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1
Straaten, J. P. van. „Studies on the human c-myc gene product“. Thesis, University of Cambridge, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.377708.
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2
Kuschak, Theodore I. „c-Myc dependent genomic instability of the ribonucleotide reductase R2 gene“. Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0020/NQ53061.pdf.
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Chana, Jagdeep. „The prognostic and therapeutic significance of C-MYC expression in melanoma“. Thesis, Imperial College London, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.314348.
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Melkoumian, Zaroui K. „Pharmacological regulation of c-myc gene expression in human breast cancer cells“. Morgantown, W. Va. : [West Virginia University Libraries], 2001. http://etd.wvu.edu/templates/showETD.cfm?recnum=2218.
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Thesis (Ph. D.)--West Virginia University, 2001.Title from document title page. Document formatted into pages; contains x, 152 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references (p. 119-149).
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Dedieu, Jean-François. „Activites et localisation du produit du premier exon de l'oncogene c-myc humain“. Paris 6, 1987. http://www.theses.fr/1987PA066331.
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6
Peres, Raquel Mary Rodrigues 1983. „Instabilidade genômica em neoplasias malignas da mama em função da concentração de alumínio intracelular : Genomic instability association with intracellular aluminum concentration in breast tumors“. [s.n.], 2013. http://repositorio.unicamp.br/jspui/handle/REPOSIP/310522.
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Orientador: Luis Otavio Zanatta SarianTese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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Resumo: Introdução: A hipótese de que os efeitos do alumínio em células humanas podem ter implicações clínicas tem sido levantada há algum tempo, especialmente no que concerne ao câncer de mama. As evidências laboratoriais mostrando altos níveis de alumínio nos tecidos da mama e os efeitos biológicos conhecidos sobre esse metal não são suficientes para estabelecer uma relação causal entre a exposição ao alumínio e o risco aumentando para o desenvolvimento do câncer de mama. O objetivo deste estudo foi estabelecer a concentração de alumínio nas áreas centrais e periféricas de tumores de mama, assim como na área glandular normal da mama e correlacionar esses achados com a instabilidade dos genes ERBB2, C-MYC e CCND1 e a aneuploidia dos cromossomos que contêm estes genes. Métodos: Para este estudo foram incluídas 176 mulheres com diagnóstico de carcinoma invasor de mama, com tumores maiores de 1cm3, sem quimioterapia neoadjuvante, operadas enter 2008 e 2010 no Hospital da Mulher Prof. Dr. José Aristodemo Pinotti - Centro de Atenção Integral à Saúde da Mulher (CAISM) - UNICAMP. Para a análise da concentração de alumínio intracelular, amostras de 150 pacientes foram consideradas viáveis; para a análise da instabilidade genômica em função da concentração de alumínio, 118 amostras foram consideradas viáveis, definindo o espaço amostral de cada um dos artigos apresentados. As amostras das áreas centrais e periféricas dos tumores de mama e das áreas glandulares normais da mama foram obtidas. A quantificação do alumínio contido nos tecidos da mama foi feita através da técnica de Espectrometria de Absorção Atômica em Forno de Grafite (GFAAS). Uma lâmina de Tissue Microarray (TMA), contendo as amostras de tumor e tecido normal foi utilizado para a realização da técnica de FISH para acessar o status dos genes ERBB2, C-MYC e CCND1 e dos centrômeros dos seus respectivos cromossomos 17, 8 e 11. Os dados clínico-patológicos foram obtidos dos prontuários de pacientes. Resultados: A média da concentração de alumínio encontrada na mama foi de 1,88 mg/kg nas áreas centrais do tumor, 2,10mg/kg nas áreas periféricas do tumor e 1,68mg/kg nas áreas de tecido glandular normal. A amplificação e/ou aneuploidia para ERBB2/CEP17, C-MYC/CEP8 e CCND1/CEP11 foi encontrada em 24%, 36,7% e 29,3% dos tumores, respectivamente. A média da concentração de alumínio nas áreas tumorais (tanto centrais quanto periféricas) não foi significativamente diferente daquela nas áreas de tecido normal. A concentração de alumínio também não foi significativamente associada a nenhum status de amplificação e/ou aneuploidia para os genes/cromossomos em questão. Conclusões: Consideramos importante que estudos experimentais in vitro continuem sendo realizados para elucidar os possíveis efeitos do alumínio nos tumores de mama, quer sejam esses efeitos relacionados ao microambiente tecidual ou mesmo a outras vias de estabilidade genômica
Abstract: Introduction: It has long been hypothesized if the effects of aluminum on human cells may have clinical implications, especially regarding to breast cancer. The current laboratorial evidence showing higher levels of aluminum in breast tissues and the known biological effects of this metal, are not sufficient to establish a causal relationship between aluminum exposure and increased risk of developing breast cancer. The objective of this study was to establish the aluminum concentration in the central and peripheral areas of breast tumors as well as in normal glandular area of the breast and to correlate these findings with the instability of ERBB2, C-MYC and CCND1, and aneuploidy of chromosomes harboring these genes. Methods: This study included 176 women diagnosed with invasive breast carcinoma with tumors larger than 1cm3 without neoadjuvant chemotherapy, operated between 2008 and 2010 at the Women's Hospital Professor. Dr. José Aristodemo Pinotti - Centro de Atenção Integral à Saúde da Mulher (CAISM) - UNICAMP. To analyze the intracellular concentration of aluminum, samples from 150 patients were considered viable; for the analysis of genomic instability as a function of the concentration of aluminum, 118 samples were considered viable. These figures define the sample of each of the two articles that this PhD thesis comprises. Evaluation of tissue aluminum content was carried out using Graphite Furnace Atomic Absorption Spectrometry (GFAAS). A TMA slide containing the tumor and normal samples was used in FISH assays to assess ERBB2, C-MYC and CCND1 and the respective chromosomes 17, 8 and 11 centromeres status. Clinicopathological data were obtained from patients' records. Results: The average aluminum content found in breast was 1.88 mg/kg in the central tumor areas, 2.10 mg/ kg in the peripheral tumor areas and 1.68 mg/ kg in the normal tissue areas. The amplification and/or aneuploid status for the ERBB2/CEP17, C-MYC/CEP8 and CCND1/CEP11 was detected in 24%, 36.7% and 29.3% of the tumors, respectively. The average aluminum content in tumor areas (either central or peripheral) was not significantly different from that in normal tissues. We found that aluminum concentration was not related to any of the gene status. Conclusions: We consider important that in vitro experimental studies continue to be done in order to elucidate the possible effects of aluminum in the development of breast tumors, whether it is influencing the tissue microenvironment or other genome stability pathways
Doutorado
Oncologia Ginecológica e Mamária
Doutora em Ciências da Saúde
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Lepique, Ana Paula. „O Gene c-myc e o controle do ciclo celular por ACTH em células adrenocorticais de camundongo da linhagem Y-1“. Universidade de São Paulo, 2000. http://www.teses.usp.br/teses/disponiveis/46/46131/tde-14102008-085011/.
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ACTH é o hormônio trófico que estimula a esteroidogênese, promove o crescimento e a manutenção do córtex adrenal. Porém, em linhagens adrenocorticais, assim como em culturas primárias, ACTH inibe a proliferação celular. A linhagem Y-1 de células adrenocorticais de camundongo tem as seguintes respostas a ACTH: aumento da esteroidogênese, arredondamento celular, bloqueio do ciclo celular em G1 e indução dos proto-oncogenes fos e jun. Esta linhagem também responde muito Sem a FGF2, um protótipo da família dos FGFs (Fibroblast Growth Factors) que regula diferenciação e proliferação de diversos tipos celulares, sendo estimulada a transitar pelas fases G0→G1→S do ciclo celular. ACTH antagoniza este efeito de FGF2, inibindo parcialmente a entrada em S induzida por FGF2. Este projeto buscou compreender o papel de c-Myc no controle do ciclo celular de Y-1, com ênfase nos efeitos de ACTH e FGF2 na expressão e atividade de c-Myc. Mostramos que os dois principais controles da expressão de c-Myc em Y-1 são transcrição e degradação da proteína, sendo a concentração de c-Myc o único controle sobre o sistema Myc/Max/Mad, uma vez que a expressão de Max e de Mad-1 , Mad-4 e Mxi é constitutiva em células Y-1. FGF2 induz a expressão de c-Myc através da indução da transcrição e aumento da estabilidade da proteína de forma totalmente dependente da via de Erk-MAPK. ACTH, por outro lado, não interfere com a transcrição de c-myc, mas promove fortemente a degradação da proteína, dependentemente da via de PKA. Utilizando um sistema de transfecção transiente, transfectamos uma quimera da proteína c-Myc com o receptor de estrógeno, MycER. Quando ativada por tamoxifen, a quimera migra para o núcleo e reverte a ação anti-mitogênica de ACTH sobre FGF2, porém, não tem efeito sobre células carenciadas tratadas ou não com ACTH apenas. Em conclusão, o antagonismo entre ACTH e FGF2 no controle da transição G0→G1→S do ciclo celular de Y-1 pode ser explicado pelas suas ações antagônicas sobre a estabilidade da proteína c-Myc.ACTH is the trophic hormone that stimulates steroidogenesis, promotes growth and maintenance of the adrenal cortex. However, in adrenal cell lines, as well as in primary cultures, ACTH inhibits cell proliferation. ACTH effects on Y-1 cells are: increasing in steroidogenesis, cell rounding, cell cycle blocking in G1 phase and induction of fos and jun proto-oncogenes expression. Y-1 cell line displays a robust response to FGF2, a member from the FGFs family (Fibroblast Growth Factors), which regulates differentiation and proliferation in many cell types, being induced to enter G0→G1→S phases of fhe cell cycle upon FGF2 stimulation. ACTH antagonizes FGF2 effect, partially inhibiting cell cycle progression stimulated by FGF2. This project aimed to investigate c-Myc role in Y-1 cell cycle control, with emphasis on ACTH and FGF2 effects on its expression and activity control. We have shown that there are two main controls of c-Myc expression in Y-1 cells, transcription and protein stability. c-Myc concentration regulates the system Myc/Max/Mad, once Max and also Mad-1, Mad-4 and Mxi expression is constitutive in Y-1 cells. FGF2 induces c-Myc expression by increasing its transcription rate and stabilizing the protein in an Erk-MAPK pathway dependent manner. ACTH, on the other hand, does not control c-myc transcription but promotes a strong degradation of the protein through the PKA pathway. Using a transient transfection system, we were able to express MycER, a chimera of c-Myc and estrogen receptor in Y-1 cells. When activated by tamoxlfen, MycER is translocated to cell nucleus, where it abolishes the anti-mitogenic effect of ACTH over FGF2. However, it has no effect on cell cycle progression of serum starved cells treated or not with ACTH only. In conclusion, their antagonist effects on c-Myc protein stability can explain the antagonist effects of ACTH and FGF2 on the control of G0→G1→S transition of Y-1 cell cycle.
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Hagemeier, Christian. „Transactivation of the hsp70 gene and protooncogenes c-fos and c-myc by human cytomegalovirus immediate early proteins“. Thesis, University of Cambridge, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.316643.
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Clarke, Matthew Alan. „Predictive computational modelling of the c-myc gene regulatory network for combinatorial treatments of breast cancer“. Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/284163.
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As cancer tumours develop, competition between cells will favour those with some mutations over others, creating a dynamic heterogeneous system made up of different cell populations, called sub-clones. This heterogeneity poses a challenge for treatment, as this variety serves to ensure there is almost always a portion of the cells which are resistant to any one targeted therapy. This can be avoided by combining therapies, but finding viable combinations experimentally is expensive and time-consuming. However, there is also cooperation between sub-clones, and being able to better model and predict these dynamics could allow this interdependence to be exploited. In order to investigate how best to tackle tumour heterogeneity, while avoiding acquired resistance, I have developed the first comprehensive computational model of the gene regulatory network in breast cancer focused on the c-myc oncogene and the differences between sub-clones. I model the system as a discrete, qualitative network, which can reproduce the conditions in heterogeneous tumours, as well as predict the effect of perturbations mimicking mutations or application of therapy. Together with experimental collaborators, I apply my computational model to an in vivo mouse model of MMTV-Wnt1 driven breast cancer, which has high and low c-myc expressing sub-clones. I show that the computational model is able to reproduce the behaviour of this system, and predict how best to target either one sub-clone individually or the tumour as a whole. I show how combination therapies offer more paths to attack the tumour, and how two drugs can work synergistically. For example, I predict how Mek inhibition will preferentially affect one sub-clone, but the addition of COX2 inhibition improves effectiveness across the tumour as a whole. In this thesis, I show how a computational network model can predict treatments in breast cancer, and assess the effects on different clones of different treatment combinations. This model can be easily extended with new data, as well as adapted to different types of cancer. This therefore represents a novel method to find viable combination therapies computationally and speed up the development of new cancer treatments.
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SILVA, FILHO João Luiz Quirino da. „Avaliação da amplificação e superexpressão do gene c-myc em subtipos moleculares de carcinoma ductal invasivo“. Universidade Federal de Pernambuco, 2016. https://repositorio.ufpe.br/handle/123456789/23420.
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REUNI
O câncer de mama é o segundo tipo de câncer mais frequente no mundo e o mais comum entre as mulheres, correspondendo a 25% de todos os cânceres do sexo feminino. No Brasil, representa a primeira incidência de neoplasia na mulher. O gene c-myc codifica fatores de transcrição que participam, direta e indiretamente, da regulação do ciclo celular, diferenciação, metabolismo, crescimento, apoptose, instabilidade genômica, angiogênese e imortalização celulares. O c-myc tem sido apontado como peça central no processo tumorigênico e sua amplificação está relacionada com carcinomas invasivos que apresentam comportamento clínico mais agressivo e prognóstico reservado. Diante disto, o presente estudo objetivou investigar a relação da amplificação do gene c-myc com fatores prognósticos entre os subtipos moleculares de câncer de mama diagnosticado com carcinoma ductal invasivo (CDI). As amostras de CDI (n=60), fixadas em formalina e embebidas em parafina, foram obtidas no Arquivo de Biópsias do Serviço de Anatomia Patológica do Hospital das Clínicas (HC) da Universidade Federal de Pernambuco (UFPE). A caracterização dos tumores em subtipos moleculares foi realizada utilizando imunohistoquímica para receptor de fator de crescimento epidérmico do tipo 2 (HER-2), receptores de estrógeno (RE) e progesterona (RP) e o fator de proliferação celular (Ki-67). A detecção da amplificação do gene c-myc foi realizada através de Hibridização in situ cromógena (CISH). Os resultados mostraram maiores frequências para os subtipos Luminal A (37,7%) e Triplo-Negativo (40%). Neste estudo tumores Luminais, notadamente Luminal A, apresentaram correlação estatistica quanto ao nível de diferenciação (p=0,0135), tamanho menor (p=0.5715), em estádio inicial no momento do diagnóstico; e com baixo a médio grau histológico e nuclear ao diagnóstico, respectivamente. Tumores dos subtipos superexpressão de HER-2 e Triplo-Negativo se relacionaram com caraterísticas prognósticas desfavoráveis, apresentando maiores taxas de invasão linfonodal, maiores chances de tumores indiferenciados e predomínio de diagnóstico entre as pacientes mais jovens, respectivamente. A maior frequência de amplificação do c-myc foi observada em 21 tumores (35%) no subtipo Triplo-Negativo, indicando que a amplificação pode estar associada a tumores mais agressivos e por isso um prognóstico reservado.
Breast cancer is the second most common cancer type worldwide and the most common among women, accounting for 25% of all female cancers. In Brazil, it represents the most incident cancer type in women. C-myc gene encodes transcription factors which are, directly and indirectly, involved in cell cycle regulation, differentiation, metabolism, growth, apoptosis, genomic instability, angiogenesis and cell immortalization. It has been considered as playing a role in tumorigenesis and its amplification is associated with more aggressive clinical behavior and poor prognosis in invasive carcinomas. This study aimed to investigate the relationship of c-myc amplification and clinicopathologic features amog the subtypes of invasive ductal carcinomas (IDC) of breast. Formalin-fixed and paraffin-embeded tissues samples (n=60) were retrieved from the Biopsies Archives of Anatomy and Pathology Sector of University Hospital at Federal University of Pernambuco. Tumors subtyping was developed using immunohistochemistry against epidermal growth factor receptor type 2 (HER-2), estrogen and progesterone receptors (ER and PR) and cell proliferating factor Ki-67. c-myc amplification was evaluated via chromogenic in situ hybridization (CISH). Results showed that the most frequent breast carcinomas subtypes were Luminal A (37.7%) and Triple-Negative (40%). Luminal tumors, mainly subtype A, showed to be well differentiated tumours regarding histological grade (p=0.0135), of small size (p=0.5715) at an early stage and presented a low and medium histologic and nuclear grade, respectively, at the time of diagnosis. Triple-Negative and HER-2 superexpression carcinomas were larger tumours, poorly differentiated (p= 0.0570), presenting higher rates of ganglionar involvement, advanced stages tumors and younger patients at the time of diagnosis, presenting the worst prognosis. We observed c-myc amplification in 21 tumours (35%) but no statistical difference was found between amplified and nonamplified and molecular subtypes of breast cancer.
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Lepique, Ana Paula. „Efeitos de ACTH, PMA e dcAMP na expressão de genes das famílias FOS e JUN do gene C-MYC e na atividade do fator de transcrição AP-1 em células adrenocorticais Y-1“. Universidade de São Paulo, 1996. http://www.teses.usp.br/teses/disponiveis/46/46131/tde-18092008-093726/.
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As células Y-1 pertencem a uma linhagem clonal de células funcionais de córtex adrenal de camundongo, que respondem a ACTH. Em células Y-1, ACTH promove a esteroidogênese (função) e tem efeitos regulatórios complexos na transição G0→G1→S do ciclo celular. ACTH promove a transição G0→G1, mas inibe a transição G1→S. É possível que a regulação do ciclo celular por ACTH seja mediada pelo controle da expressão dos proto-oncogenes das famílias fos, jun e myc. Nosso laboratório mostrou, anteriormente, que ACTH induz a expressão dos genes fos e jun, mas inibe c-myc. O objetivo deste trabalho foi identificar pontos de controle na expressão dos genes fos, jun e myc e na atividade dos fatores de transcrição AP-1 (dímeros da proteínas Fos e Jun) por ACTH, derivados de cAMP (ativadores de PKA), PMA (ativador de PKC) e FCS (soro fetal bovino). ACTH, PMA e dcAMP aumentam a atividade de ligação de AP-1 a DNA, independentemente de síntese protéica. Ensaios de elongação de cadeia nascente de RNA (run off transcription) mostram que ACTH, PMA e FCS são fortes indutores de c-fos, c-jun e junB, enquanto dcAMP induz apenas c-fos e junB. Hibridizações Northern permitiram estimar a meia-vida dos mRNAs de c-fos e c-jun em 30 min, independentemente do tratamento com ACTH ou PMA. Diferentemente de c-fos, o mRNA de fosB é superinduzido por ActinomicinaD em células Y-1 tratadas com ACTH e PMA.The Y-1 cells belong to a clonal lineage of functional mouse adrenocortical cells, which are responsive to ACTH. In Y-1 cells, ACTH promotes esteroidogenesis (function) and has complex effects on the G0→G1→S transition of the Y-1 cell cycle. ACTH induces the G0→G1 transition but inhibits the G1+S transition. Probably, the cell cycle regulation by ACTH is mediated by the expression control of the proto-oncogenes from the fos, jun and myc families. Our laboratory has previously shown that ACTH induces the fos and jun genes expression, but inhibits c-myc expression. The target of this work was to identify control points in the fos, jun and myc genes expression and in the AP-1 transcription factors (Fos and Jun proteins dimers) by ACTH, cAMP derivatives (PKA activators), PMA (PKC activator) and FCS (Fetal Calf Serum). ACTH, PMA and dcAMP raise the AP-1 DNA binding activity, independently of protein synthesis. Run off transcription assays show that ACTH, PMA and FCS are strong c-fos, c-jun and junB inducers, while dcAMP induces only c-fos and junB. Northern hybridisations allowed us to estimate the half life of the fos and jun mRNAs in about 30 min, independently of ACTH or PMA treatment. Differently of c-fos, fosB mRNA is superinduced by ActinomicinD treatment in Y-1 cells treated with ACTH or PMA.
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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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Kastler, Silvia [Verfasser]. „On the impact of risk variants in the c-MYC gene region on prostate cancer development / Silvia Kastler“. Ulm : Universität Ulm. Medizinische Fakultät, 2011. http://d-nb.info/1016659628/34.
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Winnischofer, Sheila Maria Brochado. „Caracterização do envolvimento do gene RECKna proliferação celular e progressão tumoral: inversa correlação com a expressão do oncogene c-myc“. Universidade de São Paulo, 2005. http://www.teses.usp.br/teses/disponiveis/46/46131/tde-14072016-110620/.
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Este trabalho mostra o envolvimento do gene RECK no processo de progressão do ciclo celular. Foi verificado que a expressão endógena de RECK é modulada durante a progressão do ciclo celular. A superexpressão de RECK em fibroblastos normais de camundongo promove uma diminuição da capacidade proliferativa das células e um retardo da transição das fases G0/G1-S do ciclo celular. Além disso, os resultados sugerem que um dos possíveis mecanismos de ação de RECK, que promovem este processo, envolve a indução da expressão de um inibidor de CDK, especificamente de p21, e retardo da fosforilação de pRb. Os resultados indicam, ainda, que durante a progressão do ciclo celular a expressão do gene RECK apresenta uma correlação inversa com a expressão do proto-oncogene c-myc. Estes dados corroboram os dados da literatura que mostram RECK como um alvo para o produto de diversos oncogenes, como ras e c-myc. A caracterização da repressão de RECK por c-Myc mostrou que a mesma ocorre ao nível transcricional e que sítios Sp1, presentes no promotor de RECK, são essenciais para a ação de Myc. Dados adicionais sugerem que a repressão de RECK por c-Myc parece envolver mecanismos de desacetilação de histonas. A modulação da expressão de RECK também foi avaliada durante a progressão maligna de tumores do sistema nervoso central (especificamente, gliomas). Foi verificado que a expressão de RECK não é alterada com a progressão deste tipo de tumor. Porém, foi verificado que os pacientes que manifestaram um maior tempo de sobrevida apresentaram tumores com uma significativa maior expressão do gene RECK. Estes dados sugerem que RECK possa ser um possível marcador prognóstico. A caracterização da regulação da expressão de RECK, tanto em células normais como em diferentes tipos de tumores, assim como os alvos moleculares da sua ação, são pontos muito importantes para o entendimento dos mecanismos que controlam a proliferação celular e podem contribuir para o desenvolvimento de novas formas de terapia anti-tumoral.This work shows, for the fIrst time, the involvement of the RECK gene in cell cycle progression. Our data shows that the RECK gene product regulates cell cycle progression by altering the G1 to S transition. Also, we show that RECK is able to induce p21 expression and, consequently, lead to hypophosphorylation of the Rb protein, revealing at least one molecular mechanism through which RECK modulates the cell cycle progression. It has been described that induction of the c-Myc transcription factor promotes cell proliferation and cell transformation by regulating several genes that are involved in cell cycle progression. Here, we show that activation of a Mycestrogen receptor fusion protein with 4-hydroxytamoxifen in mouse fibroblasts was suffIcient to repress the expression of the RECK gene, by acting at the RECK promoter region. In addition, we show that Myc-responsiveness seems to be mediated by the upstream Sp1 sites and to be dependent on cromatin remodelling mechanisms. RECK gene expression was aIso evaluated during human glioma progression. Our results indicate that RECK gene expression is not altered during glioma progresslOn, but a correlation was found between the abundance of RECK expression in gliomas and patient survival. The levels of RECK expression can be considered a good prognostic indicator for glioma patients. Better understanding of RECK gene regulation may contribute to uncover the mechanisms of cell cycle and tumor progression, and to the development of new strategies for cancer prevention and therapeutic intervention.
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Parkin, Neil T. „Regulation of gene expression by the 5' untranslated region of eukaryotic mRNAS : c-myc and HIV-1 as examples“. Thesis, McGill University, 1989. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=74327.
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The 5$ sp prime$ untranslated region (UTR) of c-myc and human immunodeficiency virus type 1 (HIV-1) mRNAs were used as models in a variety of in vitro and in vivo systems in order to study the role of this region in the control of eukaryotic gene expression. Using an ultraviolet light-induced crosslinking assay, a 55 kilodalton protein was identified in extracts of HeLa, mouse erythroleukemia, and other cell lines, which interacts specifically with a purine-rich RNA sequence in the 5$ sp prime$ UTR of c-myc. The function of this protein in control of c-myc expression is not known, but may be implicated in the process of transcriptional elongation. The 5$ sp prime$ UTR of HIV-1 mRNAs was shown to inhibit strongly the translation of a heterologous mRNA; this inhibition was dependent on the secondary structure predicted to form in this region, and on the accessibility of the cap structure to initiation factors. The structural requirements in the HIV-1 5$ sp prime$ UTR for trans-activation by the viral tat gene product were examined by mutagenesis studies; the base-pairing in the stem-loop structure, the sequence of the loop, and the presence of a three nucleotide bulge were found to be critical features necessary for complete trans-activation. These findings indicate that the 5$ sp prime$ UTR can have important effects on the expression of eukaryotic genes.
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Dufort, Daniel. „Characterization of a protein binding site involved in the regulation of transcription elongation within the murine c-myc gene“. Thesis, McGill University, 1993. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=41580.
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The c-myc gene was previously shown to be regulated by a conditional block to transcription elongation and sequences from its promoter were implicated in this regulation. The objective of this project was to define the promoter elements involved in the control of transcription elongation. Using heterologous promoter constructs, the ME1a1 protein binding site located in the c-myc promoter was shown to be required for the block to transcription elongation. From mutation analysis, a correlation was established between the binding of nuclear factors to ME1a1 sites in vitro and the ability of these sites to confer block to transcription elongation in vivo, strongly implicating trans-acting factors in this process. Fractionation studies demonstrated that three nuclear factors interact with the ME1a1 site, thus generating three protein-DNA complexes termed "a", "b", and "c". These factors were characterized and a cDNA encoding the protein responsible for complex "c" was isolated. This protein was shown to represent the human homologue of the Drosophila Cut homeodomain protein (hu-Cut) and to repress expression from the c-myc promoter in transient transfection assays.
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Modjtahedi, Nazanine. „Role de l'amplification du gene c-myc dans le phenotype tumoral des cellules de carcinome humain sw 613-s“. Paris 6, 1990. http://www.theses.fr/1990PA066245.
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Nous avons etudie le role de l'amplification de l'oncogene c-myc dans le phenotype tumoral en utilisant comme systeme experimental la lignee de carcinome humain sw613-s qui renferme un gene c-myc amplifie. Nous avons montre que cette lignee etait constituee d'au moins deux types cellulaires qui ont ete individualises sous forme de clones: d'une part des cellules ayant un haut niveau d'amplification et d'expression du gene c-myc qui sont tumorigenes chez la souris athymique; d'autre part des cellules a faible niveau d'amplification et d'expression qui ne sont pas tumorigenes. L'introduction de copies exogenes du gene c-myc par transfection dans les cellules non tumorigenes leur confere un phenotype tumorigene. Les cellules tumorigenes proliferent sans s'attacher, peuvent croitre dans un milieu chimiquement defini et produisent de hauts niveaux de plusieurs facteurs de croissance dont le tgh alpha. Les cellules non tumorigenes sont davantage dependantes de l'ancrage, ont une croissance restreinte en milieu defini et ne produisent pas de tgf alpha detectable. Par ailleurs nous avons identifies plusieurs autres genes dont le niveau d'expression est notablement different entre les cellules tumorigenes et non tumorigenes. En particulier, les cellules tumorigenes surexpriment les genes de plusieurs cytokeratines (k8, k18 et k19) et de la chaine h de la ferritine. Il reste maintenant a essayer de determiner quels sont les mecanismes qui regulent differentiellement l'expression de ces differents genes et si le gene c-myc participe a certains d'entre eux
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Lindström, Mikael. „Functional characterization of the alternative reading frame protein p14ARF /“. Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-917-x.
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Shiue, Jai-Jün [Verfasser]. „Modifier-Gene in BRCA1/2-Mutationsträgerinnen: SNP-Analyse (single nucleotide polymorphism) in AKAP10, AKAP13 und c-MYC / Jai-Jün Shiue“. Köln : Deutsche Zentralbibliothek für Medizin, 2014. http://d-nb.info/1049200160/34.
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Fonseca, Luciano Santos da [UNESP]. „Tumor venéreo transmissível espontâneo canino: a inserção do transposon line-1 no gene C-MYC e os critérios de malignidade“. Universidade Estadual Paulista (UNESP), 2009. http://hdl.handle.net/11449/89259.
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O Tumor Venéreo Transmissível (TVT) é uma das neoplasias mais antigas e em contínua propagação entre hospedeiros. É a segunda neoplasia mais diagnosticada em cães no Serviço de Patologia de Botucatu Dentre as alterações moleculares mais encontradas no TVT está o rearranjo do protooncogene c-MYC resultante da inserção do segmento de DNA repetitivo conhecido como LINE (Long Interspersed Element). O objetivo deste trabalho foi a identificação dos critérios citopatológicos de malignidade nos grupos linfocítóide e plasmocitóide pela técnica de Papanicolaou, a detecção do rearranjo LINE-1/c-MYC nas células do TVT e a realização do sequenciamento genético. Com a coloração de Papanicolaou, os critérios de malignidade nucleares mais observados foram espessamento da membrana nuclear, ranhura nuclear, nucléolo angular e halo perinucleolar. A Reação em Cadeia da Polimerase (PCR) amplificou um produto de 340pb em 100% das amostras analisadas e o sequenciamento genético confirmou a presença do rearranjo LINE-1/c-MYC. Concluiu-se que a especificidade desta alteração genética é indiscutível corroborando para mais estudos que permitirão o melhor entendimento quanto ao mecanismo de formação deste rearranjo. A coloração de Papanicolaou constituiu uma grande contribuição não apenas para o diagnóstico citológico do TVT, como também, ferramenta valiosa para evidenciação de critérios de malignidade que normalmente não são visualizados quando se utiliza corantes tipo Romanowsky. Para futuras investigações, este estudo poderá servir de esteio para correlacionar morfologia, critérios de malignidade e estudos moleculares ainda não realizados em conjunto para o TVT.
The Transmissible Venereal Tumor disease (TVT) is one of the neoplasias oldest and in continuous propagation between hosts and the second neoplasia more frequent diagnosed in dogs of in the Service of Pathology of Botucatu. Amongst the molecular alterations more frequently found in the TVT c-MYC resultant of the insertion of the repetitive segment of known DNA is the rearrangement of proto-oncogene as LINE (Long Interspersed Element). The objective of this work was the identification of the cytopathology criteria of malignancy in the groups linfocitóide and plasmocitóide for the technique of Papanicolaou, the detention of the LINE-1/c-MYC rearrangement in the cells of the TVT, and the accomplishment of the genetic sequencing. With the coloration of Papanicolaou, the observed nuclear criteria of malignancy more had been thicking of the nuclear membrane, nuclear groove, angular nucleolar and halo perinucleolar. The Reaction in Chain of Polimerase (PCR) amplified a product of 340pb in 100% of the analyzed samples and the genetic sequencing confirmed the presence of the LINE-1/c-MYC rearrangement and the degree of identity between the samples that 94% varied of 96%. Concluded that the especificidade of this genetic alteration is unquestionable corroborating for more studies that will allow optimum agreement how much to the mechanism of formation of this rearrangement. The Papanicolaou staining not only constituted a great contribution for the cytological diagnosis of the TVT, as well as, valuable tool for evideciacion of malignancy criteria that normally they are not visualized when Romanowsky type is used. For future inquiries, this study it will be able to serve of esteio to correlate morphology, criteria of malignidade and molecular studies not yet carried through in set for the TVT.
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Fonseca, Luciano Santos da. „Tumor venéreo transmissível espontâneo canino : a inserção do transposon line-1 no gene C-MYC e os critérios de malignidade /“. Botucatu : [s.n.], 2009. http://hdl.handle.net/11449/89259.
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Resumo: O Tumor Venéreo Transmissível (TVT) é uma das neoplasias mais antigas e em contínua propagação entre hospedeiros. É a segunda neoplasia mais diagnosticada em cães no Serviço de Patologia de Botucatu Dentre as alterações moleculares mais encontradas no TVT está o rearranjo do protooncogene c-MYC resultante da inserção do segmento de DNA repetitivo conhecido como LINE (Long Interspersed Element). O objetivo deste trabalho foi a identificação dos critérios citopatológicos de malignidade nos grupos linfocítóide e plasmocitóide pela técnica de Papanicolaou, a detecção do rearranjo LINE-1/c-MYC nas células do TVT e a realização do sequenciamento genético. Com a coloração de Papanicolaou, os critérios de malignidade nucleares mais observados foram espessamento da membrana nuclear, ranhura nuclear, nucléolo angular e halo perinucleolar. A Reação em Cadeia da Polimerase (PCR) amplificou um produto de 340pb em 100% das amostras analisadas e o sequenciamento genético confirmou a presença do rearranjo LINE-1/c-MYC. Concluiu-se que a especificidade desta alteração genética é indiscutível corroborando para mais estudos que permitirão o melhor entendimento quanto ao mecanismo de formação deste rearranjo. A coloração de Papanicolaou constituiu uma grande contribuição não apenas para o diagnóstico citológico do TVT, como também, ferramenta valiosa para evidenciação de critérios de malignidade que normalmente não são visualizados quando se utiliza corantes tipo Romanowsky. Para futuras investigações, este estudo poderá servir de esteio para correlacionar morfologia, critérios de malignidade e estudos moleculares ainda não realizados em conjunto para o TVT.Abstract: The Transmissible Venereal Tumor disease (TVT) is one of the neoplasias oldest and in continuous propagation between hosts and the second neoplasia more frequent diagnosed in dogs of in the Service of Pathology of Botucatu. Amongst the molecular alterations more frequently found in the TVT c-MYC resultant of the insertion of the repetitive segment of known DNA is the rearrangement of proto-oncogene as LINE (Long Interspersed Element). The objective of this work was the identification of the cytopathology criteria of malignancy in the groups linfocitóide and plasmocitóide for the technique of Papanicolaou, the detention of the LINE-1/c-MYC rearrangement in the cells of the TVT, and the accomplishment of the genetic sequencing. With the coloration of Papanicolaou, the observed nuclear criteria of malignancy more had been thicking of the nuclear membrane, nuclear groove, angular nucleolar and halo perinucleolar. The Reaction in Chain of Polimerase (PCR) amplified a product of 340pb in 100% of the analyzed samples and the genetic sequencing confirmed the presence of the LINE-1/c-MYC rearrangement and the degree of identity between the samples that 94% varied of 96%. Concluded that the especificidade of this genetic alteration is unquestionable corroborating for more studies that will allow optimum agreement how much to the mechanism of formation of this rearrangement. The Papanicolaou staining not only constituted a great contribution for the cytological diagnosis of the TVT, as well as, valuable tool for evideciacion of malignancy criteria that normally they are not visualized when Romanowsky type is used. For future inquiries, this study it will be able to serve of esteio to correlate morphology, criteria of malignidade and molecular studies not yet carried through in set for the TVT.
Orientador: Noeme Sousa Rocha
Coorientador: Lígia Souza Lima Silveira da Mota
Banca: Maria Denise Lopes
Banca: Adriene Pinto Vasques
Mestre
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Ye, Shanli. „DNA Sequences Involved in the Regulation of Human c-myc Gene Expression by Herpes Simplex Virus Type 1 (HSV-1)“. PDXScholar, 1995. https://pdxscholar.library.pdx.edu/open_access_etds/5221.
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The human c-myc gene is a cellular proto-oncogene composed of three exons and two introns. Transcription of c-myc is controlled by two promoters, Pl and P2. The activity of these promoters is regulated by many factors, such as cellular transcription factors E2F, YYl, and HSV-1 immediate-early proteins, ICPO, ICP4. Many regulatory elements located both upstream of and between P 1 and P2 have been identified, and some of these are required for optimum expression of c-myc. In this thesis research, a region downstream from P2 in the c-myc exon 1 was identified by its response to transactivation by HSV-1 immediate-early proteins, ICPO and ICP4. The purpose of this research was to examine this region for regulatory sites that respond to HSV-1 infection. I hypothesized that after HSV-1 infection, ICPO and ICP4 activate c-myc expression, in part, through regulatory sequences present in exon 1. To test for this hypothesis, reporter plasmids containing (I) the c-myc promoter (from - 101 bp relative to Pl) and exon 1 coupled to the bacterial CAT gene were constructed. (ii) The c-myc exon sequences used were either intact (wild-type) or they were constructed with various deletions. The activities of these plasmids were examined in transient expression assays. To analyze protein binding, electrophoretic mobility shift assay (EMSA) and completion EMSAs were carried out. The results from these experiments lead to the following conclusions: (i) ICP4 and ICPO serve as activators, whereas ICP27 inhibits c-myc gene expression. (ii) The region from +332 to +513 within the c-myc exon 1 contains an important element required for transactivation of the c-myc gene by HSV-1 proteins. (iii) Cellular proteins, including factor YYl, bind to the region from +332 to +513 in the c-myc exon 1. Although the exact mechanism by which HSV-1 immediate-early proteins regulate cmyc gene expression is still not clear, it gives rise to a possibility that this regulation is caused by turning on or activation of the cellular regulatory proteins by ICP4 and ICPO. The cellular proteins in turn activate the c-myc gene expression by interacting with the ciselement downstream from P2.
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Gazin, Claude. „Structure du locus c-myc humain : mise en evidence d'une proteine codee par le premier exon et determination de certaines de ses proprietes structurales et fonctionnelles“. Paris 6, 1988. http://www.theses.fr/1988PA066248.
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La sequence nucleotidique au locus c-myc humain revele trois exons, dont le deuxieme et le troisieme codent pour une proteine homologue a u-myc alors que le premier exon code pour une proteine de 118 aminoacides. L'utilisation d'anticorps antipeptides permet de mettre en evidence la proteine de l'exon 1 (mychex 1) dans les cellules humaines et la realisation de transcriptions et des traductions in vitro indique, de facon independante, que la proteine detectee correspond bien a l'exon 1 du genie c myc proteine mychex 1 (dimere de 58 kd), conservee dans l'ensemble du regne animal, presente la capacite d'interagir avec l'adn avec une specificite de sequence qui correspond a celle de nfi, facteur nucleaire dans le controle de la transcription et de la replication
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Corral, Marisol. „Caracterisation de genes cellulaires dont l'expression est associee a la cancerisation hepatique“. Paris 6, 1987. http://www.theses.fr/1987PA066124.
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Law, Wendy. „Characterization of FH3-derived and MC29-derived Gag-Myc fusion proteins : correlation of transcriptional repression and protein stability with cellular transformation /“. Thesis, Connect to this title online; UW restricted, 2000. http://hdl.handle.net/1773/5069.
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Massé, Karine. „Caractérisation des isoformes C et D de la NDP kinase chez la souris : étude préliminaire du rôle des isoformes A et B sur l'expression du protooncogène“. Bordeaux 2, 1999. http://www.theses.fr/1999BOR28669.
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Paleske, Lisa von [Verfasser], und Andreas [Akademischer Betreuer] Trumpp. „Identification of a novel enhancer region 1.7 Mb downstream of the c-myc gene controlling its expression in hematopoietic stem and progenitor cells / Lisa von Paleske ; Betreuer: Andreas Trumpp“. Heidelberg : Universitätsbibliothek Heidelberg, 2016. http://d-nb.info/1180735145/34.
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Harr, Michael W. „The interactive transcript abundance index [c-Myc*p73alpha]/[p21*Bcl-2] correlates with spontaneous apoptosis and response to CPT-11 : implications for predicting chemoresistance and cytotoxicity to DNA damaging agents“. Connect to Online Resource-OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=mco1176730845.
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Thesis (Ph.D.)--University of Toledo, 2007."In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biomedical Sciences." Major advisor: James Willey. Includes abstract. Title from title page of PDF document. Bibliography: pages 47-51, 73-76, 120-174.
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Dixon, Vincent. „Etudes sur la correlation entre l'etat differencie des cellules cibles b et l'infection par le virus de la leucemie aviaire (alv)“. Paris 7, 1988. http://www.theses.fr/1988PA077212.
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Corcos, Daniel. „Etude de l'expression des proto-oncogenes dans le foie normal et cancereux chez le rat“. Paris 7, 1988. http://www.theses.fr/1988PA077042.
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Augmentation correlee de l'expression des trois genes ras dans les tumeurs et egalement dans les parties non tumorales des foies cancereux. L'etude des variations physiologiques de l'expression des protooncogenes a revele un controle alimentaire de l'expression du gene c-myc
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Evans, Joanne R. „The investigation of internal ribosome entry in the c-myc and c-myb genes“. Thesis, University of Leicester, 2003. http://hdl.handle.net/2381/29681.
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The c-myc gene contains an internal ribosome entry site (IRES) within its 5' untranslated region. The IRES was shown to have different activities between cell lines suggesting a requirement for protein trans-acting factors that are present in these cell lines in varying amounts. In addition a number of proteins have been shown to interact with the IRES by north-western and UV cross-linking analysis. Investigation of the protein factors involved in c-myc IRES translation identified PCBP1 (Poly (rC) binding protein 1), PCBP2, HnRNPK (heterogeneous nuclear ribonucleoprotein K), UNR (upstream of N-ras) and UNRIP (unr interacting protein) as having a role in c-myc IRES translation, PCBP1, PCBP2, HnRNPK and UNR were found to directly interact with the IRES RNA by UV cross-linking and electrophoretic mobility shift assays (EMSAs). Investigation of the proteins effect on c-myc IRES activity showed stimulation of IRES activity in HeLa cells by PCBP1 and PCBP2. The factor HnRNPK was found to have a slight stimulatory effect in vivo. In addition PCBP1 and PCBP2 were found to stimulate IRES activity in vitro in combination with UNR and UNRIP. Using the yeast three-hybrid system a number of additional proteins were found to interact with the c-myc IRES RNA. A novel Fibrillarin-like protein was identified and shown to strongly interact with the IRES by EMSA. Studies to determine a direct role of this factor in c-myc IRES translation were inconclusive. The study of translation of the c-myc gene identified an IRES within its 5'UTR. Investigation of the role of trans-acting factors in its translation showed a possible role of the factors PCBP2, HnRNPk and ITAF45 (IRES trans-acting factor 45).
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LIDEREAU, WEINSTEIN ROSETTE. „La variabilite genetique des proto-oncogenes ras, myc et mos comme marqueur de predisposition et d'evolution dans le cancer du sein“. Paris 7, 1987. http://www.theses.fr/1987PA077129.
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Feist, Maren [Verfasser], Dieter [Akademischer Betreuer] Kube, Detlef [Gutachter] Doenecke und Jörg [Gutachter] Grosshans. „Synergism of IL10R and TLR9 signaling affects gene expression, proliferation and metabolism in B cells: A comparative study of STAT3/NF-kB and c-Myc mediated effects / Maren Feist ; Gutachter: Detlef Doenecke, Jörg Grosshans ; Betreuer: Dieter Kube“. Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2016. http://d-nb.info/1116080001/34.
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Andeol, Yannick. „Contribution a l'etude des oncogenes cellulaires de la famille ras : caracterisation dans trois lignees tumorales humaines“. Paris 6, 1987. http://www.theses.fr/1987PA066065.
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VILAREM, PUIG MARIE-JOSE. „Etude des mecanismes d'activite cytotoxique et moleculaire du bd-40, une aza-ellipticine douee de pouvoir antitumoral“. Paris 6, 1987. http://www.theses.fr/1987PA066219.
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DEPREZ, ROY ISABELLE. „Construction et utilisation de vecteurs adenoviraux pour le transfert de sequences antisens dirigees contre c-myc ou le transfert du gene du facteur atrial natriuretique dans le but d'inhiber la migration et la proliferation des cellules musculaires lisses vasculaires in vitro et in vivo“. Paris 12, 2000. http://www.theses.fr/2000PA120015.
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Les cellules musculaires lisses vasculaires (cml) jouent un role majeur dans le remaniement hypertrophique de la paroi arterielle. Notre travail visait a diminuer la proliferation et la migration des cml en bloquant l'expression de la proteine c-myc ou en surexprimant le facteur atrial natriuretique (anf). Des vecteurs adenoviraux ont donc ete developpes pour transferer des antisens contre c-myc ou le gene de l'anf. Le traitement des cml avec la construction ad-as-myc permet une synthese importante d'antisens ; une diminution de la proteine c-myc ; une diminution majeure de la migration sans diminution importante de la proliferation ; et une diminution de 40% de l'hyperplasie neointimale apres desendothelialisation de la carotide de rat. Cette construction semble bloquer l'hyperplasie neointimale essentiellement par inhibition de la migration cellulaire. Le traitement des cml avec la construction val eint2 entraine une synthese tres importante d'antisens ; une diminution majeure de la proteine c-myc ; une inhibition de la proliferation et de la migration des cml. Cette construction presente donc un fort potentiel pour inhiber la formation d'une neointima. Le promoteur vai semble important pour l'efficacite de l'antisens dans la cellule. Le traitement dans les cml d'artere pulmonaire avec ad-anf entraine une diminution de la proliferation cellulaire associee a une induction d'apoptose. En revanche, le traitement des cml de carotide avec ad-anf inhibe leur migration sans modification de la proliferation corroborant les resultats obtenus dans la carotide de rat ou l'hyperplasie neointimale est inhibee d'environ 30%. Le traitement de cml par des vecteurs adenoviraux codant pour des antisens contre c-myc ou pour exprimant l'anf entraine dans la carotide de rat une diminution de la neointima expliquee en partie par l'inhibition de la migration et de la proliferation observee in vitro. Nos resultats montrent que le transfert d'antisens contre c-myc est efficace pour inhiber la formation d'une neointima.
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Al-Sallami, Dheyaa Abdul Salam. „INTERROGATION OF CHROMOSOME 8Q24.21 REGION FOR GENES CRUCIAL FOR CARCINOGENESIS USING CRISPR-CAS9 APPROACHES“. OpenSIUC, 2016. https://opensiuc.lib.siu.edu/theses/1994.
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8q24.21 is a highly amplified region in cancer and associated with many epithelial cancer such as bladder, breast, colorectal and prostate cancer. The proto-oncogene c-myc is located in this region and surrounded by many lncRNAs genes such as PCAT family, CCAT family, PRNCR1. In this study, we used CRISPR-Cas9 constructs to knock out PCAT1, PRNCR1, CASC8, CASC11 and also the sequences between PCAT1-CASC11 and CASC8-CASC11in the prostate cancer cell PC3. The transfected cells with CRISPR-Cas9 targeting CASC11 gene had less proliferation ability comparing with the transfected cells with CRISPR-Cas9 targeting PCAT1, PRNCR1 or CASC8. The role of CASC11 in cancer progression and development is obscure. In our study, The CASC11 Knockout efficiency was 90% compare to the control cell. Furthermore, the study showed the importance of CASC11 in cell proliferation by significantly decreasing in the forming colonies and the growth rate comparing to the control. Also, MMP2, MMP3 and MMP9 expression levels were detected in the transfected cell by using real time PCR and the result revealed the crucial role for CASC11 in metastasis and migration. The slug and vimentin expression levels were reduced in the transfected and the double transfected clones which indicate the possible role of CASC11 in epithelial mesenchymal transition and cell motility. Taken together, our study revealed that the lncRNA CASC11 plays important roles in prostate cancer progression and metastasis by promoting the cell proliferation and migration.
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Sobczak, Joëlle. „Etude de l'expression genetique dans le foie de rat en hypertrophie compensatrice“. Paris 6, 1988. http://www.theses.fr/1988PA066543.
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Lauder, Angus James. „Regulation of the c myb gene by interleukin 2“. Thesis, Institute of Cancer Research (University Of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.271255.
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James, Leonard Philip. „Myc and Mad target genes /“. Thesis, Connect to this title online; UW restricted, 2000. http://hdl.handle.net/1773/5093.
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Hsu, Jui-Cheng. „Transcriptional regulation of the stem cell/progenitor gene c-Myb“. Thesis, University of Nottingham, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.546247.
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Robson, Samuel Charles. „Life or cell death : identifying c-Myc regulated genes in two distinct tissues“. Thesis, University of Warwick, 2008. http://wrap.warwick.ac.uk/1064/.
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The c-myc oncogene is over-expressed or deregulated in many human cancers. c-myc encodes a transcription factor, the oncoprotein c-Myc (Myc), which acts as a master regulator of genes involved in such diverse cellular processes as replication and growth, loss of differentiation, invasion, and angiogenesis. Myc can also act as its own tumour suppressor by promoting cell death in the form of apoptosis. Thus, for putative cancer cells to arise, apoptosis must be blocked. Conditional MycERTAM transgenic mice allow regulated activation of Myc in distinct cell populations (skin suprabasal keratinocytes and pancreatic islet β-cells) and have highlighted contrasting behaviour between these two adult tissues in vivo: proliferation in the skin, and apoptosis in the pancreas. Given the crucial dependence on tissue location in vivo, we still do not know enough about the key divergence in Myc-regulated genes and proteins under conditions favouring opposing outcomes. To address this, we performed high-throughput transcriptome analysis using oligonucleotide microarrays. The in vivo transcriptional response to deregulated Myc was analysed for skin keratinocytes and laser-captured pancreatic islets following a time-course of MycERTAM activation. Due to the multi-factorial nature of the experimental design, novel statistical tools were developed allowing the use of linear models for inference of changes in gene-expression based on multiple experimental variables. Comparison of the transcriptional response between the two tissues identified potential signalling pathways which may promote apoptosis of β-cells or survival of skin keratinocytes: the DNA damage response pathway, and the Insulin-like growth factor 1 (Igf1) signalling pathway respectively. In addition, a marked change in expression was detected in members of the steroid hormone-regulated Kallikrein serine protease family in suprabasal keratinocytes but not for β-cells. These have been found to play an important role in regulating Igf1/Igf1-receptor ligation through proteolysis of the Igf1 binding proteins, are previously categorised markers for several human cancers, and may indicate a tissue-specific regulatory mechanism for determining ultimate Myc function in vivo.
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Madisen, Linda. „Lymphoid specific elements deregulate c-myc transcription following chromosomal translocation in murine plasmacytoma and human Burkitt's lymphoma cells /“. Thesis, Connect to this title online; UW restricted, 1996. http://hdl.handle.net/1773/6324.
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Schmidt, Marcelo Kruel. „Expressão imunohistoquímica do C-MYC na seqüência metaplasia-displasia-adenocarcinoma no esôfago“. reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2005. http://hdl.handle.net/10183/4697.
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Introdução e Objetivos: O esôfago de Barrett (BE) desenvolve-se como conseqüência de uma agressão acentuada sobre a mucosa esofágica causada pelo refluxo gastresofágico crônico. É uma lesão precursora e exerce papel importante no desenvolvimento do adenocarcinoma esofágico (ACE). Inúmeras alterações genéticas estão presentes ao longo da transformação tumoral de uma célula, sendo o c-Myc um dos principais genes envolvidos na carcinogênese humana. O objetivo do presente estudo foi determinar a expressão do c-myc em pacientes com EB e com adenocarcinoma esofágico, e avaliar esta prevalência relacionada com a seqüência metaplasia-displasia-adenocarcinoma. Métodos: A expressão da proteína do C-myc foi determinada através da análise imunohistoquímica em quatro grupos diferentes: 31 pacientes com tecido normal, 43 pacientes com EB sem displasia, 11 pacientes com displasia em EB e 37 pacientes com o adenocarcinoma esofágico. O material foi obtido de peças de biópsias ou de ressecção cirúrgica de pacientes atendidos pelo Grupo de Cirurgia de Esôfago, Estômago e Intestino Delgado (GCEEID) do Hospital de Clínicas de Porto Alegre (HCPA) no período de janeiro 1998 a fevereiro 2004. Dados demográficos e endoscópicos (sexo, idade, raça, tamanho hiatal da hérnia e extensão do epitélio colunar esofágico), e as características morfológicas e histopatológicas tumorais (invasão tumoral, comprometimento linfonodal, e diferenciação histológica do tumor) foram analisados. A expressão de c-Myc foi avaliada usando o sistema de escore de imunorreatividade (Immunoreactive Scoring System – ISS). Resultados: Expressão aumentada do c-myc foi encontrada em apenas 9,7% das amostras de epitélio normal, em 37,2% dos pacientes com EB, em 45,5% dos pacientes com displasia e em 73% dos pacientes com adenocarcinoma, com diferença estatística significativa entre os grupos. Nenhuma associação foi identificada quando a expressão do c-Myc foi comparada as características morfológicas e histológicas do tumor ou aos dados endoscópicos. Entretanto, uma correlação linear da expressão do c-myc ao longo da seqüência metaplasia-displasia-adenocarcinoma foi observada. Conclusão: O estudo demonstrou um aumento significativo da expressão do c-Myc no EB, na displasia, e no adenocarcinoma em relação aos controles, bem como uma progressão linear da positividade deste gene ao longo desta seqüência. Estes resultados apontam para um papel importante deste marcador no desenvolvimento do ACE a partir do EB. Esta expressão aumentada do c-Myc em pacientes com EB poderá ajudar a identificar pacientes com risco elevado para o desenvolvimento de adenocarcinoma, contribuindo para um diagnóstico precoce desta doença.Background & Aims: Barrett’s esophagus (BE) develops as a result of severe esophageal mucosa injury from gastroesophageal reflux. BE is premalignant lesion and plays important role in the development of esophageal adenocarcinoma. Several genetic alterations have been identified in the transforming process through a normal cell to tumor one, where the c-myc is one of the most important genes involved in the development of human tumors. The aim of the present study was to determine the expression of the c-myc in patients with BE and esophageal adenocarcinoma, and to evaluate this prevalence in relation to the metaplasia-displasia-adenocarcinoma sequence. Methods: The c-myc protein expression was determined by immunohistochemical analysis in four different groups: 31 patients with normal tissue, 43 patients with BE without dysplasia, 11 patients with dysplasia in BE and 37 patients with esophageal adenocarcinoma. The material was obtained from esophageal biopsy or dissection of esophagectomy specimens of patients from the Esophagus, Stomach and Small Bowel Surgery Group of the Hospital de Clínicas de Porto Alegre from January 1998 to February 2004. Demographic and endoscopic data (sex, age, race, hiatal hernia size and intestinal metaplasia extension), and morphologic and histopathologic tumor characteristics (deep tumor invasion, lymph node status, and tumor differentiation) were analyzed. The c-myc expression was assessed using the Imunoreactive Scoring System (IRS). Results: Overexpression of c-myc was found in only 9.6% of normal tissue specimens, 37,2% of Barrett’s esophagus, 45,5% of BE patients with displasia and 73% adenocarcinoma samples, with significant statistic difference among these groups. No association was identified when the c-myc expression was compared with morphologic and histologic tumor features or endoscopic data. However, linear correlation of c-myc overexpression along the metaplasia-displasia-adenocarcinoma sequence was observed. Conclusion: The study demonstrated a significant increase of the expression of c-myc in Barrett’s esophagus, dysplasia and adenocarcinoma in relation to the control group, as well as a linear progression of this gene expression in this sequence. These results put forward to an important role of this marker in the development of ACE from EB. The increased expression of the c-myc in patients with EB may help to identify patients with increased risk for adenocarcinoma development, contributing to an early diagnosis of this disease.
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Alam, Goleeta N. „Role of the Lineage Gene Phox2B in Neuroblastoma Development“. University of Toledo Health Science Campus / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=mco1243891387.
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Lopes, Rodrigo Antonio [UNESP]. „Detecção e expressão dos genes supressores p53 E c-Myc em tumores palpebrais de cães“. Universidade Estadual Paulista (UNESP), 2008. http://hdl.handle.net/11449/92207.
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Os objetivos deste estudo foram detectar a presença e a expressão dos genes supressores p53 e c-Myc em tumores palpebrais, pelas técnicas de PCR, RTPCR, PCR-ELISA E RT-PCR-ELISA que até o então não foram descritas nestes tumores e nesta espécie. Foram utilizadas 10 amostras de tumores que foram fixados em formol e incluídos em parafina. O material foi obtido junto aos arquivos do Serviço de Patologia Veterinária, sendo nove amostras de tumores localizados nas pálpebras e terceira pálpebra e uma de tumor mamário para controle. Todos os tumores tiveram o seu diagnóstico firmado empregando-se a coloração de H.E e imunoistoquímica para citoqueratina AE1/AE3 e vimentina (V9), marcadores de tecido epitelial e mesenquimal, respectivamente. Os resultados indicaram que os tumores palpebrais e da terceira pálpebra aqui estudados verificou-se a presença do gene supressor p53 em 8 amostras (88,8%, n=8), e entre as amostras positivas (n=8), ele esteve expresso em 75 % delas. O gene supressor c-Myc esteve presente em 5 amostras (55,5%) e com expressão em 100% delas (n=5). Foi possível concluir que os tumores palpebrais e da terceira pálpebra de cães expressam o p-53 e c-Myc identificados pelas técnicas de PCR e RT-PCR, no entanto, as técnicas de PCR ELISA e RT-PCR ELISA foram mais importantes para avaliação da presença e expressão do oncogenes estudados, pois permitiram identificar produtos amplificados que não foram visualizados em gel de agarose.
The aims of this study were to detect the presence and the expression of p53 and c-Myc suppressor genes in eyelid tumors of dogs, by the PCR, RT-PCR, PCR-ELISA and RT-PCR-ELISA techniques, which until then they were not described in these tumors and in this specie. Ten samples of tumors were fixed in formalin and included in paraffin. The material was obtained from the archives of the Department of Veterinary Pathology, being nine samples of epithelial tumors located in the eyelids and the third eyelid, and a breast tumor which was used as a positive control of the reactions. All the samples had reached their diagnosis employing up the HE technique, and the immunohistochemistry for cytokeratin AE1/AE3 and vimentin (V9). The results showed that the eyelid and the third eyelid tumors, here studied, (88.8%, n=8) of them demonstrated the presence of the p53 gene and between the positive samples (n=8), the expression was around 75%. The c-Myc gene was present in 55.5% (n=5) of the samples, with 100% of expression (n=5). Thus, it was possible to conclude that the eyelid and the third eyelid tumors of dogs express the p53 and c-Myc genes, identified by the techniques of PCR and RT-PCR, however, the PCR ELISA and RT-PCR ELISA techniques were of extreme importance for assessing the presence and expression of these studied genes, and they allowed to identify amplified products that were not visible on the electrophoresis on the agarose gel.
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Lopes, Rodrigo Antonio. „Detecção e expressão dos genes supressores p53 E c-Myc em tumores palpebrais de cães /“. Araçatuba, 2008. http://hdl.handle.net/11449/92207.
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Resumo: Os objetivos deste estudo foram detectar a presença e a expressão dos genes supressores p53 e c-Myc em tumores palpebrais, pelas técnicas de PCR, RTPCR, PCR-ELISA E RT-PCR-ELISA que até o então não foram descritas nestes tumores e nesta espécie. Foram utilizadas 10 amostras de tumores que foram fixados em formol e incluídos em parafina. O material foi obtido junto aos arquivos do Serviço de Patologia Veterinária, sendo nove amostras de tumores localizados nas pálpebras e terceira pálpebra e uma de tumor mamário para controle. Todos os tumores tiveram o seu diagnóstico firmado empregando-se a coloração de H.E e imunoistoquímica para citoqueratina AE1/AE3 e vimentina (V9), marcadores de tecido epitelial e mesenquimal, respectivamente. Os resultados indicaram que os tumores palpebrais e da terceira pálpebra aqui estudados verificou-se a presença do gene supressor p53 em 8 amostras (88,8%, n=8), e entre as amostras positivas (n=8), ele esteve expresso em 75 % delas. O gene supressor c-Myc esteve presente em 5 amostras (55,5%) e com expressão em 100% delas (n=5). Foi possível concluir que os tumores palpebrais e da terceira pálpebra de cães expressam o p-53 e c-Myc identificados pelas técnicas de PCR e RT-PCR, no entanto, as técnicas de PCR ELISA e RT-PCR ELISA foram mais importantes para avaliação da presença e expressão do oncogenes estudados, pois permitiram identificar produtos amplificados que não foram visualizados em gel de agarose.Abstract: The aims of this study were to detect the presence and the expression of p53 and c-Myc suppressor genes in eyelid tumors of dogs, by the PCR, RT-PCR, PCR-ELISA and RT-PCR-ELISA techniques, which until then they were not described in these tumors and in this specie. Ten samples of tumors were fixed in formalin and included in paraffin. The material was obtained from the archives of the Department of Veterinary Pathology, being nine samples of epithelial tumors located in the eyelids and the third eyelid, and a breast tumor which was used as a positive control of the reactions. All the samples had reached their diagnosis employing up the HE technique, and the immunohistochemistry for cytokeratin AE1/AE3 and vimentin (V9). The results showed that the eyelid and the third eyelid tumors, here studied, (88.8%, n=8) of them demonstrated the presence of the p53 gene and between the positive samples (n=8), the expression was around 75%. The c-Myc gene was present in 55.5% (n=5) of the samples, with 100% of expression (n=5). Thus, it was possible to conclude that the eyelid and the third eyelid tumors of dogs express the p53 and c-Myc genes, identified by the techniques of PCR and RT-PCR, however, the PCR ELISA and RT-PCR ELISA techniques were of extreme importance for assessing the presence and expression of these studied genes, and they allowed to identify amplified products that were not visible on the electrophoresis on the agarose gel.
Orientador: Alexandre Lima de Andrade
Coorientador: Tereza Cristina Cardoso da Silva
Banca: Débora Aparecida Pires de Campos Zuccari
Banca: Cláudia Valéria Seullner Brandão
Mestre
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Cericatto, Rodrigo. „Expressão gênica do receptor estrogênico-a, bcl-2 e c-myc em fibroadenomas e no tecido mamário normal circunjacente“. reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2003. http://hdl.handle.net/10183/4629.
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Tesell, Jessica M. „The Notch1-c-Myc Pathway Mediates Leukemia-Initiating Cell Activity in Mouse T-ALL Models: A Dissertation“. eScholarship@UMMS, 2013. http://escholarship.umassmed.edu/gsbs_diss/671.
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Although cure rates have significantly improved for children with T-cell acute lymphoblastic leukemia (T-ALL), 20-30% undergo induction failure or relapse with most succumbing to disease. Leukemia-initiating cells (L-ICs) are hypothesized to be resistant to conventional chemotherapy and radiation and are thereby responsible for disease recurrence. Using an in vivo limiting dilution assay, we previously showed that the murine T-ALL L-IC is quite rare, with only 0.003-0.05% of cells capable of initiating disease, and demonstrated that the L-IC is a subset of the leukemic DN3 thymic progenitor population. Work described in this thesis validates the L-IC assay using two transplantation methods to rule out effects of homing and/or microenvironment on T-ALL L-IC survival and maintenance. Using this assay, we demonstrate that sustained Notch1 signaling is required for T-ALL initiation in vivo and show that treatment with a Notch1 inhibitor reduces or in some cases eliminates the L-IC population. We further analyze the effects of inhibiting c-Myc, a Notch1-regulated gene, on L-IC frequency and uncover an essential role for c-Myc in L-IC survival and expansion. Suppressing c-Myc by using specific shRNAs or a c-Myc inhibitor reduces the L-IC population and interferes with leukemia initiation. Together, these findings reveal a critical role of the Notch1-c-Myc pathway in T-ALL initiation and suggest that therapeutics targeted at this pathway could be used to treat and/or prevent disease relapse in patients.
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PEREIRA, Cynthia Mara Brito Lins. „Expressão dos genes C-MYC, HER-2 e receptores hormonais como preditores de resposta à quimioterapia neoadjuvante em câncer mamário“. Universidade Federal do Pará, 2010. http://repositorio.ufpa.br/jspui/handle/2011/2859.
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O câncer de mama é um dos tumores de maior incidência na mulher, e por isso, muitas pesquisas vêm sendo realizadas, desde a avaliação das características epidemiológicas, à dinâmica biocelular e o tratamento desta doença. Na avaliação de respostas ao tratamento, os fatores preditivos são marcadores que auxiliam na escolha da melhor droga a ser usada. Esta dissertação teve o objetivo de avaliar os genes de receptores de estrogênio e progesterona, HER-2 e C-MYC em tumores localmente avançados da mama, como fatores preditivos de resposta à quimioterapia neoadjuvante. Estudaram-se fragmentos da neoplasia maligna mamária de 50 pacientes com carcinoma ductal infiltrativo, com estadiamento clínico E-III e tratadas com quimioterapia neoadjuvante. Utilizaram-se as técnicas de imunohistoquímica e de hibridização in situ por fluorescência (FISH). A análise dos receptores hormonais não apresentou diferença estatisticamente significativa comparando as pacientes com resposta satisfatória à quimioterapia, das insatisfatórias; a análise do HER-2 apresentou significância apenas para as respostas satisfatórias, onde houve baixa amplificação deste gene. Em relação ao C-MYC observou-se uma diferença estatisticamente significativa comparando a alta amplificação deste gene a uma resposta insatisfatória à quimioterapia. O estudo concluiu que o gene C-MYC pode ser um importante marcador de predição nos tratamentos quimioterápicos neoadjuvantes usados em câncer mamário.
Breast cancer is a higher incidence of tumors in women, and therefore many studies have been performed since the assessment of the epidemiological characteristics, the dynamics biocelular and treatment of this disease. In evaluating responses to treatment, the risk factors are markers that help in choosing the best drug to use. This work aimed to evaluate the genes of estrogen and progesterone receptors, HER-2 and C-MYC in locally advanced breast tumors as predictors of response to neoadjuvant chemotherapy. We studied fragments of mammary malignancy in 50 patients with infiltrating ductal carcinoma, with clinical stage III and E-treated with neoadjuvant chemotherapy. We used the techniques of immunohistochemistry and fluorescence in situ hybridization (FISH). The analysis of hormone receptors showed no statistically significant difference comparing patients with satisfactory response to chemotherapy, the poor and the analysis of HER-2 showed significance only for satisfactory answers, where there was poor amplification of this gene. Regarding C-MYC was observed a statistically significant difference comparing the high amplification of this gene to a poor response to chemotherapy. The study concluded that the C-MYC gene may be an important marker for predicting the treatments used in neoadjuvant chemotherapy for breast cancer.