Dissertations / Theses: 'Oncogene expression'

1

Ellis, D. K. "Cellular oncogene expression during retinal transdifferentiation." Thesis, University of Nottingham, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.371121.

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2

Chan, Yuk Fai. "Manipulation of EWS oncogene expression using RNAi /." View abstract or full-text, 2005. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202005%20CHAN.

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3

Appleby, Mark William. "Oncogene expression and the modulation of keratinocyte self renewal." Thesis, University of Cambridge, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.306476.

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4

Watson, Dorothy M. A. "Cyclic nucleotide binding and oncogene expression in breast cancer." Thesis, University of Edinburgh, 1989. http://hdl.handle.net/1842/19398.

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5

Radhakrishnan, Vijayababu, Charles Putnam, Wenqing Qi, and Jesse Martinez. "P53 suppresses expression of the 14-3-3gamma oncogene." BioMed Central, 2011. http://hdl.handle.net/10150/610345.

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BACKGROUND:14-3-3 proteins are a family of highly conserved proteins that are involved in a wide range of cellular processes. Recent evidence indicates that some of these proteins have oncogenic activity and that they may promote tumorigenesis. We previously showed that one of the 14-3-3 family members, 14-3-3gamma, is over expressed in human lung cancers and that it can induce transformation of rodent cells in vitro.METHODS:qRTPCR and Western blot analysis were performed to examine 14-3-3gamma expression in non-small cell lung cancers (NSCLC). Gene copy number was analyzed by qPCR. P53 mutations were detected by direct sequencing and also by western blot. CHIP and yeast one hybrid assays were used to detect p53 binding to 14-3-3gamma promoter.RESULTS:Quantitative rtPCR results showed that the expression level of 14-3-3gamma was elevated in the majority of NSCLC that we examined which was also consistent with protein expression. Further analysis of the expression pattern of 14-3-3gamma in lung tumors showed a correlation with p53 mutations suggesting that p53 might suppress 14-3-3 gamma expression. Analysis of the gamma promoter sequence revealed the presence of a p53 consensus binding motif and in vitro assays demonstrated that wild-type p53 bound to this motif when activated by ionizing radiation. Deletion of the p53 binding motif eliminated p53's ability to suppress 14-3-3gamma expression.CONCLUSION:Increased expression of 14-3-3gamma in lung cancer coincides with loss of functional p53. Hence, we propose that 14-3-3gamma's oncogenic activities cooperate with loss of p53 to promote lung tumorigenesis.

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6

Williams, Alistair Robert William. "Expression of oncogenes in human colorectal neoplasms." Thesis, University of Edinburgh, 1988. http://hdl.handle.net/1842/19415.

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7

Amouyel, Philippe. "Expression des proto-oncogenes ets dans les astrocytes et dans les tumeurs astrocytaires." Lille 2, 1988. http://www.theses.fr/1988LIL2M054.

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8

Ritchie, Andrew John. "Endocrinology, oncogene expression and outcome in carcinoma of the lung." Thesis, Queen's University Belfast, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.357457.

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9

Richards, Sally. "Inhibition of oncogene expression by the formation of Triplex DNA." Thesis, Institute of Cancer Research (University Of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368703.

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10

Faulkner, Lee. "Expression of the c-fgr proto-oncogene in monoblastoid cells." Thesis, University College London (University of London), 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.309109.

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11

Marcos-Gutierrez, Camelia Victoria. "Expression, function and conservation of the c-Ret proto-oncogene." Thesis, Open University, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.361457.

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12

Chung, Maureen. "Expression of the c-fos proto-oncogene, mutant p53 anti-oncogene and statin in colorectal carcinoma and adjacent mucosa." Thesis, McGill University, 1992. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=56961.

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The purpose of this study was to provide evidence for a field defect around colorectal carcinomas using c-fos, mutant p53 and statin markers. Tissue from ten colorectal carcinomas and mucosa at 1, 5 and 10 cm from the primary lesion was obtained from surgical specimens and frozen in liquid nitrogen. Detergent-extracted protein was separated by electrophoresis through polyacrylamide gells and western blots performed using monoclonal antibodies against c-fos, mutant p53 and statin. Expression of c-fos within the carcinoma was increased relative to its expression at 1 cm, which was increased relative to 5 or 10 cm. The reverse results were obtained for statin with the lowest expression detected in the carcinoma, intermediate expression at 1 cm, and highest values at 5 and 10 cm. Increased mutant p53 expression was detected only within the carcinoma. These results indicate that c-fos gain and statin loss may occur before p53 mutation and be initial steps in oncogenesis.

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Demoly, Pascal. "Expression du proto-oncogene c-fos dans l'epithelium bronchique de l'asthmatique." Montpellier 1, 1992. http://www.theses.fr/1992MON11169.

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Menzel, Garry Edward. "Regulation of proto-oncogene expression during mitogenic activation of T-cells." Thesis, University of Cambridge, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.315120.

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15

Shipillis, Nicholas. "Investigation of system properties related to MYCN oncogene expression in neuroblastoma." Thesis, University of Manchester, 2012. https://www.research.manchester.ac.uk/portal/en/theses/investigation-of-system-properties-related-to-mycn-oncogene-expression-in-neuroblastoma(2e3ba06b-faec-449e-85be-730213e697b9).html.

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Neuroblastoma (NB) is one the most common cancers in infancy and childhood, andpossession of amplified MYCN gene sequence (gene locus 2p24) is related toaggressive disease and poor prognosis, with a clear distinction established regardingthe survival of patients based on the gene copy-number of MYCN. However, theexpression of MYCN has been reported to vary between patients of even the sameNB subgroups and more importantly its significance in relation to NB prognosis isstill not clearly established with various reports presenting contradicting results.In this study, a bottom-up Systems Biology approach is suggested for studying boththe significance of MYCN expression, but also the distribution of control in therelated pathways that regulate this expression. An initial model was constructeddescribing the basic steps in MYCN expression and it was parameterised with valuesobtained from the literature. The results from the model simulations and analysisgenerated the hypothesis that the expression of MYCN cannot be used exclusively asa predictive factor without taking into account the relative levels of its dimerisationpartner, the protein MAX. Additionally, it was predicted that the amplification ofMYCN had a more pronounced relative effect at lower rather than at higher MYCNgene copy numbers.In order to create separate models for 4 NB cell-lines, it was necessary to performabsolute measurements for MYCN at the DNA, mRNA and protein level, as well asfor the MAX protein. The MYCN gene copy numbers were measured using theqPCR method, while a new data analysis method was suggested for performingabsolute quantification with the use of house-keeping genes, appropriate statisticalmethods and no reference samples. The relative amounts of MYCN mRNA werealso measured using qPCR and the results obtained were in agreement with thesuggested levels from the literature.The absolute measurement of the N-Myc and MAX proteins was attempted usingtwo complementary methods, western blots and ELISA. A series of optimisationexperiments and data analysis steps were taken that resulted in the refinement of theexperimental conditions to the point where they can be used for successfulquantification of the absolute levels of the N-Myc protein. Alternatively, theprocedure used for the MAX protein proved problematic and was not as successful.Overall, this study was successful in becoming the first step for an expanded bottomupsystems biology study regarding the significance of MYCN expression in NB.The combination of both the modelling and experimental parts of this workillustrated some of the potential benefits of Systems Biology approaches in studyingdisease. In this case the resulting model, once fully parameterised with experimentaldata, can be expanded in a number of suggested ways that address questions like therole and control of MYCN expression in relation to the cell-cycle deregulation ormulti-drug resistance in NB, giving in the process a better understanding regardingsuitable treatment targets for individual NB cases.

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16

El, Khyari Saïd. "Implication des oncogenes nucleaires et de surface dans les mecanismes cellulaires de chimioresistance." Aix-Marseille 2, 1993. http://www.theses.fr/1993AIX22951.

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Tuthill, Matthew Charles. "N-myc oncogene expression in neuroblastoma is dependent on Sp1 and Sp3." Thesis, University of Hawaii at Manoa, 2003. http://hdl.handle.net/10125/987.

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Regulation of N-myc oncogene expression is an important determinant of the biological behavior of neuroblastoma. The N-myc promoter contains several potential binding sites for transcription factors of the Sp1 family. Mutation of a CT-box motif contained within a 26 base pair region required for N-myc downregulation by retinoic acid decreased basal transcriptional activity and altered DNA-protein interactions of the promoter, while mutations flanking this motif did neither. On gel shift this region generated 3 specific DNA-protein complexes that were reliant on wild type sequence of the core CT element within it. Both Spl and Sp3 bound to the wild type probe as distinct complexes in specifically retarded bands, while neither protein was present on mutated sequences. Lysates from Drosophila S2 cells expressing exogenous Sp1 and Sp3 proteins were able to reproduce the gel shift complexes seen with neuroblastoma nuclear extract. Transient transfections of S2 cells showed that individually or together, Sp1 and Sp3 were able to trans-activate a N-myc CT-box-containing luciferase reporter construct in a dose-dependent manner. Conversely, transfection of CT-box oligonucleotide was able to decrease endogenous N-myc expression in neuroblastoma cells. Together these results suggest that the CT-box element serves a critical functional role, and in the basal state allows for N-myc transactivation by Spl and Sp3.

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Rao, Mira A. "Regulated expression of the v-rel oncogene in vitro and in vivo." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape8/PQDD_0026/MQ50863.pdf.

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19

Liang, Huiling. "Genomic structure and expression of the MDM2 proto-oncogene in human cancer." Thesis, University of Newcastle Upon Tyne, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.297574.

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20

Candelière, G. Antonio (Giuseppe Antonio). "Expression of the c-fos proto-oncogene during normal and pathological bone development." Thesis, McGill University, 1994. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=28429.

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The expression of the c-fos proto-oncogene during normal and pathological bone development was studied. The regulation of c-fos expression in bone cells by calcitriol and its contribution to the etiology of fibrous dysplasia was addressed. We have shown that treatment of osteoblasts with calcitriol, the active form of vitamin D, transiently stimulated the expression of c-fos, fos-B, c-jun and jun-B in a specific and dose-dependent manner. The expression of the Fos protein correlated with the expression of the c-fos gene. Finally, calcitriol appeared to modulate c-fos transcription in osteoblasts, whereas it stimulated c-jun and jun-B expression by a post-transcriptional mechanism distinct from mRNA stabilization. The transcriptional stimulation of c-fos was explored further and we identified a novel vitamin D response element (VDRE) in the c-fos promoter. We report that a 36 bp sequence centered around position-161 upstream of the c-fos transcription start site is responsive to 1,25-(OH)$ rm sb2D sb3$ in osteoblastic cells. This sequence binds the VDR, and mutations that abrogate binding to this element also abolish transcriptional activation by 1,25-(OH)$ sb2D sb3,$ demonstrating that we have identified a functional VDRE. Structure-function analysis revealed that the c-fos VDRE has an unusual structure that does not correspond to the classical direct repeat (DR)-type elements. Supporting this observation, our results show that the VDR requires a novel dimerizing partner to bind the c-fos VDRE. Finally, we report increased expression of c-fos in bone lesions from patients with fibrous dysplasia. The elevated c-fos mRNA levels were detected only in fibrous dysplasia lesions and not in samples from patients with other bone diseases where high bone turnover and fibrous marrow tissue are present. Our results support the implication of c-fos in the etiology of fibrous dysplasia.

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21

Grover, Rajiv. "Oncogene expression in malignant melanoma : markers of prognosis and targets for gene therapy." Thesis, Queen Mary, University of London, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.266579.

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22

Feller, J. Kyle. "Correlation of amplification and expression of the c-myc oncogene in Kaposi's sarcoma." Thesis, Boston University, 2012. https://hdl.handle.net/2144/12373.

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Thesis (M.A.)--Boston University PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.
The c-myc proto-oncogene is involved in various cellular processes including cell growth, proliferation, and apoptosis. Overexpression and deregulated expression of the gene have been previously linked to several lineage-unrelated, aggressive, poorly differentiated tumors. Oncogenic expression of c-myc has also been implicated in several vascular neoplasms as having a crucial role in angiogenesis. This gives c-myc a dual oncogenic function in that tumor growth requires both cell proliferation and angiogenesis to ensure survival and confer an effective malignancy. In vitro studies have shown that the c-Myc protein is an important regulatory molecule of spindle cell proliferation and migration in Kaposi's sarcoma (KS), an angioproliferative tumor that is commonly associated with HIV. In light of the above and recent findings demonstrating amplification of c-myc in select angiosarcomas secondary to irradiation or chronic lymphedema, our primary aim was to ascertain the same in KS. We also attempted to determine what correlation existed, if any, between the immunohistochemical (IHC) expression of the c-Myc protein and c-myc gene copy amplification using fluorescent in situ hybridization (FISH). Samples analyzed during this study included archival tissue samples of KS (N=24 ). For FISH analyses, a dual-labeled technique was employed and probes against the c-myc gene and chromosome 8 (CEP-8) were used. For IHC, the monoclonal anti-c-myc antibody, 9E10, was used and tissue from hemangiomas (N=11) and non-radiation induced angiosarcomas (N=6) served as the controls. PCR for detection of KS-associated herpesvirus (KSHV) DNA was performed on all KS cases. While FISH analyses revealed no amplification of c-myc in any of the cases of KS, IHC analyses revealed positive staining for c-Myc in 13/24 cases (54%) with stain localization throughout the cell. As such, no correlation could be found between gene amplification and protein expression. KSHV-PCR analyses revealed that 19/24 cases (79%) were positive for KSHV-DNA. Ten of 24 cases (42%) were positive for c-Myc IHC and KSHV-PCR, while one case (4%) was negative for both indicating a lack of correlation (using McNemar's test for statistical analysis) between c-Myc IHC protein levels and presence of KSHVDNA. Our findings indicate that c-myc gene amplification is not normally found in KS and cannot be correlated with the expression of the c-Myc protein. Thus, unlike other tumors we have discussed where gene amplification was a common occurrence; it seems to have little clinical significance in KS. The absence of c-myc amplification raises the question of why 54% of the samples in this study still exhibited protein expression as determined by IHC. To grasp a further understanding of what is truly going on in these cases, it would be necessary to use techniques such as RT-PCR or in situ hybridization to study c-myc at the RNA level.

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23

Lanaud, Philippe. "Etude de l'expression neuronale des oncogenes a expression immediate et precoce dans differents modeles d'epilepsie chez le rat." Besançon, 1992. http://www.theses.fr/1992BESA3711.

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24

Bauters, Christophe. "Expression des oncogenes nucleaires c-myc et c-fos dans les surcharges hemodynamiques du coeur de rat adulte." Lille 2, 1990. http://www.theses.fr/1990LIL2M006.

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25

MARECHAL, GAEL. "Oestrogenes et expression de l'oncogene c-fos dans les cellules d'endometres de cobaye en culture primaire." Besançon, 1991. http://www.theses.fr/1991BESA3086.

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26

Galdemard, Catherine. "Regulation transcriptionnelle de l'expression du proto-oncogene fgf-3 dans les cellules d'adenocarcinome du colon humain : bases fondamentales de l'oncogenese)." Paris 11, 1997. http://www.theses.fr/1997PA11T006.

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Leroy, Janine Marie Gisele. "Controle da expressão de TRAIL, OSM, FAIM e NIPA pelo oncogene bcr-abl." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/42/42133/tde-17092008-131050/.

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A leucemia mielóide crônica (LMC) é uma doença mieloproliferativa e sua patogênese está associada à expressão de um neogene, bcr-abl, que codifica uma proteína tirosina quinase Bcr-Abl. Esse trabalho tem como objetivos o estudo dos mecanismos envolvidos na resistência à morte das células Bcr-Abl positivas e a identificação de alterações gênicas nessas células. Dados de expressão gênica global obtidos por \"microarray\" mostraram uma superexpressão nas células HL-60.Bcr-Abl com relação a HL-60 dos genes faim e nipa, que foi confirmada por qRT-PCR em diferentes linhagens celulares Bcr-Abl positivas. Já os genes de trail e osm, apresentaram uma diminuição significativa em HL-60.Bcr-Abl, que foi confirmada para trail, porém osm não teve seu resultado validado. A avaliação da expressão dos genes em células de pacientes portadores de LMC, em diferentes fases da doença também foi estudada. Com esses resultados, o presente estudo visa a melhor compreensão de como alterações na expressão desses genes contribuem na fisiopatologia da LMC.
Chronic myelogenous leukemia (CML) is a stem cell disease characterized by the presence of the Bcr-Abl oncoprotein, which is the cause of the malignant transformation and the extreme resistance to apoptosis displayed by CML patients. Our aim was to analyze the alteration in global gene expression in Bcr-Abl expressing cells. Data obtained from microarray analysis showed significant up-regulation of nipa and faim in HL60.Bcr-Abl and down-regulation of osm and trail. These results were further confirmed by Real-Time PCR to nipa, faim and trail, but not for osm expression in HL-60.Bcr-Abl cells. To evaluate the potential of some of the modified genes as therapeutic targets or prognostic markers for CML, we also analyzed the expression of these genes in samples from CML patients.

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Opitz, Armin Walter. "Structural and functional investigations of a molecular imaging nanoparticle for magnetic resonance imaging of oncogene expression in the pancreas." Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 490 p, 2008. http://proquest.umi.com/pqdweb?did=1459924631&sid=13&Fmt=2&clientId=8331&RQT=309&VName=PQD.

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Thesis (Ph.D.)--University of Delaware, 2008.
Principal faculty advisors: Norman J. Wagner, Dept. of Chemical Engineering, University of Delaware; Eric Wickstrom, Dept. of Biochemistry and Molecular Biology, Thomas Jefferson University. Includes bibliographical references.

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Ritchie, Andrew John. "Endocrinology, oncogene and tumour suppressor gene expression in Barrett's oesophagus, oesophageal and gastric cardia carcinoma." Thesis, Queen's University Belfast, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.238950.

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30

Bradbury, Andrew W. "Cyclic AMP binding proteins and ras p21 oncogene expression in human colorectal cancer and mucosa." Thesis, University of Edinburgh, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.531024.

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OLIVEIRA, Talita Helena Araújo de. "Avaliação e correlação do perfil de expressão do oncogene E5 do papilomavírus humano e do miRNA- 203 do hospedeiro na carcinogênese cervical." Universidade Federal de Pernambuco, 2016. https://repositorio.ufpe.br/handle/123456789/19531.

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Submitted by Fabio Sobreira Campos da Costa (fabio.sobreira@ufpe.br) on 2017-07-12T15:28:57Z No. of bitstreams: 2 license_rdf: 811 bytes, checksum: e39d27027a6cc9cb039ad269a5db8e34 (MD5) Dissertação Final - talita.pdf: 2175488 bytes, checksum: 400478ce39315d3a295c2c268c514539 (MD5)
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CNPQ
O HPV é o principal fator transformadordo câncer cervical. No seu ciclo viral é expressa a oncoproteína E5, responsável por várias alterações na célula hospedeira e,foi sugerido in vitro, que ela altera a proliferação celular através da regulação negativa do microRNA-203, que em condições normais atua inibindo a proliferação e condicionando a diferenciação dos queratinócitos. Entretanto os mecanismos que envolvem E5 e o microRNA-203 ainda não estão bem elucidados. Este estudo tem como objetivo avaliar o perfil de expressão da oncoproteína E5 e do microRNA-203 em biópsias de colo uterino, observando a existência de correlação entre ambos. A expressão gênica relativa do microRNA-203 e E5 nas amostras clínicas (n=90), referente a todas as etapas da carcinogênese cervical (Normal, NIC I, NIC II, NIC III e câncer), foi obtida por qPCR.As análises mostraram uma diminuição do perfil de expressão do microRNA-203 no câncer em comparação com amostras normais (p<0,01) enquanto o RNAm de E5 do HPV 16 aumentou sua expressão em NIC III e no câncer em relação a lesões de baixo grau (NIC I) (p<0,001 e p<0,01, respectivamente). Os resultados apontam que o microRNA-203 está regulado negativamente no câncer cervical, porém sem correlação estatisticamente significante com a expressão de E5. O perfil apresentado nos diferentes estágios sugere que omicroRNA-203e o oncogene E5 são capazes de diferenciar estágios da carcinogênese cervical.
The Human papillomavirus (HPV) is the main transforming factor in cervical cancer. The HPV expresses the oncoprotein E5 which is responsible for several changes in the host cells and recent in vitro studies have suggested that it plays a role in the regulation of cell proliferation through microRNA-203. This microRNA acts by inhibiting cell proliferation and stimulating cell differentiation in normal conditions. However, the mechanisms involving E5 and microRNA-203 are not yet well elucidated. The aim of the present study is to evaluate both E5 and microRNA-203 expression profiles in biopsies of women from Pernambuco andobserve if there is any correlations between them. Expression of microRNA-203 in clinical samples (n=90), observed at all carcinogenic process (Normal, CIN I, CIN II, CIN III and cancer), was obtained by real-time qPCR. The analysis here performed demonstrates a decreased expression of microRNA-203 in cancer samples when compared to the normal ones (p<0,01) while E5 increased its expression in CIN III and cancer when compared to low-grad lesion (CIN I) (p<0,001 and p<0,01, respectively). Our data shows that miR-203 is downregulated in cancer, although no statistical significant correlation was found between its expression and E5.Both expression profiles suggest their ability to differentiatelesions.

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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 of cumulative cooperating mutations in the pre-leukemic progenitor cells that enhance their expansion to induce leukemia is not known. The standard treatment for inv(16) AML is based on the use of non-selective cytotoxic chemotherapy, resulting in a good initial response, but with limited long-term survival. Therefore, there is a need for developing targeted therapies with improved efficacy in leukemic cells and minimal toxicity for normal cells. Here, we used conditional Nras+/LSL-G12D; Cbfb+/56M; Mx1Cre knock-in mice to show that allelic expression of oncogenic N-RasG12D expanded the multi-potential progenitor (MPP) compartment by 8 fold. Allelic expression of Cbfbeta-SMMHC increased the MPPs and short-term hematopoietic stem cells (ST-HSCs) by 2 to 4 fold both alone and in combination with N-RasG12D expression. In addition, allelic expression of oncogenic N-RasG12D and Cbfbeta-SMMHC increases survival of pre-leukemic stem and progenitor cells. Differential analysis of bone marrow cells determined that Cbfb+/MYH11 and Nras+/G12D; vii Cbfb+/MYH11 cells included increased number of blasts, myeloblasts and promyelocytes and a reduction in immature granulocytes, suggesting that expression of N-RasG12D cannot bypass Cbfbeta-SMMHC driven differentiation block. N-RasG12D and Cbfbeta-SMMHC synergized in leukemia, in which Nras+/G12D; Cbfb+/MYH11 mice have a shorter median latency than Cbfb+/MYH11 mice. In addition, the synergy in leukemogenesis was cell autonomous. Notably, leukemic cells expressing N-RasG12D and Cbfbeta-SMMHC showed higher (over 100 fold) leukemia-initiating cell activity in vivo than leukemic cells expressing Cbfbeta-SMMHC (L-IC activity of 1/4,000 and 1/528,334, respectively). Short term culture and biochemical assays revealed that pre-leukemic and leukemic cells expressing N-RasG12D and Cbfbeta-SMMHC have reduced levels of pro-apoptotic protein Bim compared to control. The Nras+/G12D; CbfbMYH11 pre-leukemic and leukemic cells were sensitive to pharmacologic inhibition of MEK/ERK signaling pathway with increasing apoptosis and Bim protein levels but not sensitive to PI3K inhibitors. In addition, knock-down of Bcl2l11 (Bim) expression in Cbfbeta-SMMHC pre-leukemic progenitors decreased their apoptosis levels. In collaboration with Dr. John Bushweller’s and other research laboratories, we recently developed a CBFbeta-SMMHC inhibitor named AI-10-49, which specifically binds to CBFbeta-SMMHC, prevents its binding to RUNX proteins and restores CBF function. Biochemical analysis in human leukemic cells showed that AI-10-49 has significant specificity in reducing the viability of leukemic cells expressing CBFbeta-SMMHC (IC50= 0.83μM), and negligible toxicity in normal cells. Likewise, mouse Nras+/G12D; viii Cbfb+/MYH11 leukemic cells were sensitive to AI-10-49 (IC50= 0.93μM). By using the NrasLSL-G12D; Cbfb56M mouse model, we also show that AI-10-49 significantly prolongs the survival of mice bearing the leukemic cells. Preliminary mechanistic analysis of AI-10-49 activity has shown that AI-10-49 increased BCL2L11 transcript levels in a dose and time dependent manner in murine and human leukemic cells, suggesting that the viability through BIM-mediated apoptosis may be targeted by both oncogenic signals. My thesis study demonstrates that Cbfbeta-SMMHC and N-RasG12D promote the survival of pre-leukemic myeloid progenitors primed for leukemia by activation of the MEK/ERK/Bim axis, and define NrasLSL-G12D; Cbfb56M mice as a valuable genetic model for the study of inv(16) AML targeted therapies. For instance, the novel CBFbeta-SMMHC inhibitor AI-10-49 shows a significant efficacy in this mouse model. This small molecule will serve as a promising first generation drug for targeted therapy of inv(16) leukemia and also a very useful tool to understand mechanisms of leukemogenesis driving by CBFbeta-SMMHC.

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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 of cumulative cooperating mutations in the pre-leukemic progenitor cells that enhance their expansion to induce leukemia is not known. The standard treatment for inv(16) AML is based on the use of non-selective cytotoxic chemotherapy, resulting in a good initial response, but with limited long-term survival. Therefore, there is a need for developing targeted therapies with improved efficacy in leukemic cells and minimal toxicity for normal cells. Here, we used conditional Nras+/LSL-G12D; Cbfb+/56M; Mx1Cre knock-in mice to show that allelic expression of oncogenic N-RasG12D expanded the multi-potential progenitor (MPP) compartment by 8 fold. Allelic expression of Cbfbeta-SMMHC increased the MPPs and short-term hematopoietic stem cells (ST-HSCs) by 2 to 4 fold both alone and in combination with N-RasG12D expression. In addition, allelic expression of oncogenic N-RasG12D and Cbfbeta-SMMHC increases survival of pre-leukemic stem and progenitor cells. Differential analysis of bone marrow cells determined that Cbfb+/MYH11 and Nras+/G12D; vii Cbfb+/MYH11 cells included increased number of blasts, myeloblasts and promyelocytes and a reduction in immature granulocytes, suggesting that expression of N-RasG12D cannot bypass Cbfbeta-SMMHC driven differentiation block. N-RasG12D and Cbfbeta-SMMHC synergized in leukemia, in which Nras+/G12D; Cbfb+/MYH11 mice have a shorter median latency than Cbfb+/MYH11 mice. In addition, the synergy in leukemogenesis was cell autonomous. Notably, leukemic cells expressing N-RasG12D and Cbfbeta-SMMHC showed higher (over 100 fold) leukemia-initiating cell activity in vivo than leukemic cells expressing Cbfbeta-SMMHC (L-IC activity of 1/4,000 and 1/528,334, respectively). Short term culture and biochemical assays revealed that pre-leukemic and leukemic cells expressing N-RasG12D and Cbfbeta-SMMHC have reduced levels of pro-apoptotic protein Bim compared to control. The Nras+/G12D; CbfbMYH11 pre-leukemic and leukemic cells were sensitive to pharmacologic inhibition of MEK/ERK signaling pathway with increasing apoptosis and Bim protein levels but not sensitive to PI3K inhibitors. In addition, knock-down of Bcl2l11 (Bim) expression in Cbfbeta-SMMHC pre-leukemic progenitors decreased their apoptosis levels. In collaboration with Dr. John Bushweller’s and other research laboratories, we recently developed a CBFbeta-SMMHC inhibitor named AI-10-49, which specifically binds to CBFbeta-SMMHC, prevents its binding to RUNX proteins and restores CBF function. Biochemical analysis in human leukemic cells showed that AI-10-49 has significant specificity in reducing the viability of leukemic cells expressing CBFbeta-SMMHC (IC50= 0.83μM), and negligible toxicity in normal cells. Likewise, mouse Nras+/G12D; viii Cbfb+/MYH11 leukemic cells were sensitive to AI-10-49 (IC50= 0.93μM). By using the NrasLSL-G12D; Cbfb56M mouse model, we also show that AI-10-49 significantly prolongs the survival of mice bearing the leukemic cells. Preliminary mechanistic analysis of AI-10-49 activity has shown that AI-10-49 increased BCL2L11 transcript levels in a dose and time dependent manner in murine and human leukemic cells, suggesting that the viability through BIM-mediated apoptosis may be targeted by both oncogenic signals. My thesis study demonstrates that Cbfbeta-SMMHC and N-RasG12D promote the survival of pre-leukemic myeloid progenitors primed for leukemia by activation of the MEK/ERK/Bim axis, and define NrasLSL-G12D; Cbfb56M mice as a valuable genetic model for the study of inv(16) AML targeted therapies. For instance, the novel CBFbeta-SMMHC inhibitor AI-10-49 shows a significant efficacy in this mouse model. This small molecule will serve as a promising first generation drug for targeted therapy of inv(16) leukemia and also a very useful tool to understand mechanisms of leukemogenesis driving by CBFbeta-SMMHC.

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34

BOUSSADIA, OREDA. "Deletion du promoteur du gene unr murin par recombinaison homologue : etude de l'interference transcriptionnelle dans le locus unr / n-ras et du role biologique de la proteine unr." Paris 11, 1996. http://www.theses.fr/1996PA11T017.

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35

Adenis, Antoine. "Recepteurs d'hormones et de facteur de croissance, proteinases, produits d'oncogene et d'anti-oncogene, dans les cancers colorectaux humains ; expression et valeur pronostique." Lille 2, 1997. http://www.theses.fr/1997LIL2T010.

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Zhang, Yi [Verfasser], Rosalia [Gutachter] Deeken, and Wolfgang [Gutachter] Dröge-Laser. "Regulation of Agrobacterial Oncogene Expression in Host Plants / Yi Zhang. Gutachter: Rosalia Deeken ; Wolfgang Dröge-Laser." Würzburg : Universität Würzburg, 2014. http://d-nb.info/1102827614/34.

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Pleasant, Chaucola K. "TARGETING EXPRESSION OF AN ONCOGENE BY SPLICING INTERFERENCE (SPLICEi) IN HUMAN MAMMARY CARCINOMA CELL CULTURE MODEL." Cleveland State University / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=csu1328206596.

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Choo, Chee-Keong. "Human papillomavirus type 16 E6 and E7 oncogene expression in relation to host cell growth and differentiation." Case Western Reserve University School of Graduate Studies / OhioLINK, 1994. http://rave.ohiolink.edu/etdc/view?acc_num=case1057943758.

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Hamon, Martial. "Expression des oncogenes nucleaires dans l'aorte de lapin apres angioplastie : influence de l'heparine sur l'expression de c-myc, c-fos et c-jun." Lille 2, 1991. http://www.theses.fr/1991LIL2M347.

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40

Roncalli, Massimo. "Proto-oncogene and tumour suppressor gene expression in normal and abnormal growth with emphasis on neuroendocrine tumours." Thesis, Imperial College London, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.281771.

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Mastromina, Ioanna. "Investigation into the expression, role and regulation of the Myc oncogene during vertebrate embryonic body axis elongation." Thesis, University of Dundee, 2017. https://discovery.dundee.ac.uk/en/studentTheses/76216355-3572-4642-aaf8-72a9948af467.

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42

László, Csaba F. "Translation regulation of UV-light-induced transcription factor NF-kappa-B and oncogene COX-2." View abstract, 2009. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&res_dat=xri:pqdiss&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:3353542.

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43

Boßler, Felicitas Martha [Verfasser], and Walter [Akademischer Betreuer] Nickel. "AKT-dependent Repression of Human Papillomavirus E6/E7 Oncogene Expression under Hypoxia / Felicitas Martha Boßler ; Betreuer: Walter Nickel." Heidelberg : Universitätsbibliothek Heidelberg, 2019. http://d-nb.info/1177045451/34.

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44

Tsang, Tom Chun-Chang. "Viraljun oncogene serves as a suppressor of phorbol ester TPA induced tumor cell invasion and stromelysin gene expression." Diss., The University of Arizona, 1994. http://hdl.handle.net/10150/186681.

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Carcinogenesis in the mouse skin is a multistep process involving initiation, promotion, and progression. In order for the benign papilloma cells that have been initiated and promoted to become malignant, genetic alterations are believed to be involved. The viral jun (v-jun) oncogene encodes a transcription factor that can participate in the transactivation of genes through the AP-1 complex. Evidence indicates that the ability of v-jun to transform cells and stimulate transcription depends on the cell type. The question that I have attempted to answer in my dissertation studies is whether expression of the v-jun gene in benign tumor forming mouse keratinocytes that already express an activated c-rasᴴᵃ oncogene would cause malignant progression. Our results showed that the v-jun transfection did not result in malignant progression; instead, we made the unexpected observation that the ability of these cells to invade reconstituted basement membrane matrix (in vitro) in response to the phorbol ester, 12-O-tetradecanoyl-phorbol-13-acetate (TPA) was suppressed. This phenomenon could partially be explained by the suppression of the induction by phorbol ester of expression of the metalloproteinase, stromelysin (transin). Of interest was the finding that TPA induction of other cellular genes known to be regulated by AP-1 was not inhibited in the benign tumor cells expressing v-jun. The suppressor activity shown by v-jun is different than that of other tumor suppressor genes in that it appears to be specific for the process of tumor invasion. A potential implication of this unexpected finding is that it may provide insight on how to develop cancer therapeutic strategies that can specifically inhibit tumor invasion. I have constructed a set of cassette cloning vectors that can be used for rapid adaptation of DNA restriction fragments. In addition, I have formulated a new model with regards to the mechanism of function for the 70 kDa family of heat shock proteins (hsp 70). This model proposes that hsp 70 serves as a cross-linker molecule between many cellular proteins and the cytoskeletal matrix, and this model may have significant implications on many cellular processes.

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45

Bossen, Judith [Verfasser], Thomas [Akademischer Betreuer] Roeder, and Holger [Gutachter] Heine. "Impact of oncogene expression in the respiratory system of Drosophila melanogaster / Judith Bossen ; Gutachter: Holger Heine ; Betreuer: Thomas Roeder." Kiel : Universitätsbibliothek Kiel, 2018. http://d-nb.info/1232726435/34.

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46

LEYGUE, ETIENNE. "Expression et e2-dependance du proto-oncogene c-myc dans les cellules epitheliales mammaires humaines normales (emh) en culture." Paris 6, 1994. http://www.theses.fr/1994PA066632.

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Le proto-oncogene c-myc, gene clef de la multiplication cellulaire, est implique comme intermediaire de l'effet proliferatif de l'oestradiol (e2) dans les lignees cancereuses mammaires humaines. Sur un modele original de culture de cellules epitheliales mammaires humaines normales (emh), nous avons montre que la croissance etait stimulee par e2 et freinee par les antioestrogenes. Il importait donc de verifier si l'effet proliferatif de e2 faisait intervenir le proto-oncogene c-myc. L'arnm et la proteine c-myc ont ete caracterises dans les cellules emh par northern blot, immunocytochimie et western blot. Le taux d'arnm est identique a celui des cellules cancereuses e2-dependantes mcf-7 et inferieur a celui des cellules e2-independantes mda-mb-231. En revanche, le taux de proteine est inferieur a celui des mda-mb-231 et des mcf-7. Ces resultats, ainsi que ceux obtenus par protection a la rnase suggerent l'existence de mecanismes differents controlant l'expression de c-myc dans ces trois types cellulaires. L'expression de c-myc est e2-dependante dans les cellules emh. E2 induit une stimulation diphasique de l'arnm et de la proteine. Les modifications de cet effet en presence d'actinomycine d et de cycloheximide sont en faveur d'une action transcriptionnelle de e2. L'antioestrogene 4-ohtam inhibe la stimulation de la proteine par e2. Le proto-oncogene c-myc parait donc jouer un role dans les mecanismes par lesquels e2 et les antioestrogenes controlent la croissance du tissu mammaire sain et cancereux. Des modifications de ces mecanismes peuvent intervenir dans la deregulation de la croissance cellulaire et participer au processus qui en plusieurs etapes conduit une cellule normale a devenir cancereuse. Une meilleure comprehension des differences observees dans ces voies communes controlant la multiplication cellulaire pourrait permettre de mieux definir les points les plus sensibles aux efforts therapeutiques a entreprendre

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Vriz, Sophie. "Caracterisation du proto-oncogene c-myc chez le xenope et regulation de son expression au cours du developpement embryonnaire." Paris 6, 1990. http://www.theses.fr/1990PA066358.

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Nous nous sommes interesses a la regulation de l'expression des deux proto-oncogenes c-myc chez le xenope. Dans un premier temps nous avons caracterise ces deux genes au niveau de la sequence nucleotidique correspondant a leurs adnc. Nous avons ensuite etudie leur expression au cours du developpement embryonnaire et du processus de regeneration des membres. Nous avons enfin teste l'implication de la region 3 non codante des arnm myc dans la degradation de ceux-ci. 1) les genes c-myc i et c-myc ii s'expriment differemment au cours de l'ovogenese et du developpement precoce. C-myc i est transcrit dans l'ovocyte et dans l'embryon a partir du stade gastrula, contrairement a c-myc ii qui est exprime uniquement dans l'ovocyte. Nous avons montre que la difference de taille observee entre les deux arnm, c-myc i et c-myc ii, correspond a une difference au niveau de la sequence 5 non codante. 2) au cours du processus de regeneration des membres, l'expression des genes c-myc est correlee a la proliferation cellulaire. Nous detectons un grand nombre de transcrits c-myc dans les couches cellulaires qui ont une intense activite de division, alors que tres peu de messages myc sont detectes dans les cellules engagees dans une voie de differenciation (muscle et derme). 3) la comparaison des sequences 3 non codantes de 7 adnc-myc nous a permis d'identifier 3 sequences contigues (a, b et c) de 10, 11 et 12 nucleotides respectivement, parfaitement conservees au cours de l'evolution. Leur implication dans la regulation de la demi-vie des arnm c-myc est discutee

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Junetha, Syed Jabarulla. "Chemical Biology Approaches for Regulating Eukaryotic Gene Expression." 京都大学 (Kyoto University), 2015. http://hdl.handle.net/2433/202664.

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Popov, Nikita. "Expression and activity of Myc network proteins during cell cycle progression and differentiation /." Sundbyberg, 2004. http://diss.kib.ki.se/2004/91-7349-856-4/.

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Walker, Darius M. "Characterization of ESE-1 protein expression and function in transformed mammary cell-lines /." Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2007.

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Thesis (Ph.D. in Biophysics & Genetics) -- University of Colorado Denver, 2007.
Typescript. Includes bibliographical references (leaves 118-124). Free to UCD affiliates. Online version available via ProQuest Digital Dissertations;

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Dissertations / Theses on the topic 'Oncogene expression'

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