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Dissertations / Theses on the topic 'Fos oncogenes'

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Published: 4 June 2021

Last updated: 20 February 2023

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1

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 line between the mitogenic effect and the c-fos and c-myc modulation induced by these immunomodifiers. The impact of lps, tpa and dibutyryl-cyclic amp on mhc class ii antigen (ia) has been revealed by radio-immuno-assay. These compounds inhibited constitutive or induced by interferon-gamma ia expression. This inhibition seemed to be in relation with c-fos expression. The ia expression was therefore analysed either after c-fos translation blockage by a dna antisense either after overexpression of c-fos by transfection of p388d1 cells with a plasmid containing the c-fos gene. The first results seemed to confirm an inverse correlation between the c-fos induction and the inhibition of ia expression

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2

Tiniakos, Konstantina G. "Production, characterisation and clinical application of monoclonal antibodies to the human c-jun and c-fos oncoproteins." Thesis, University of Newcastle Upon Tyne, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.246089.

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3

Jang, Woochan. "The presence of fos-like immunoreactivity in neurons in the vomeronasal epithelium of mice /." free to MU campus, to others for purchase, 1997. http://wwwlib.umi.com/cr/mo/fullcit?p9842591.

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4

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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5

Spray, Kristina Jean. "Neural circuitry underlying expression of fos-like immunoreactivity in intermediate nucleus of the solitary tract following expression of taste aversion learning /." Thesis, Connect to this title online; UW restricted, 2002. http://hdl.handle.net/1773/8998.

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6

Whitelaw, Philippa F. "The expression of cellular oncogenes c-myc and c-fos in rat skeletal muscle : changes during development and hypertrophy." Thesis, University of Aberdeen, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295585.

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A study has been made on the expression of cellular oncogenes c-myc and c-fos in rate skeletal muscle both in vitro in cell lines and primary culture and in vivo during development and after the induction of two models of hypertrophy. Using the technique of Northern hybridisation, results showed that the pattern of expression of c-myc and c-fos mRNA in primary myoblast cells and in established myoblast and fibroblast cells in culture were similar; stimulation of quiescent cells to proliferate induced expression from the c-fos gene within 30 minutes and the c-myc gene by 2 hours. The findings demonstrate that c-myc and c-fos mRNA levels are increased in terminally differentiated rat skeletal muscle both in vitro and in vivo. They confirm work which showed that c-myc is not exclusively connected with cell proliferation (Endo and Nadal-Ginard 1986) and extend previous work into the increased expression of c-myc and c-fos mRNA in cardiac muscle induced to hypertrophy (Mulvagh et al., 1987; Izumo et al., 1988; Komuro et al., 1988). The possible location of the elevated expression within the muscle after hypertrophy and the relative contributions from an inflammatory response, satellite cells and myofibres are discussed. Elevation of c-myc and c-fos mRNA in hypertrophy induced both surgically by tenotomy and pharmocologically with clenbuterol argue against a significant contribution from infiltrating fibroblasts, while from the literature, the activation of satellite cells appears to occur later. It is concluded that the elevated expression of c-myc in skeletal muscle is probably located within the myofibres and may be linked to mechanisms of cell enlargement. However further confirmation with in situ hybridisation and immunohistochemistry is required.

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7

Allbutt, Haydn. "The rat spinal cord following traumatic injury: An anatomical and behavioural study examining NADPH-d and fos." University of Sydney, 2004. http://hdl.handle.net/2123/1335.

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Doctor of Philosophy
The general aim of this current work was to examine spinal cord injury (SCI), and in particular to examine the pathology of injury as it relates to changes in sensory transmission. Due to the limited possibilities for experimentation in humans, a range of animal models of SCI have been developed and are reviewed here. The weight drop SCI model is the most similar to the clinical presentation of SCI in humans and has been widely used in the rat. It was selected for the series of experiments reported in this thesis. Many of the functional deficits produced by SCI result from a cascade of biochemical events set into motion by the injury. Included amongst these is the activation of the enzyme nitric oxide synthase which produces the gaseous neuromodulator, nitric oxide (NO). NO is amongst the most widely distributed and widely utilised molecule in virtually all living organisms, and it is an important signalling molecule in the nervous system. One of the major functions performed by NO appears to relate to sensory transmission, and thus alterations in sensory transmission observed as a result of SCI may involve alterations to NO synthesis. One of the principal aims of this thesis was to examine the effect of SCI on the NO producing cells of the spinal cord and to consider what any changes in NO synthesis may suggest in regards to sensation. NO producing cells were examined using NADPH diaphorase (NADPH-d) histochemistry. As the symptoms of SCI such as motor loss and changes in sensory processing are functional changes, it was also useful to examine changes in neuronal function as a result of SCI. Widespread neuronal function was examined via immunohistochemical detection of the gene product of the immediate early gene, c-fos. It is not known how extensive the biochemical changes resulting from SCI may be, thus another of the aims of the present thesis was to examine the effects of SCI on NO synthesis not only at the level of injury, but also distant to the injury. Findings of the present thesis indicated that traumatic SCI resulted in a decrease in the number of NADPH-d positive cells from the superficial dorsal horn (SDH) of the spinal cord, while the number of these cells are increased in the ventral horn. These changes were restricted to spinal segments adjacent to the injury. Fos expression was also altered by injury and was found to decrease. The most profound changes were found to occur in lamina III, although the other laminae also demonstrated similar changes. Changes in fos expression however were notably more widespread than those for NADPH-d and were not restricted to the level of the injury, occurring at all levels of the spinal cord examined. It was interpreted that alterations in NO synthesis appear to be modulated by the local injury-induced environment while fos expression may be altered by widespread changes to the global level of activity within the central nervous system. Having observed that the number of NADPH-d positive cells of the SDH is reduced following injury, it was of interest to determine whether these cells were in fact killed, or whether they were still present but with reduced NADPH-d activity. Cell counts suggested that the NADPH-d positive cells, which were likely to represent a population of inhibitory interneurons, were not killed following injury, but rather are disrupted such that their normal biochemistry is altered. Since these cells were likely to be inhibitory and were located in laminae involved in sensory transmission, the question arose how disruption of these cells may relate to the neuropathic pain observed to develop following SCI. Thus both NADPH-d and fos expression were again examined, but this time in conjunction with the sensory function of the rats. Sensory thresholds to pain-like behaviour were determined prior to and after injury using Von Frey filaments. Rats that demonstrated a decrease in sensory threshold of at least two Von Frey filament gradations (>70%) were classed as allodynic, while those with a less than a 70% decrease in threshold were classed as non-allodynic. A subpopulation of each of the groups of rats (uninjured, non-allodynic and allodynic) underwent a somatic stimulation paradigm. It was found that stimulation resulted in an increase in the number of NO producing cells but only in the allodynic group of animals. Since this group of animals by definition would perceive this stimulation as noxious, it is likely that the noxious nature of the stimulation resulted in the increased number of NO producing cells observed. This effect occurred only in segments adjacent to the injury. When fos expression was examined in the uninjured animals it was noted that somatic stimulation resulted in a decrease in fos expression, almost exclusively in lamina III. Following injury, there was no change in fos expression in lamina III observed. Instead the only change observed was an increase in fos expression in the deep dorsal horn (DDH, lamina IV and V). This occurred most profoundly in the allodynic group. These results suggested that SCI may lead to misprocessing of sensory signals such that non-noxious somatic stimuli are processed in the DDH rather than lamina III following SCI. It is proposed here that this change in laminae processing may be responsible for the perception of pain towards a non-noxious stimulus, and that the reported injury-induced loss of NO producing inhibitory interneurons in the SDH may be responsible for this alteration in sensory processing following SCI. Sensation is also processed by a number of supraspinal structures and a number of these have been implicated in the development of neuropathic pain states. The effects of SCI on neuronal activity as well as NO synthesis were examined in the periaqueductal grey region of the mid brain (PAG). SCI was shown to result in reduced neuronal activity in the PAG. This reduction in activity did not follow the somatotopy of the lateral column of the PAG (lPAG). It was suggested the reduced activity may not be solely caused by reduced spinal input as a result of SCI. Reduced neuronal activity in the PAG may indicate reduced PAG function, which includes descending modulation of spinal sensory transmission. Injury was not found to alter NADPH-d expression in the PAG. The effect of traumatic lumbar SCI on the parietal (sensorimotor) cortex of the rat was also examined, as loss of inputs following SCI have been shown to result in a profound reorganisation of the cortex. Results indicated that SCI results in a virtual cessation of neuronal activity in areas 1 and 2 of the parietal cortex, likely as a result of lost afferent drive. Theories of cortical plasticity suggest that while the primary inputs via the lumbar spinal cord may be lost following SCI, other less dominants input will remain and become more dominant. It has been proposed previously that cortical reorganisation involves a rapid reorganisation of the entire sensory system. It was interpreted that a similar process may explain the system-wide reduction in neuronal activity observed in the present series of studies.

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8

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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9

Van, Belle Eric. "Effets de l'inhibition de l'enzyme de conversion de l'angiotensine sur l'expression des oncogenes nucleaires c-myc, c-fos et c-jun et sur l'hyperplasie intimale induites par l'angioplastie experimentale." Lille 2, 1993. http://www.theses.fr/1993LIL2M261.

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10

MATSUYAMA, MUTSUSHI, R. KAZUHIKO UTSUMI, AKIRA MASUDA, MASAHIDE TAKAHASHI, WORAWIDH WAJJWALKUI, and YOSHIHISA SAKAI. "Expression of Proto-Oncogenes and Tumor Suppressor Genes in in vitro Cell Lines Derived from a Thymus, Thymoma, and Malignant Thymoma of Rats." Nagoya University School of Medicine, 1993. http://hdl.handle.net/2237/17542.

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11

Gentry, Aleksandra. "Growth control of chondrocytes by the c-fos proto-oncogene." Thesis, King's College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.399494.

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12

Basset-Seguin, Nicole. "Role du proto-oncogene c-fos dans la physiopathologie cutanee." Montpellier 1, 1993. http://www.theses.fr/1993MON1T016.

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13

Rost, Nathalie. "Expression et régulation du gène de la proenképhaline dans un modèle expérimental de tumeur cérébrale chez le rat." Grenoble 1, 1991. http://www.theses.fr/1991GRE10048.

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L'expression du gène précurseur de la met-enképhaline (PPE) a été analysée dans un modèle expérimental de tumeur cérébrale chez le rat, provoquée par l'injection stéréotaxique de cellules gliales malignes C6 dans le striatum. Une étude par hybridation in situ a montré une expression élevée de ce gène dans la tumeur, en l'absence in vitro, pour la lignée C6, par Yoshikawa et al. (1986). L'expression élevée du gène PPE, dans les cellules C6, ne résulterait pas d'une amplification de l'ADN, ni de l'absence d'un rétrocontrôle enképhalinergique. Le fait de trouver une expression de gènes codant pour des neuromodulateurs dans les cellules gliales normales, et malignes dans le cas présent, remet en question le concept de leur rôle exclusif de neurotransmetteur et suggère l'implication éventuelle de ce type de gènes dans la carcinogenèse. Nous avons aussi montré que, suite à une déafférentation dopaminergique, l'expression du gène PPE diminue dans la tumeur. La destruction des afférences dopaminergiques entraîne une série de changements, au niveau de plusieurs peptides striataux, variable suivant l'étendue de la lésion. La nature du/des composés responsables de la modulation de l'expression du gène PPE reste à définir. D’autre part, l'analyse de certains oncogènes, dans le modèle tumoral, a révélé l'expression des oncogènes nucléaires FOS et JUN au sein de la tumeur. Une éventuelle corrélation, entre l'expression de ces gènes codant pour des facteurs régulateurs de la transcription et l'expression du gène PPE pourrait permettre une approche originale du processus tumoral.

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14

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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15

Tisserand, Julie. "Mise en évidence d'un rôle suppresseur de tumeur pour la protéine tyrosine-kinase FES dans le mélanome." Thesis, Aix-Marseille, 2016. http://www.theses.fr/2016AIXM5035.

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Le mélanome est un cancer de la peau agressif et au mauvais pronostic. Si de nouvelles solutions thérapeutiques efficaces ont été développées, les taux de réponses sont variables et transitoires. Découvrir de nouveaux mécanismes oncogéniques dans cette pathologie reste donc nécessaire. Durant mes travaux, j’ai pu démontrer que la protéine tyrosine-kinase FES est exprimée dans les mélanocytes normaux. Cette expression est largement perdue dans un panel de lignées cellulaires de mélanome, au niveau protéique et transcriptionnel ainsi que dans des cultures primaires d’échantillons de patients. La perte de FES est due à une hyper-méthylation de son promoteur et est réversible. En ré-exprimant FES de manière stable dans deux lignées cellulaires de mélanomes, j’ai montré que cette réexpression entraînait une diminution des capacités oncogéniques des cellules. De plus, en analysant les données d’une cohorte de mélanomes (TCGA), j’ai pu établir qu’une diminution importante ou une perte d’expression de FES se retrouve dans près de 40% des patients, et qu’elle est corrélée à une hyper-méthylation du gène FES. Les patients ayant une faible expression de FES présentent un moins bon pronostic soulignant l’importance de ce phénomène. Enfin, en croisant un modèle murin déficient pour le gène Fes avec un modèle de mélanome, nous observons que les tumeurs sous fond Fes KO sont plus prolifératives et plus volumineuses.Ainsi, par des analyses in vitro, sur des données de patients ou en croisant des modèles murins, j’ai pu démontrer que FES est exprimée au niveau des mélanocytes normaux et y exerce un rôle de suppresseur de tumeur
Among skin cancers, melanoma is the most aggressive and has the worst prognosis. In the last years, new therapeutic tools have been developed but responses differ between patients and are often transient due to resistance mechanisms. This highlights the need to improve understanding of molecular mechanisms of the disease. During my thesis, I have shown for the first time that FES tyrosine kinase is expressed in normal melanocytes, and that its expression is lost at the protein and RNA levels in most melanoma cell lines. The same result is observed in a panel of 12 patients’ short-term cultures. The lack of expression is due to FES promoter hyper-methylation and can be reverted using a hypomethylating agent. By restoring FES expression in two melanoma cell lines, I observe a decrease of oncogenic properties of the cells. Moreover, the analysis of the TCGA data on melanoma indicate that FES expression is strongly decreased or lost in about 40% of patients, and that this loss of expression is correlated with FES promoter methylation. Importantly, patients with low level of FES mRNA have poor prognosis compared to FES expressing patients. Finally, Fes knock-out mice crossed with an inducible melanoma mouse model indicate that tumors proliferation and size are more important under a Fes KO background.In conclusion, by using melanoma cells in vitro, data from melanoma patients and mouse models, I have demonstrated that FES is expressed in normal melanocytes and clearly plays a tumor suppressor role.in melanoma

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16

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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17

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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18

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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19

Baker, David Alan. "Mutational analysis of the proto-oncogenes c-fms and c-kit." Thesis, Imperial College London, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.362390.

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20

André, Catherine. "Les oncogenes c-kit et c-fms : recepteurs a activite tyrosine kinase." Paris 7, 1992. http://www.theses.fr/1992PA077214.

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Les produits des oncogenes c-fms et c-kit, les pdgfra et pdgfrb appartiennent a la sous-classe iii des recepteurs a activite tyrosine kinase (rtk). Leurs genes sont localises par paire chez l'homme et la souris. Nous avons clone et sequence l'oncogene c-kit humain, sa structure genomique est homologue a celle de c-fms; les deux genes: 60 kb pour c-fms, 80 kb pour c-kit, leur structure exons/introns est identique dans le domaine catalytique. L'organisation genomique de c-kit et c-fms, la localisation chromosomique particuliere des genes de la sous-classe iii des rtk, ainsi que leurs fonctions communes, nous ont conduit a emettre l'hypothese selon laquelle ces genes auraient evolue a partir d'un gene ancestral commun, apres cis et trans duplications. Nous nous sommes interesses a l'implication de c-fms et c-kit dans l'hematopoiese. (1) en collaboration avec l'equipe de pierre tambourin (inserm-u. 152, hopital cochin), nous avons mis en evidence, au sein de l'intron 1 de l'oncogene c-fms (m-csfr), un site preferentiel d'integration du retrovirus de friend (f-mulv), implique dans 20% des leucemies myeloblastiques de la souris. (2) nous avons montre l'expression de c-kit dans les progeniteurs myeloides/erythroides et les mastocytes. Actuellement, nous recherchons l'implication de c-kit et de son ligand, kl, dans l'anemie de fanconi et d'autres aplasies, en collaboration avec le pr. Eliane gluckman (service des greffes de moelle osseuse a l'hopital st louis)

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21

McGarry, Lynn C. "Mediation of transformation by the v-fos oncogene : regulation of the invasive phenotype by histone deacetylases." Thesis, Open University, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.403835.

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22

Passegue, Emmanuelle. "Régulation de l'expression des proto-oncogènes c-fos et jun B par le TRH dans une lignée clonale de cellules à prolactine (GH3B6) : recherche d'une implication fonctionnelle." Paris 11, 1995. http://www.theses.fr/1995PA11T033.

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23

Hagerimana, Aline. "Étude de la modulation de c-fos par le facteur activateur des plaquettes (PAF) dans les cellules du muscle lisse vasculaire et les monocytes." Sherbrooke : Université de Sherbrooke, 2002.

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24

Patel, Shreya. "MiRNAs Trageting Proto-Oncogene C-FMS mRNA in Breast and Ovarian Cancer Cells." Thesis, The University of Arizona, 2014. http://hdl.handle.net/10150/321928.

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25

ANTOINE, MURIEL. "Regulation du proto-oncogene c-fos par le ca#2#+ et les kinases ca#2#+/calmoduline dependantes dans les cellules corticotropes." Université Louis Pasteur (Strasbourg) (1971-2008), 1997. http://www.theses.fr/1997STR13254.

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Le ca#2#+ exerce un role essentiel dans le controle des genes hormonaux hypophysaires (prolactine, proopiomelanocortine), et du proto-oncogene c-fos. Nos travaux ont montre que la proteine c-fos est un element regulateur majeur de la transcription du gene de la proopiomelanocortine dans les cellules corticotropes. Nous nous sommes interesse aux mecanismes d'action du signal calcique sur la transcription de c-fos ainsi qu'aux voies de signalisation impliquees dans ces regulations transcriptionnelles. Nous avons montre que dans une lignee cellulaire derivees de cellules corticotropes (att20), une entree de ca#2#+ dans la cellule provoque une augmentation du niveau des arnm et l'apparition de la proteine c-fos dans le noyau. Une technique de transfection transitoire de genes rapporteurs indique que ces regulations s'exercent au niveau transcriptionnel. Parmi les effecteurs de la voie calcique, nous avons etudie l'effet des ca#2#+/calmoduline kinases (camk) de type ii et iv sur le promoteur c-fos et nous avons mis en evidence des reponses specifiques des elements cis-activants sre (serum responsive element), fap (c-fos ap1-like element), cre (camp responsive element) et rce (retinoblastoma control element) a chaque camk. Ceci indique une action de ces kinases par des mecanismes distincts. La reponse de l'element rce aux camk est interessante car cet element est sous le controle du produit de susceptibilite au retinoblastome (rb) et des facteurs de transcription de la famille sp (sp1, sp3). Ceci suggere un possible lien entre la voie ca#2#+ et le cycle cellulaire. Nous montrons que l'effet stimulateur des camk sur c-fos et sur l'element rce est bloque lorsque rb est surexprime. De plus, a l'aide de proteines chimeres, nous montrons que cette regulation passe par le facteur de transcription sp1. Ces travaux suggerent une possible regulation croisee entre la voie ca#2#+ et le cycle cellulaire. Ce mecanisme serait susceptible de coordonner l'activite endocrine de la cellule avec l'arret du cycle cellulaire lors de la differenciation.

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26

Demoly, Pascal. "Etude immunohistochimique de l'expression du proto-oncogène fos et de la protéine PCNA dans l'asthme et la bronchite chronique." Montpellier 1, 1995. http://www.theses.fr/1995MON1T009.

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27

Morton, Jennifer P. "The role of Fas signalling and the c-MYC oncogene in T cell apoptosis and transformation." Thesis, University of Glasgow, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.390740.

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28

BOUTILLIER, ANNE-LAURENCE. "Etude de la regulation transcriptionnelle du gene de la pomc hypophysaire par la proteine kinase amp cyclique dependante et le proto-oncogene c-fos." Strasbourg 1, 1993. http://www.theses.fr/1993STR13177.

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Dans l'hypophyse, les cellules qui expriment la proopiomelanocortine (pomc) representent un systeme de regulations endocrines impliquant des interactions multihormonales complexes, importantes dans la reponse au stress. La synthese et la secretion des peptides derives de la pomc sont controlees par des facteurs hypothalamiques tels que la crh ou les catecholamines et par les glucocorticoides. Le but de mon travail de these etait de dissequer les mecanismes moleculaires intracellulaires par lesquels la crh module la transcription du gene de la pomc. A l'aide de techniques de biologie moleculaire, j'ai montre que la pka est le relais essentiel dans la stimulation de la transcription du gene de la pomc par la crh, dans les cellules corticotropes (lignee att20). De plus, cette stimulation s'effectue en deux etapes: tout d'abord, elle met en jeu une reponse precoce impliquant des modifications post-traductionnelles de facteurs de transcription preexistants, et ensuite une reponse tardive impliquant la neosynthese de proteines. En effet, dans le premier exon du gene de la pomc, j'ai caracterise un site ap1 fonctionnel, qui lie les oncoproteines cfos et cjun, montrant qu'elles participent a cette reponse tardive. Cela nous a permis de proposer un nouveau modele de regulation negative de la transcription du gene de la pomc par les glucocorticoides, dans les cellules corticotropes

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29

Fort, Philippe. "Etude de gènes réglés au cours du cycle cellulaire opérons de sporulations de Bacillus subtilis et proto-oncogène C-Fos de fibroblastes de Hamster." Grenoble 2 : ANRT, 1986. http://catalogue.bnf.fr/ark:/12148/cb375976472.

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30

MACHWATE, MOHAMED, and Philippe Ascher. "Etude de la formation osseuse dans un modele d'hypodynamie et au cours du developpement chez le rat : implication du proto-oncogene c-fos dans la proliferation et la differenciation osteoblastique." Paris 6, 1994. http://www.theses.fr/1994PA066180.

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Le but de cette these etait d'etudier quelques aspects de la regulation de la formation osseuse, ainsi que le niveau d'implication du proto-oncogene c-fos dans ces processus chez le rat. Dans la premiere partie de ce travail, nous avons montre que l'alteration de l'activite de formation osseuse observee en condition d'hypodynamie chez le rat suspendu est due a la diminution du recrutement des precurseurs osteoblastiques presents au niveau du stroma medullaire. Le traitement par l'insulin growth factor-i (igf-i) a partiellement prevenu la perte osseuse chez le rat suspendu en stimulant le recrutement des precurseurs osteoblastiques presents au niveau du stroma medullaire. L'igf-i semble ainsi etre implique, du moins en partie, dans la mediation des effets des contraintes mecaniques. Dans la deuxieme partie, nous avons montre que le proto-oncogene c-fos est implique dans la proliferation des osteoblastes pendant la periode prenatale et dans leur differenciation apres la naissance chez le rat. L'utilisation d'un oligonucleotide antisens capable d'inhiber l'expression de la proteine c-fos nous a permis, par ailleurs, de montrer que le proto-oncogene c-fos est implique dans les mecanismes intracellulaires de transduction des effets du transforming growth factor-b (tgf-b) sur les cellules osteoblastiques de rat en culture

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31

Murugadoss, Karthik. "Convergence of regulatory mutations into oncogenic pathways across multiple tumor types." Thesis, Massachusetts Institute of Technology, 2017. http://hdl.handle.net/1721.1/111510.

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Thesis: S.M., Massachusetts Institute of Technology, Computation for Design and Optimization Program, 2017.
Cataloged from PDF version of thesis.
Includes bibliographical references (pages 65-74).
Cancer sequencing efforts have largely focused on profiling somatic variants in the protein-coding genome and characterizing their functional impact. In this study, we develop a computational pipeline to identify non-coding mutational drivers across multiple tumor types. We describe the non-coding mutational profiles of 854 samples, spread across 15 tumor types, in the context of their respective tissue type-specific reference epigenomes, using recent pan-cancer whole-genome sequencing data. We develop a novel method to detect significantly recurrent non-coding mutations by reestimating the background mutation density while adjusting for epigenomic covariates. Existing databases on enhancer-gene links allow us to capture the convergence of disparate mutations onto downstream target genes. We then systematically identify key immunomodulatory and tumor-suppressive genes enriched for non-coding mutations in their regulatory neighborhood and evaluate these in a pan-cancer context. Taken together, we show that low-frequency alterations converge into high-frequency recurrent events on downstream targets through tissue-specific regulatory interactions.
by Karthik Murugadoss.
S.M.

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McVeigh, Jennifer Lyn. "Studying the biological function of the Fps/Fes proto-oncogene by generating and analyzing transgenic mice expressing a targeted inactivating mutation in the gene." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq22357.pdf.

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33

Lascombe, Isabelle. "Mecanismes moleculaires de l'action des estrogenes dans l'endometre : etude dans des cellules en croissance normale ou cancereuses." Besançon, 1997. http://www.theses.fr/1997BESA3709.

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34

Vuillermoz, Christophe. "Arguments en faveur de l'existence d'une repression de l'action estrogenique dans les cellules d'endometre en croissance normale." Besançon, 1994. http://www.theses.fr/1994BESA3701.

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35

Buzyn, Agnès. "Etude de l'immunite anti-tumorale specifique dans les leucemies myeloides et perspectives d'applications therapeutiques." Paris 5, 2000. http://www.theses.fr/2000PA05N127.

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36

Gauthier-Rouvière, Cécile. "Médiateurs précoces de l'activation mitogénique induite par les facteurs de croissance ou l'oncogène ras : implication du facteur de réponse au sérum p67SRF et des protéine kinase C et caséine kinase II dans la régulation transcriptionnelle du gène c-fod." Montpellier 1, 1991. http://www.theses.fr/1991MON11247.

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37

Alibhai, Imran Nizamudin. "Regulation of FOSB MRNA isoforms by drugs of abuse." Access to abstract only; dissertation is embargoed until after 5/15/2007, 2005. http://www4.utsouthwestern.edu/library/ETD/etdDetails.cfm?etdID=144.

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Ordener, Catherine. "Etude de l'action des estrogenes et des facteurs de croissance sur la proliferation cellulaire et l'expression genique dans les cellules d'endometre en croissance normale." Besançon, 1995. http://www.theses.fr/1995BESA3702.

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39

Vesvres, Marie-Hélène. "Etude des bases anatomiques du contrôle par les opiacés de l'activité des neurones striataux." Bordeaux 2, 1995. http://www.theses.fr/1995BOR28345.

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40

Liphaus, Bernadete de Lourdes. ""Expressão das proteínas Fas e Bcl-2 em células mononucleares de crianças e adolescentes com lúpus eritematoso sistêmico"." Universidade de São Paulo, 2005. http://www.teses.usp.br/teses/disponiveis/5/5141/tde-16022006-162336/.

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Para verificar a expressão das proteínas Fas e Bcl-2 em linfócitos e suas correlações com a atividade da doença foram avaliados 38 pacientes com lúpus eritematoso sistêmico de início na infância e 25 controles sem doença autoimune. Observou-se que as porcentagens de linfócitos T CD3+ e CD8+ e linfócitos B que expressavam a proteína Fas e a intensidade média de fluorescência da proteína Bcl-2 nos linfócitos T CD3+, CD4+ e CD8+ dos pacientes com lúpus foram significativamente maiores quando comparadas aos controles. Os pacientes com doença ativa apresentavam porcentagens de linfócitos B que expressavam a proteína Fas significativamente maiores que os pacientes com doença inativa e os controles e houve correlação direta entre estas porcentagens e o SLEDAI (p=0.02, r=0.38)
In order to verify the expression of Fas and Bcl-2 proteins on lymphocytes and their relationship with disease activity 38 patients with juvenile-onset systemic lupus erythematosus and 25 healthy controls were studied. The measurements showed that percentages of lymphocytes T CD3+ and CD8+ and B lymphocytes positively stained for Fas antigen and mean fluorescence intensity of Bcl-2 on CD3+, CD4+ and CD8+ T cells from lupus patients were significantly increased compared to healthy controls. Lupus patients with active disease presented percentages of lymphocytes B positive for Fas antigen significantly higher compared to patients with inactive disease and healthy controls and there was a statistically significant direct correlation between these percentages and SLEDAI score (p=0.02, r=0.38).

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Miret, Mas Carlos. "Alteraciones de la apoptosis como mecanismo patogénico en el lupus eritematoso sistémico." Doctoral thesis, Universitat de Barcelona, 2003. http://hdl.handle.net/10803/2165.

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La apoptosis es un proceso de muerte celular programada que está involucrada en la selección del repertorio de linfocitos T y en el mantenimiento de la tolerancia inmunológica, ya que es el mecanismo por el que se eliminan las células que podrían dar lugar a respuestas autoinmunes. Existen evidencias de que la alteración en los mecanismos apoptóticos están implicados en la patogenia y la actividad de las enfermedades autoinmunes sistémicas, de las cuales, el lupus eritematoso sistémico (LES) es la más representativa. Se han identificado en el ser humano algunos genes que codifican oncoproteínas y citocinas cuya transcripción parece ser crucial en este proceso: unos pro-apoptóticos (fas, p53 y TNF-alfa) y otros anti-apoptóticos (bcl-2 y IL-10). Se sospecha que cambios en la expresión de los mismos podrían desempeñar algún papel en la patogenia del LES, al favorecer la proliferación de determinadas poblaciones celulares de efecto autorreactivo.
Con los trabajos de la presente tesis doctoral nos propusimos: determinar la implicación de los oncogenes (bcl-2, fas y p53) y las citocinas (IL-10 y TNF-alfa) en la disregulación apoptótica que presentan los pacientes con LES; estudiar la interrelación existente entre ellos; y analizar la relación de las posibles disregulaciones de los elementos que participan en la apoptosis con la actividad de la enfermedad lúpica.
Los resultados obtenidos muestran cómo los oncogenes fas, bcl-2 y p53, las citocinas IL-10 y TNF-alfa, y la fracción proteica soluble del Fas (sFas) tienen una notable importancia en la patogenia y la actividad de la enfermedad lúpìca. Las vías apoptóticas del Fas y p53 son independientes entre sí. Sin embargo, diversas citocinas (IL-10, TNF-alfa), oncoproteínas (Bcl-2) y fracciones proteicas solubles (sFas) pueden ser las encargadas de relacionarlas entre sí. La interferencia de estas vías apoptóticas produciría una eliminación deficiente de los linfocitos autorreactivos. Ello favorecería su supervivencia, lo que provocaría las alteraciones de disregulación inmunológica propias del LES.

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42

Paues, Jakob. "Brain Stem Involvement in Immune and Aversive Challenge." Doctoral thesis, Linköping : Linköping University, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-7579.

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43

Athanassiadis, Tuija. "Neural circuits engaged in mastication and orofacial nociception." Doctoral thesis, Umeå : Department of Integrative Medical Biology, Umeå university, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-26342.

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44

Hamza-Talha, Saliha. "Stimulation rapide du renouvellement de l'atp par des facteurs de croissance dans des fibroblastes de souris swiss : relation avec d'autres evenements precoces." Paris 6, 1987. http://www.theses.fr/1987PA066423.

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Depuis la mise en evidence de similitude entre des facteurs de croissance (fc) et des produits d'oncogenes, differents evenements biochimiques precocement induits par les fc sont decrits, cependant, leur chronologie n'est pas clairement determinee. Mise en evidence d'un nouvel evenement precoce: une stimulation du renouvellement de l'atp dans des cultures quiescentes de cellules 3t3 swiss incubees en presence de fc ou d'un promoteur de tumeur, utpa: activation de l'echange sodium-proton et de l'atpase sidium-potassium. Les mouvements cellulaires, induits precocement par les fc de par le tpa, sont impliques dans la degradation et le renouvellement rapides de l'atp. De plus, ils favorisent la stimulation par les fc de l'accumulation de certains arn messagers (actine et c-fos) et de la synthese d'arn ribosomiques

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45

"Involvement of thec-fos oncogene in Friend erythroleukemia cell proliferation and differentiation." Tulane University, 1990.

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Previous studies suggest that the product of the c-fos proto-oncogene may have multifunctional properties affecting both cell proliferation and differentiation. This study has investigated the role of c-fos in Friend erythroleukemia cell (FELC) proliferation and differentiation using two approaches. In the first approach, the expression of c-fos mRNA was examined in FELC treated with Hexamethylene bisAcetamide (HMBA), hemin or aphidicolin. These three agents, which have different effects on FELC proliferation, have also been reported to induce differentiation. However, only HMBA induced the complete erythroid differentiation program in FELC including the accompanying limitation of proliferative capacity. Hemin had no effect on FELC proliferation or heme synthesis, but did induce globin mRNA expression. Aphidicolin inhibited FELC proliferation but did not induce either heme synthesis or globin production. After removal of aphidicolin, proliferation was restored and differentiation could be induced by subsequent addition of HMBA to FELC. Cell replication and HMBA-induced differentiation were both inhibited with continuous exposure of FELC to aphidicolin. C-fos was constitutively expressed in uninduced FELC. There was no change in c-fos mRNA levels either preceding or during induction of differentiation by HMBA, or during the initiation of globin mRNA synthesis by hemin. C-fos mRNA levels were not affected by direct inhibition of DNA replication by aphidicolin. With the second approach, the proliferative and differentiative response of FELC to antisense oligodeoxynucleotide inhibition of c-fos expression was evaluated. Exposure of FELC to c-fos antisense oligodeoxynucleotide (Fos-AS) resulted in irreversible inhibition of cell replication and prevented induction of differentiation by HMBA. Treatment with both aphidicolin and Fos-AS also had profound effects on the ploidy of FELC. These results suggest that c-fos expression is required for the continuous proliferation of FELC. Since at least one round of proliferation was required for induction of FELC differentiation, the expression of the c-fos oncogene, while not directly inducing or inhibiting differentiation, nonetheless, has an indirect effect on the ability of FELC to differentiate through its role in the regulation of proliferation
acase@tulane.edu

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46

TANG, SHI-JIE, and 唐世杰. "Analysis of fos proto-oncogene expression in the butyrate-induced F-98 glioma cell differentiation." Thesis, 1991. http://ndltd.ncl.edu.tw/handle/51915182103797079621.

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47

Huang, Ying-Tang, and 黃胤唐. "Inhibitions of protein kinase C and proto-oncogene expressions iny apigenin; Studies on the mechanisms of TPA-induced c-fos andns." Thesis, 1996. http://ndltd.ncl.edu.tw/handle/79460443897144740955.

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博士
國立臺灣大學
生化學研究所
84
Apigenin(Api)是一種低毒性和不具致突變性的植物性的flavonoid。它可以抑制腫瘤促進劑(TPA)在老鼠皮膚上的促癌作用。但其抑制機轉仍不是很清楚。在我們的實驗中發現：Api是一種ATP型式的protein kinase C (PKC)的抑制劑，它對PKC的IC50=10μM。此外，它對數種的tyrosine kinases也有抑制作用，其中以對FGF receptor的抑制效果最好(IC50=20 μM)，對pp60v-src的抑制效果最差(IC50>200μM)。10、50和100μM Api 和100ng/ml TPA同時處理細胞，則可以抑制TPA所誘增c-jun的表現，其抑制的程度分別是50％，80％和100％。Api僅須要10μM就可以完全抑制TPA 所誘增c-fos的表現。25μM的Api就可以完全抑制TPA所造成的細胞生長效應。由以上我們的實驗結果，可以來說明Api之所以能抑制TPA的促癌作用的機轉。腫瘤促進劑(TPA)可以誘導許多基因的表現，如c-fos和c-jun，但對於c-fos和c-jun的誘導作用之機制和兩者之間的關係仍不是很清楚。因此，本部份的實驗就想針對這些方面作一番探討。在我們的實驗結果中發現：TPA可以在一小時內，使得細胞內的cAMP的含量和c-fos的表現，作劇烈的升降。以protein kinase A(PKA)的專一性抑制劑－H-89處理細胞，則發現H-89可以抑制TPA所誘增的c-fos，且呈濃度效應，但對TPA所誘增的c-jun則沒有影響。這種抑制效應並非來自抑制PKC和MAPK的活化與活性，而可能是與降低某些transcriptional factors 對於serum response element及其它regulatory elements的結合力有關。自由基的清除者－ DMSO，它可以清除TPA所誘增的‧OH基和抑制c-jun的表現，但對TPA所誘增的c-fos則沒有影響。DMSO的抑制效果並非自抑制MAPK的活化與活性，而可能是與改變一些transcrptional factors對於TPA response element的結合能力有所關連。由以上的實驗結果，可以來說明 TPA對 c-fos和c-jun的誘導作用，在開始的前30分鐘是互相獨立分開調控，而這些調控因子可以分別被H-89和DMSO所抑制。 Apigenin, a low toxic and non-mutagenic plant flavonoid, suppresses 12-O-tetradecanoyl-phorbol-13-acetate (TPA)-mediated tumor promotion on mouse skin. TPA has the ability to activate protein kinase C (PKC) and induce protooncogene expression. Our study shows that apigenin is a PKC inhibitor in competition with ATP, and exhibits an IC50 value of 10 μM. Apigenin also restrains the amount of TPA-stimulated phosphoprotein. Among the analysis of inhibitory effects of apigenin on several protein tyrosine kinases, the FGF receptor has a lowest IC50 (=20μM), and pp60v-src has a highest IC50 (>200μM). Treatment of 10, 50, and 100 μM apigenin with 100 ng/ml TPA resulted in 50%, 80%, and 100% suppression of TPA-induced c-jun expression, respectively. Treatment of 10 μM apigenin with TPA significant- ly inhibited TPA-induced c-fos expression. TPA- stimulated cell growth can be suppressed by 25μM apigenin. Our results provide some clues in the understanding of apigenin's inhibitory effects on TPA-mediated tumor promotion. In our data, we found that TPA can dramatically change the status of c- fos and cAMP during 1hr. We used H-89, a protein kiase A specific inhibitor, to treat with NIH 3T3 cells, we found that TPA-induced c-fos transcription is inhibited, but not c-jun. Neither the inhibition of PKC activity nor the inhibition of MAPK1/2 activity was contributed to the inhibitory effect. The effect was caused by the change of transcriptional factors of serum response element (SRE) binding activity. DMSO, a kind of free radical scavengers, could inhibit TPA-induced c-jun transcription, but not c-fos. DMSO could not inhibit MAPK1/2 activity. The inhibitory effect was contributed to the change of transcriptional factors of TPA-response element and/or other regulatory element(s) binding activity.

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48

Huang, Yin-Tang, and 黃胤唐. "Inhibitions of protein kinase C and proto-oncogene expressions iny apigenin; Studies on the mechanisms of TPA-induced c-fos andns." Thesis, 1996. http://ndltd.ncl.edu.tw/handle/20745636675011657579.

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