation (cas des cellules NB4) ou en être dissociée conduisant à la mort des cellules (cas des cellules NB4-LR1 résistantes à la maturation induite par l’ATRA). A partir de la lignée NB4-LR1 a été sélectionnée la lignée NB4-LR1SFD ré

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18

Ferrari, Ana Luiza. "Expressão dos protooncogenes c-fos, c-myc e c-jun em miométrio e mioma humanos." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2006. http://hdl.handle.net/10183/6629.

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19

Beaulieu, Marie-Ève. "Biologie structurale de c-Myc et Max évidences pour un nouveau mécanisme de transrépression par Myc." Thèse, Université de Sherbrooke, 2011. http://hdl.handle.net/11143/5809.

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The transcription factor c-Myc plays a central role in cell growth and proliferation owing to the large number of genes it transactivates or transrepresses and to the fact that these genes are in turn implicated in these cellular processes. Also, c-Myc's deregulation and/or overexpression contribute to most aspects of tumoral cellular biology. As a heterodimer with Max, c-Myc activates the transcription of genes leading to cell proliferation and represses the transcription of cytostatic genes such as p15[superscript ink4b] and p21[superscript CiP1]. In contrast to the transactivation mechanism

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20

Pulverer, Bernd J. "Regulation of nuclear protooncogens c-Jun and c-Myc by protein serine-kinases." Thesis, Open University, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.315301.

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21

Lux, Christoph. "Untersuchungen zur transkriptionellen Regulation des Proto-Onkogens c-myc." Diss., lmu, 2005. http://nbn-resolving.de/urn:nbn:de:bvb:19-44401.

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22

Zhang, Yandong. "Pim kinases phosphorylate p21 CiP1/WAF1 and c-Myc." Online access for everyone, 2007. http://www.dissertations.wsu.edu/Dissertations/Summer2007/y_zhang_062907.pdf.

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23

Royla, Nadine [Verfasser]. "Analysis of metabolic feedbacks regulating c-MYC / Nadine Royla." Berlin : Freie Universität Berlin, 2018. http://d-nb.info/1170814441/34.

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24

Riley, Timothy E. W. "Post-transcriptional regulation of the c-myc proto-oncogene." Thesis, University of Cambridge, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.257194.

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25

Ferre, François. "Pouvoir transformant et régulation de l'oncogène humain c-myc." Lille 1, 1986. http://www.theses.fr/1986LIL10081.

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26

Lucas, John Mark. "Regulation of the C-MYC and FGF-4 Oncogenes /." The Ohio State University, 1994. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487859879939229.

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27

Ferre, François. "Pouvoir transformant et régulation de l'oncogène humain c-myc." Grenoble 2 : ANRT, 1986. http://catalogue.bnf.fr/ark:/12148/cb375975871.

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28

Arabi, Azadeh. "Regulation of the ribosomal RNA transcription by c-MYC oncoprotein /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-947-5/.

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29

TEYSSIER, MAGALI. "Expression des oncogenes c-fos et c-myc et immunomodulation de la lignee monocytaire." Paris 11, 1992. http://www.theses.fr/1992PA112239.

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The p388d1 murine macrophage cell line has been chosen to study events resulting from the transduction of immunomodulatory signals. Owing to the frequent implication of the c-myc gene in the tumorigenicity of hematopoietic cells, the normal c-myc status in this cell line is demonstrated by southern analysis. The early modulation of the c-fos and c-myc proto-oncogene expression has been studied by northern analysis and the dna synthesis by #3h-thymidine incorporation after treatment of p388d1 cells by tpa, calcium ionophore a23187, mdp and csf-1. No correlation could be evidenced in this cell l

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30

Eriksson, Jonathan. "WT1 påverkar proliferationen för cancercellinjer troligen via reglering av c-Myc." Thesis, Umeå universitet, Biomedicinsk laboratorievetenskap, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-58625.

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31

Sunohara, Maxwell. "Targeting the Process of c-MYC Stabilization in Chronic Myelogenous Leukemia." Thesis, Université d'Ottawa / University of Ottawa, 2017. http://hdl.handle.net/10393/35884.

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Currently there is no curative therapy for Chronic Myelogenous Leukemia (CML), and patients must remain on the current prescribed treatment, tyrosine kinase inhibitors (TKI), indefinitely. Although many patients can survive in the chronic phase of the disease under TKI treatment, some patients do progress to the terminal blast crisis phase of the disease. Patients in this terminal phase do not respond to TKI treatment. We evaluated the therapeutic benefit of targeting the oncogene c-MYC in CML, using the CML cell line K562. This was achieved by inhibiting the enzyme O-linked β-N-acetylglucosam

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32

Lima, Caroline Rocha de Oliveira. "Classificação morfológico, critérios de malignidade, expressão gênica de C-MYC e imunoistoquímica de C-MYC, p53, p21 e p27 no tumor venéreo transmissível canino." Universidade Federal de Goiás, 2013. http://repositorio.bc.ufg.br/tede/handle/tede/3258.

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33

Arnaud, Nicolas. "Les lymphomes B diffus à grandes cellules de type activé : rôle de NF-κB et c-Myc". Thesis, Limoges, 2017. http://www.theses.fr/2017LIMO0105/document.

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A l’instar du lymphome de Burkitt (LB) avec la translocation de MYC, les lymphomes diffus à grandes cellules B (DLBCL) par d'autres mécanismes (mutation, amplification, dérégulation du promoteur) sont associés à une dérégulation de c-Myc, facteur de transcription maitre de la prolifération. Les DLBCL sont classés en deux sous-groupes: « centre germinatif » (GCB) et « cellule B activée » (ABC) avec activation constitutive de NF-κB. Cette activation constitutive de NF-κB peut être le résultat d'altérations génétiques (MYD88, A20, TRAF2 et TRAF5) ou de l'activation du BCR ou CD40. Ces caractérist

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34

Hoelzel, Michael. "Regulation von Teilungswahrscheinlichkeit und Zellzyklusdauer durch das Onkoprotein c-Myc." Diss., lmu, 2004. http://nbn-resolving.de/urn:nbn:de:bvb:19-23912.

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35

Helander, Sara. "Structural biology of transcriptional regulation in the c-Myc network." Doctoral thesis, Linköpings universitet, Kemi, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-106185.

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The oncogene c-‐Myc is overexpressed in many types of human cancers and regulation of c-‐Myc expression is crucial in a normal cell. The intrinsically disordered N-‐terminal transactivation domain interacts with a wide range of proteins regulating c-‐Myc activity. The highly conserved Myc box I region includes residues Thr58 and Ser62, which are involved in the phosphorylation events that control c-‐Myc degradation by ubiquitination. Aggressive cell growth, leading to tumor formation, occurs if activated c-‐ Myc is not degraded by ubiquitination. Such events may be triggered by defects i

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36

Paulin, Fiona E. M. "A study of c-myc translational regulation in multiple myeloma." Thesis, University of Leicester, 1997. http://hdl.handle.net/2381/29701.

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In cell lines derived from patients with multiple myeloma (MM), a B-cell neoplasia, a 10-20 fold elevation in the level of c-myc protein has been observed. This was not accompanied by a concomitant increase in c-myc mRNA levels and there was no alteration in the half life of the protein suggesting that a translational mechanism could be responsible for the elevated c-myc protein levels.;Sequence analysis of c-myc exon 1, a region previously implicated in translational control, revealed no gross sequence abnormalities of the c-myc gene in the MM cell lines. However, in 4 out of 5 MM cell lines

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37

Labrie, Mireille. "Rôle des protéines BH3 dans l'apoptose dépendante de C-MYC." Thesis, Université Laval, 2005. http://www.theses.ulaval.ca/2005/23275/23275.pdf.

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La dérégulation de l'oncogène c-myc sensibilise les cellules à la mort programmée induite par le cisplatine en agissant sur la voie mitochondriale de l'apoptose. Les membres de la famille de protéines Bcl-2 sont essentiels à la régulation de ce sentier apoptotique. Parmi ceux-ci on retrouve une sous-famille de protéines pro-apoptotiques incluant Bid, Bad, Bim, Noxa et PUMA qui ont comme caractéristique de posséder un domaine BH3 unique. Suite à divers stress cellulaires, ces protéines BH3 interagissent avec les autres membres de la famille Bcl-2 via le domaine BH3 et favorisent ainsi la sort

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38

Ryan, Kevin M. "Regulation of myeloid differentiation by c-myc and its antagonists." Thesis, University of Glasgow, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318117.

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39

Kenneth, Niall S. "Mechanisms of RNA polymerase III transcriptional activation by c-Myc." Thesis, University of Glasgow, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.439250.

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40

Littlewood, Trevor David. "An investigation of the functions of the c-Myc oncoprotein." Thesis, Anglia Ruskin University, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.357338.

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41

Lapham, Abigail. "Mechanisms of transcriptional repression by the proto-oncogene c-Myc." Thesis, University of Southampton, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.420247.

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42

Seth, Alpna. "Functional Analysis of the c-MYC Transactivation Domain: A Dissertation." eScholarship@UMMS, 1992. https://escholarship.umassmed.edu/gsbs_diss/315.

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Many polypeptide growth factors act by binding to cell surface receptors that have intrinsic tyrosine kinase activity. Binding of these growth factors to their cognate receptors results in the initiation of mitogenic signals which then get transduced to the interior of the cell. A critical target for extracellular signals is the nucleus. A plethora of recent evidence indicates that extracellular signals can affect nuclear gene expression by modulating transcription factor activity. In this study, I have determined that the transactivation domain of c-Myc (protein product of the c-myc proto-onc

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43

Penglong, Tipparat. "Molecular Basis of Erythroid Cell Proliferation and Differentiation." Thesis, Paris 11, 2015. http://www.theses.fr/2015PA11T022.

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Pour assurer la production de milliards de globules rouges, l’érythropoièse doit parfaitement contrôler les processus de prolifération et de différenciation. Ces deux processus sont régulés par l’expression de gènes spécifiques dépendant d’une coordination entre l’activité des facteurs de transcription (FT) et les fonctions épigénétiques portées par exemple par les protéines à bromodomaine. Cette étude se concentre sur les conséquences de l’association ou la dissociation du FT clef de l’érythropoièse GATA-1 avec les FT déterminant pour le cycle cellulaire, pRb et E2F. Dans la première partie d

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44

Veyrune, Jean-Luc. "Devenir des ARNm c-fos et c-myc dans le cytoplasme : dégradation, traduction et localisation." Montpellier 2, 1996. http://www.theses.fr/1996MON20218.

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Les messagers des proto-oncogenes c-fos et c-myc font partie des arnm eucaryotes les plus instables. Cette instabilite a ete reliee a differentes sequences localisees soit dans la partie 3' non codante comprenant une region riche en au, soit dans les parties codantes du messager. Il a ete montre que la partie 3' non codante de ces messagers confere une tres mauvaise efficacite de traduction. De plus nous savons que l'utilisation de drogues bloquant la synthese des proteines (puromycine, cycloheximide) entraine le phenomene de super induction du a une stabilisation des messagers. Ces donnees ex

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45

Cheung, Ronald Se-Yuen. "Contrasting tumorigenic growth interactions of apoptosis-deficient MYC alleles with Transforming Growth Factor-alpha /." Thesis, Connect to this title online; UW restricted, 2006. http://hdl.handle.net/1773/5000.

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46

Al-Sallami, Dheyaa Abdul Salam. "INTERROGATION OF CHROMOSOME 8Q24.21 REGION FOR GENES CRUCIAL FOR CARCINOGENESIS USING CRISPR-CAS9 APPROACHES." OpenSIUC, 2016. https://opensiuc.lib.siu.edu/theses/1994.

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8q24.21 is a highly amplified region in cancer and associated with many epithelial cancer such as bladder, breast, colorectal and prostate cancer. The proto-oncogene c-myc is located in this region and surrounded by many lncRNAs genes such as PCAT family, CCAT family, PRNCR1. In this study, we used CRISPR-Cas9 constructs to knock out PCAT1, PRNCR1, CASC8, CASC11 and also the sequences between PCAT1-CASC11 and CASC8-CASC11in the prostate cancer cell PC3. The transfected cells with CRISPR-Cas9 targeting CASC11 gene had less proliferation ability comparing with the transfected cells with CRISPR-C

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47

Kuschak, Theodore I. "c-Myc dependent genomic instability of the ribonucleotide reductase R2 gene." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0020/NQ53061.pdf.

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48

Chana, Jagdeep. "The prognostic and therapeutic significance of C-MYC expression in melanoma." Thesis, Imperial College London, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.314348.

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49

Ross, David Anthony. "Clinical significance of the p53 and c-myc proteins in melanoma." Thesis, University College London (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.338852.

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50

Lombardi, Olivia. "Investigating the role of mRNA capping enzyme in C-MYC function." Thesis, University of Dundee, 2017. https://discovery.dundee.ac.uk/en/studentTheses/4816aeec-c481-4494-9a07-56e74a83c08e.

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C-MYC is a transcription factor and a potent driver of many human cancers. In addition to regulating transcription, C-MYC promotes formation of the mRNA cap which is important for transcript maturation and translation. However, the mechanistic details of C-MYC-dependent mRNA capping are not fully understood. Since anti-cancer strategies to directly target the C-MYC protein have had limited success, enzymatic co-factors or effectors of C-MYC present attractive alternatives for therapeutic intervention of C-MYC-driven cancers. mRNA capping enzyme (CE) initiates mRNA cap formation by catalysing t

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