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Dissertations / Theses on the topic 'Ras Proto-oncogene proteins B-raf'

Author: Grafiati

Published: 4 June 2021

Last updated: 15 February 2022

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1

Iritani, Brian Masao. "Control of B lymphocyte development by Ras and Raf /." Thesis, Connect to this title online; UW restricted, 1997. http://hdl.handle.net/1773/8322.

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2

Omholt, Katarina. "Activating proto-oncogene mutations in human cutaneous melanoma /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-191-1/.

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3

Estrozi, Bruna. "Avaliação anatomoclínica e molecular do melanoma cutâneo em pacientes jovens (idade 18-30 anos)." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/5/5144/tde-01042015-144721/.

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A incidência do melanoma cutâneo em pacientes adultos jovens tem aumentado consideravelmente nos últimos anos. Há, contudo, carência de conhecimentos clinicopatológicos e moleculares sobre os melanomas que ocorrem nessa faixa etária. O presente estudo teve por objetivo avaliar 132 casos de melanoma cutâneo primário em pacientes com idade entre 18 e 30 anos, com ênfase no estudo das características clínicas, histopatológicas e avaliação molecular das mutações nos genes BRAF, NRAS e KIT. Em relação aos achados clínicos e histopatológicos, houve predomínio de indivíduos do sexo feminino (61,4%),

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4

Appleman, Victoria A. "Mechanisms of KRAS-Mediated Pancreatic Tumor Formation and Progression: A Dissertation." eScholarship@UMMS, 2012. https://escholarship.umassmed.edu/gsbs_diss/600.

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Pancreatic cancer is the 4th leading cause of cancer related death in the United States with a median survival time of less than 6 months. Pancreatic ductal adenocarcinoma (PDAC) accounts for greater than 85% of all pancreatic cancers, and is marked by early and frequent mutation of the KRAS oncogene, with activating KRAS mutations present in over 90% of PDAC. To date, though, targeting activated KRAS for cancer treatment has been very difficult, and targeted therapies are currently being sought for the downstream effectors of activated KRAS. Activation of KRAS stimulates multiple signaling pa

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5

Dutenhefner, Simone Elisa. "Pesquisa da mutação T1799A do gene BRAF e a presença de metástases linfáticas no carcinoma papilífero da tireoide." Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/5/5132/tde-24012012-163817/.

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Muitos pacientes submetidos à tireoidectomia por Carcinoma Papilífero da Tireoide (CPT) têm doença linfonodal subclínica no momento da cirurgia. A mutação BRAF T17799A (V600E) é um evento comum no CPT e alguns estudos demonstram correlação entre a mutação e características de maior agressividade tumoral, incluindo a presença de metástases linfonodais. O esvaziamento eletivo do compartimento central ganha aceitação, uma vez que alguns estudos evidenciam que a presença de metástases linfonodais aumenta o risco de recidiva e mortalidade. Devido ao grande potencial de complicações do esvaziamento

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6

Borysova, Meghan E. K. "Novel roles for B-Raf in mitosis and cancer." [Tampa, Fla] : University of South Florida, 2009. http://purl.fcla.edu/usf/dc/et/SFE0002899.

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7

Freitas, Isabella Nicacio de. "Caracterização imuno-histoquímica e molecular dos pacientes com suspeita clínica de Síndrome de Lynch." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/5/5168/tde-09022015-095440/.

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Suspeita-se da Síndrome de Lynch (SL) a partir da história pessoal e familial do indivíduo. Posteriormente, os dados histopatológicos, imuno-histoquímicos e moleculares podem ser utilizados para aprimorar o diagnóstico da doença. Entretanto, um grande desafio no diagnóstico da Síndrome de Lynch é a baixa acurácia dos critérios clínicos utilizados. OBJETIVOS: Avaliar a frequência de SL em pacientes submetidos a tratamento cirúrgico por câncer colorretal e com história familial de câncer. Avaliar quais dos critérios clínicos e/ou moleculares seriam mais informativos no diagnóstico desta Síndrome

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8

Urcia, Roby Joseph. "The modulation of tumour suppressor MST2 and proto-oncogene Raf-1 kinases by the scaffold protein CNK1." Thesis, University of Glasgow, 2011. http://theses.gla.ac.uk/4183/.

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An emerging concept in the regulation of signal transduction specificity is the mediation of scaffold proteins embedded in the circuitry of signalling pathways. The multidomainbased architecture of scaffold proteins facilitates the assembly and modulation of protein complexes to regulate cellular signals to bring about an exacting biological output. The work presented in this thesis aimed to investigate the mechanisms of the protein scaffold CNK1 (connector enhancer of Ras 1) in the pro-apoptotic MST2 pathway and the prooncogenic Raf-1 signalling pathways. Here, by using several molecular, bio

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9

PAPIN, CATHERINE. "Etude biochimique et fonctionnelle des isoformes de l'oncoproteine b-raf (doctorat : bases fondamentales de l'oncogenese)." Paris 11, 1998. http://www.theses.fr/1998PA11T026.

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10

Benisty, Hannah 1986. "Post-transcriptional determinants of RAS protein abundance." Doctoral thesis, Universitat Pompeu Fabra, 2019. http://hdl.handle.net/10803/668206.

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The RAS oncogenes KRAS, NRAS and HRAS are mutated in one third of human cancers where they exhibit different mutation patterns. A potential factor contributing to this mutation bias is the variation of RAS expression levels. Here, I investigate some of the determinants of RAS protein abundance. First, I examine whether codon bias among RAS genes and within other cancer gene families plays a role in cell context-specific expression. I further describe a tRNA expression program that favors oncogene translation in proliferating cells. Second, I investigate why oncogenic RAS mutants exhibit a hi

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11

Yasmin, Lubna. "Exoenzyme S of Pseudomonas aeruginosa : cellular targets and interaction with 14-3-3." Doctoral thesis, Umeå : Univ, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1411.

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12

Filho, João Bosco de Oliveira. "Mutação em NRAS causa uma síndrome autoimune linfoproliferativa humana." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/5/5144/tde-04112008-174252/.

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A subfamília p21 RAS de pequenas GTPases, incluindo KRAS, HRAS e NRAS, participa de muitas redes de sinalização, incluindo proliferação celular, organização do citoesqueleto e apoptose, e é o alvo mais freqüente de mutações ativadoras em câncer. Mutações germinativas em KRAS e HRAS causam graves anormalidades desenvolvimentais levando às síndromes de Noonan, cárdio-facial-cutânea e Costello, porem mutações ativadoras germinativas em NRAS não foram descritas até hoje. A síndrome autoimune linfoproliferativa (ALPS) é o mais comum defeito genético de apoptose linfocitária, cursando com autoimunid

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13

Driscoll, David R. "The Impact of mTORC2 Signaling on the Initiation and Progression of KRAS-Driven Pancreatic Neoplasias: A Dissertation." eScholarship@UMMS, 2003. http://escholarship.umassmed.edu/gsbs_diss/821.

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Pancreatic ductal adenocarcinoma (PDAC), the most common form of pancreatic cancer, develops through progression of premalignant pancreatic intraepithelial neoplasias (PanINs). In mouse-models, KRAS-activation in acinar cells induced an acinar-to-ductal metaplasia (ADM), and mutation of the Kras oncogene is believed to initiate PanIN formation. ADM is also promoted by pancreatic injury, which cooperates with activated KRAS to stimulate PanIN and PDAC formation from metaplastic ducts. Our lab, and others, have shown that the downstream PI3K/AKT pathway is important for KRAS-mediated proliferati

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14

Driscoll, David R. "The Impact of mTORC2 Signaling on the Initiation and Progression of KRAS-Driven Pancreatic Neoplasias: A Dissertation." eScholarship@UMMS, 2016. https://escholarship.umassmed.edu/gsbs_diss/821.

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Pancreatic ductal adenocarcinoma (PDAC), the most common form of pancreatic cancer, develops through progression of premalignant pancreatic intraepithelial neoplasias (PanINs). In mouse-models, KRAS-activation in acinar cells induced an acinar-to-ductal metaplasia (ADM), and mutation of the Kras oncogene is believed to initiate PanIN formation. ADM is also promoted by pancreatic injury, which cooperates with activated KRAS to stimulate PanIN and PDAC formation from metaplastic ducts. Our lab, and others, have shown that the downstream PI3K/AKT pathway is important for KRAS-mediated proliferati

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15

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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16

Kinkade, Rebecca. "Rb-Raf-1 interaction as a therapeutic target for proliferative disorders." [Tampa, Fla] : University of South Florida, 2008. http://purl.fcla.edu/usf/dc/et/SFE0002426.

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17

Quattrochi, Brian J. "Subtle Controllers: MicroRNAs Drive Pancreatic Tumorigenesis and Progression: A Dissertation." eScholarship@UMMS, 2015. https://escholarship.umassmed.edu/gsbs_diss/776.

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Pancreatic ductal adenocarcinoma (PDAC) is among the most lethal malignancies in the United States, with an average five-year survival rate of just 6.7%. One unifying aspect of PDAC is mutational activation of the KRAS oncogene, which occurs in over 90% of PDAC. Therefore, inhibiting KRAS function is likely an effective therapeutic strategy for this disease, and current research in our lab and others is focused on identifying downstream effectors of KRAS signaling that may be therapeutic targets. miRNAs are powerful regulators of gene expression that can behave as oncogenes or tumor suppressor

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18

Quattrochi, Brian J. "Subtle Controllers: MicroRNAs Drive Pancreatic Tumorigenesis and Progression: A Dissertation." eScholarship@UMMS, 2004. http://escholarship.umassmed.edu/gsbs_diss/776.

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Pancreatic ductal adenocarcinoma (PDAC) is among the most lethal malignancies in the United States, with an average five-year survival rate of just 6.7%. One unifying aspect of PDAC is mutational activation of the KRAS oncogene, which occurs in over 90% of PDAC. Therefore, inhibiting KRAS function is likely an effective therapeutic strategy for this disease, and current research in our lab and others is focused on identifying downstream effectors of KRAS signaling that may be therapeutic targets. miRNAs are powerful regulators of gene expression that can behave as oncogenes or tumor suppressor

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19

Gilkes, Daniele M. "Multiple modes of MDMX regulation affect p53 activation." [Tampa, Fla.] : University of South Florida, 2008. http://purl.fcla.edu/usf/dc/et/SFE0002312.

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20

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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21

Valluet, Agathe. "Utilisation de modèles murins pour l'étude du rôle physiologique des isoformes de BRaf et du rôle des protéines Raf dans le lignage mélanocytaire." Paris 7, 2010. http://www.theses.fr/2010PA077167.

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Le laboratoire s'intéresse à la voie de signalisation ERK, particulièrement aux protéines Raf (ARaf, BRaf et I CRaf). Nous avons montré que le gène BRAF codait de multiples isofbrmes présentant une expression tissu-j spécifique. La présence des séquences codées par les exons 8b/9b module les propriétés biochimiques et I oncogéniques de BRaf Mon projet de recherche a consisté à analyser le phénotype de souris knockout dans | lesquelles chacun des exons a été invalidé. Les résultats ont montré que l'épissage alternatif n'est pas essentiel pour I le développement ni pour la myélination du cerveau

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22

Bessa, Tiphany Coralie de. "Mecanismo associados à perda da regulação da nox1 NADPH oxidase pela dissulfeto isomerase proteica em células com ativação sustentada da via ras." Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/5/5131/tde-03072018-090616/.

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Dissulfeto isomerase proteica como a PDIA1 tem sido implicada na progressão do câncer, porém os mecanismos envolvidos ainda não foram claramente identificados. Previamente, nós demonstramos um importante efeito da PDIA1 induzindo a superexpressão da Nox1 NADPH oxidase, associada à geração de espécie reativas de oxigênio (ROS). Uma vez que a perda na regulação de ROS envolve o crescimento tumoral, nós propusemos que a PDIA1 atua como um mecanismo regulador proximal na produção de ROS em tumores. No presente estudo, nós focamos no câncer colorretal (CRC) com distintos efeitos na ativação de KRas

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23

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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24

Alexandre, Cristianne da Silva. "As células linhagem negativa (Lin) de medula óssea atenuam a progressão da doença renal crônica." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/5/5148/tde-10032008-150329/.

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Introdução: A doença renal crônica continua sendo um desafio no campo da pesquisa médica. Atualmente um interesse crescente tem surgido no intuito de avaliar o potencial de células tronco em retardar o avanço de doenças crônicas progressivas. Material e Métodos: Para determinar o efeito dessas células em um modelo de progressão de doença renal crônica foram usadas células linhagem negativa (Lin ) separadas magneticamente e injetadas em ratos submetidos à injúria renal. Ratos singênicos Fischer 344 foram submetidos à nefrectomia 5/6 (Nx) e divididos em 3 grupos: Nx (não tratados); NxSC1 (submet

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25

Carie, Adam E. "Tumor suppressive effects of the Beta-2 adrenergic receptor and the small GTPase RhoB." [Tampa, Fla.] : University of South Florida, 2008. http://purl.fcla.edu/usf/dc/et/SFE0002330.

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26

Delyon, Julie. "PDE4 : cible thérapeutique dans le mélanome cutané." Thesis, Sorbonne Paris Cité, 2017. http://www.theses.fr/2017USPCC312/document.

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Le mélanome cutané métastatique était un cancer au pronostic particulièrement péjoratif, jusqu’au développement récent de 2 classes pharmacologiques: l’immunothérapie, pour tous les mélanomes, et les thérapies ciblées, principalement pour les mélanomes porteurs de la mutation BRAF (50% des mélanomes cutanés). Mais l’apparition de résistance, et l’absence de thérapies ciblées sur les mélanomes non mutés BRAF, incitent à rechercher de nouvelles cibles thérapeutiques. Notre travail portait sur l’étude in vitro de la phosphodiestérase de type 4 (PDE4), une enzyme régulant la voie de l’AMPc, princi

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27

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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28

Kumar, A., Mojgan Najafzadeh, B. K. Jacob, A. Dhawan, and Diana Anderson. "Zinc oxide nanoparticles affect the expression of p53, Ras p21 and JNKs: an ex vivo/in vitro exposure study in respiratory disease patients." 2015. http://hdl.handle.net/10454/9369.

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No<br>Zinc oxide (ZnO) nanoparticles are the mostly used engineered metal oxide nanoparticles in consumer products. This has increased the likelihood of human exposure to this engineered nanoparticle (ENPs) through different routes. At present, the majority of the studies concerning ZnO ENPs toxicity have been conducted using in vitro and in vivo systems. In this study, for the first time we assessed the effect of ZnO ENPs on the major cellular pathways in the lymphocytes of healthy individuals as well as in susceptible patients suffering from lung cancer, chronic obstructive pulmonary disease

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