Relevant bibliographies by topics / Myc Genes

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Academic literature on the topic 'Myc Genes'

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Published: 4 June 2021
Last updated: 13 February 2022

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Journal articles on the topic "Myc Genes"

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Grandori, C. "Myc target genes." Trends in Biochemical Sciences 22, no. 5 (May 1997): 177–81. http://dx.doi.org/10.1016/s0968-0004(97)01025-6.

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Collum, R. G., D. F. Clayton, and F. W. Alt. "Structure and expression of canary myc family genes." Molecular and Cellular Biology 11, no. 3 (March 1991): 1770–76. http://dx.doi.org/10.1128/mcb.11.3.1770.

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We found that the canary N-myc gene is highly related to mammalian N-myc genes in both the protein-coding region and the long 3' untranslated region. Examined coding regions of the canary c-myc gene were also highly related to their mammalian counterparts, but in contrast to N-myc, the canary and mammalian c-myc genes were quite divergent in their 3' untranslated regions. We readily detected N-myc and c-myc expression in the adult canary brain and found N-myc expression both at sites of proliferating neuronal precursors and in mature neurons.
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Collum, R. G., D. F. Clayton, and F. W. Alt. "Structure and expression of canary myc family genes." Molecular and Cellular Biology 11, no. 3 (March 1991): 1770–76. http://dx.doi.org/10.1128/mcb.11.3.1770-1776.1991.

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We found that the canary N-myc gene is highly related to mammalian N-myc genes in both the protein-coding region and the long 3' untranslated region. Examined coding regions of the canary c-myc gene were also highly related to their mammalian counterparts, but in contrast to N-myc, the canary and mammalian c-myc genes were quite divergent in their 3' untranslated regions. We readily detected N-myc and c-myc expression in the adult canary brain and found N-myc expression both at sites of proliferating neuronal precursors and in mature neurons.
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Kinzler, K. W., B. A. Zehnbauer, G. M. Brodeur, R. C. Seeger, J. M. Trent, P. S. Meltzer, and B. Vogelstein. "Amplification units containing human N-myc and c-myc genes." Proceedings of the National Academy of Sciences 83, no. 4 (February 1, 1986): 1031–35. http://dx.doi.org/10.1073/pnas.83.4.1031.

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Li, Feng, Yunyue Wang, Karen I. Zeller, James J. Potter, Diane R. Wonsey, Kathryn A. O'Donnell, Jung-whan Kim, Jason T. Yustein, Linda A. Lee, and Chi V. Dang. "Myc Stimulates Nuclearly Encoded Mitochondrial Genes and Mitochondrial Biogenesis." Molecular and Cellular Biology 25, no. 14 (July 2005): 6225–34. http://dx.doi.org/10.1128/mcb.25.14.6225-6234.2005.

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ABSTRACT Although several genes involved in mitochondrial function are direct Myc targets, the role of Myc in mitochondrial biogenesis has not been directly established. We determined the effects of ectopic Myc expression or the loss of Myc on mitochondrial biogenesis. Induction of Myc in P493-6 cells resulted in increased oxygen consumption and mitochondrial mass and function. Conversely, compared to wild-type Myc fibroblasts, Myc null rat fibroblasts have diminished mitochondrial mass and decreased number of normal mitochondria. Reconstitution of Myc expression in Myc null fibroblasts partially restored mitochondrial mass and function and normal-appearing mitochondria. Concordantly, we also observed in primary hepatocytes that acute deletion of floxed murine Myc by Cre recombinase resulted in diminished mitochondrial mass in primary hepatocytes. Our microarray analysis of genes responsive to Myc in human P493-6 B lymphocytes supports a role for Myc in mitochondrial biogenesis, since genes involved in mitochondrial structure and function are overrepresented among the Myc-induced genes. In addition to the known direct binding of Myc to many genes involved in mitochondrial structure and function, we found that Myc binds the TFAM gene, which encodes a key transcriptional regulator and mitochondrial DNA replication factor, both in P493-6 lymphocytes with high ectopic MYC expression and in serum-stimulated primary human 2091 fibroblasts with induced endogenous MYC. These observations support a pivotal role for Myc in regulating mitochondrial biogenesis.
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Versteeg, R., C. van der Minne, A. Plomp, A. Sijts, A. van Leeuwen, and P. Schrier. "N-myc expression switched off and class I human leukocyte antigen expression switched on after somatic cell fusion of neuroblastoma cells." Molecular and Cellular Biology 10, no. 10 (October 1990): 5416–23. http://dx.doi.org/10.1128/mcb.10.10.5416.

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Neuroblastomas often show amplification and high expression of the N-myc oncogene. N-myc expression could be explained as a consequence of gene amplification, but an alternative possibility is that expression primarily results from the inactivation or loss of some factor that normally represses the N-myc gene. To test this idea, we fused N-myc-overexpressing neuroblastoma cell lines with lines that do not express N-myc. In the resulting hybrids, N-myc expression turned out to be switched off, although amplified N-myc copies were still present. This suggests that N-myc overexpression in neuroblastomas results, at least in part, from the inactivation of a suppressor gene that is present in normal cells. In rat neuroblastomas, it has been found that N-myc can switch off class I major histocompatibility complex (MHC) expression. Therefore, we analyzed in our hybrid cells whether suppression of N-myc results in reexpression of human class I MHC genes. Because this was found to be the case, the picture emerges of a hierarchic pathway that connects a putative tumor-suppressor gene with the expression of N-myc and consequently of class I MHC, thus affecting the potential immunogenic properties of neuroblastomas.
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Versteeg, R., C. van der Minne, A. Plomp, A. Sijts, A. van Leeuwen, and P. Schrier. "N-myc expression switched off and class I human leukocyte antigen expression switched on after somatic cell fusion of neuroblastoma cells." Molecular and Cellular Biology 10, no. 10 (October 1990): 5416–23. http://dx.doi.org/10.1128/mcb.10.10.5416-5423.1990.

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Neuroblastomas often show amplification and high expression of the N-myc oncogene. N-myc expression could be explained as a consequence of gene amplification, but an alternative possibility is that expression primarily results from the inactivation or loss of some factor that normally represses the N-myc gene. To test this idea, we fused N-myc-overexpressing neuroblastoma cell lines with lines that do not express N-myc. In the resulting hybrids, N-myc expression turned out to be switched off, although amplified N-myc copies were still present. This suggests that N-myc overexpression in neuroblastomas results, at least in part, from the inactivation of a suppressor gene that is present in normal cells. In rat neuroblastomas, it has been found that N-myc can switch off class I major histocompatibility complex (MHC) expression. Therefore, we analyzed in our hybrid cells whether suppression of N-myc results in reexpression of human class I MHC genes. Because this was found to be the case, the picture emerges of a hierarchic pathway that connects a putative tumor-suppressor gene with the expression of N-myc and consequently of class I MHC, thus affecting the potential immunogenic properties of neuroblastomas.
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Dunnick, Wesley, James Baumgartner, Lee Fradkin, Cynthia Schultz, and Paul Szurek. "Methylation of plasmacytoma c-myc genes." Gene 39, no. 2-3 (January 1985): 287–92. http://dx.doi.org/10.1016/0378-1119(85)90325-7.

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Rimpi, S., and J. A. Nilsson. "Metabolic enzymes regulated by the Myc oncogene are possible targets for chemotherapy or chemoprevention." Biochemical Society Transactions 35, no. 2 (March 20, 2007): 305–10. http://dx.doi.org/10.1042/bst0350305.

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The Myc oncogenes are dysregulated in 70% of human cancers. They encode transcription factors that bind to E-box sequences in DNA, driving the expression of a vast amount of target genes. The biological outcome is enhanced proliferation (which is counteracted by apoptosis), angiogenesis and cancer. Based on the biological effects of Myc overexpression it was originally assumed that the important Myc target genes are those encoding components of the cell cycle machinery. Recent work has challenged this notion and indicates that Myc target genes encoding metabolic enzymes deserve attention, as they may be critical arbiters of Myc in cancer. Thus targeting metabolic enzymes encoded by Myc-target genes may provide a new means to treat cancer that have arisen in response to deregulated Myc oncogenes.
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Leffak, M., and C. D. James. "Opposite replication polarity of the germ line c-myc gene in HeLa cells compared with that of two Burkitt lymphoma cell lines." Molecular and Cellular Biology 9, no. 2 (February 1989): 586–93. http://dx.doi.org/10.1128/mcb.9.2.586.

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To study the cell type specificity of the direction of replication of the human c-myc genes and the relationship of replication polarity to transcriptional activity, we analyzed the directions of replication of the c-myc genes in two Burkitt lymphoma cell lines, CA46 and ST486, and in HeLa cells. On the basis of in vitro runoff replication of forks initiated in intact cells, we found that transcribed c-myc genes in the germ line configuration in HeLa cells were replicated in the direction of transcription from origins in the 5'-flanking DNA, while the repressed, unrearranged c-myc genes of CA46 and ST486 cells were replicated in the antitranscriptional direction. In contrast, the transcribed c-myc genes of CA46 cells were replicated in the transcriptional direction, while the translocated, amplified c-myc genes of ST486 cells showed no preferred polarity of replication. The data also provided evidence for the existence of an endogenous barrier to DNA polymerases in the flanking DNA immediately 5' to the HeLa c-myc genes.
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Dissertations / Theses on the topic "Myc Genes"

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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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Cairo, Stefano. "The promyelocytic leukaemia gene product PML interacts with Myc and influences the expression of Myc target genes." Thesis, Open University, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.406451.

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Vulcani-Freitas, Tânia Maria [UNIFESP]. "Perfil de expressão dos genes MYC, MYCN, TERT, ASPM e PRAME em Meduloblastoma." Universidade Federal de São Paulo (UNIFESP), 2010. http://repositorio.unifesp.br/handle/11600/9928.

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Meduloblastoma (MB) é o tumor maligno de sistema nervoso central (SNC) mais comum em criança, compreendendo 20% dos tumores primários de SNC e 40% dos tumores cerebelares da infância. Devido sua forte tendência metastática, o tratamento padrão pós-operatório inclui radio e quimioterapia, cujo impacto causa distúrbios endócrinos e de crescimento, e disfunção neurocognitiva a longo prazo. Frente a esses efeitos negativos, muitas pesquisas em meduloblastoma têm sido realizadas com intuito de obter conhecimento biológico desses tumores para tentar identificar fatores prognósticos moleculares que possam orientar os tratamentos, tornando-os mais específicos e menos agressivos. Alguns estudos em MB têm sugerido que a expressão do oncogene MYC está associada com diminuição da sobrevida e sua superexpressão com maior agressividade do tumor. Por isso, MYC pode ser um indicador importante de prognóstico, além de modulador do comportamento desta doença. Enquanto o gene MYC é expresso em uma variedade de tecidos, a expressão de MYCN, outro membro da família MYC, é restrita a estágios precoces do desenvolvimento embrionário de alguns tecidos apenas, entre eles, o sistema nervoso central e periférico, sendo um mediador importante dos efeitos de ativação na proliferação de células precursoras cerebelares. Dessa forma, quando a expressão de MYCN está desregulada, ela aumenta a tumorigenicidade dessas células podendo dar origem ao MB. Além disso, o gene MYC também é considerado importante regulador da transcrição TERT, gene que codifica uma subunidade catálica de da telomerase, enzima importante para carcinogênese e imortalização de células neoplásicas. A atividade anormal da telomerase está presente em 90% dos cânceres e o aumento de sua atividade está associado a eventos clínicos desfavoráveis. Outro gene importante é o ASPM (abnormal spindle-like microcephaly associated) que desempenha função fundamental na neurogênese e proliferação celular durante o desenvolvimento cerebral. Esse gene codifica uma proteína de centrossomo e fuso mitótico que permite a divisão celular simétrica em células neuroepiteliais durante o desenvolvimento e aumento do tamanho cerebral. Alterações em ASPM é a causa mais comum de microcefalia primária em humanos e de falha de segregação, induzindo a aneuploidias e instabilidade genética. Além desses genes, outro gene estudado recentemente, como alvo em xv imunoterapia, é o gene PRAME que codifica um antígeno tumoral que está presente em vários tumores, incluindo meduloblastoma. O gene PRAME possui baixa ou ausência de expressão em tecidos normais, por isso é pode ser um forte candidato como alvo em imunoterapia, que é um tratamento menos tóxico. OBJETIVOS: O objetivo desse estudo foi investigar a expressão dos genes MYC, MYCN, TERT, ASPM e PRAME em fragmentos tumorais de meduloblastoma de crianças e tentar correlacionar com os parâmetros clínicos e verificar se há correlação de MYC, MYCN, TERT entre si, uma vez que estão correlacionados. MÉTODOS: Análise de expressão gênica foi realizada através de PCR quantitativa em tempo real, utilizando sistema SYBR Green, em 37 amostras tumorais de crianças, com média de idade de 8 anos. Para comparação de perfil de expressão foi usada duas amostra de cérebro normal. A análise estatística foi realizada nos programas Graph Pad Prism 4 e VassarStats RESULTADOS: Todas nossas amostras superexpressaram o gene MYCN com valor de quantificação relativa (RQ) mediana igual a 31 com p=0.001; assim como, todas nossas amostras também superexpressaram o gene ASPM com mediana igual a 586, p<0.0001. Do total de amostras, 95%, 81% e 84% superexpressaram TERT, MYC e PRAME respectivamente, sendo os valores de RQ (mediana) iguais a 322, p=0.01; 9.2, p<0.0001; 33, p<0.0001. Apesar da elevada expressão dos genes estudados na maioria das amostras estudadas, houve apenas correlação estatística entre a superexpressão de MYCN (p=0.008) e os pacientes que foram a óbito, e de TERT e os pacientes que recidivaram (p=0.0431). Não encontramos outra correlação estatística entre a superexpressão dos genes e as características clínicas dos pacientes. CONCLUSÃO: Os genes MYC, MYCN e TERT estavam superexpressos nas amostras de meduloblastoma analisadas em uma freqüência muito superior ao demonstrado na literatura, o que sugere que esses três genes podem ajudar na identificação de tumores agressivos, uma vez que o pognóstico desses pacientes continua baseado apenas em parâmentros clínicos. A superexpressão de ASPM em todas as amostras estudadas sugere que este gene pode estar envolvido na origem de MB, como parte da neurogênse anormal durante o desenvolvimento embrionário, porém estudoas funcionais devem ser realizados para confirmar essa hipótese. Por fim, o gene PRAME pode ser candidato à marcador de célula tumoral em MB, podendo no futuro ser candidato como alvo em imunoterapias.
To investigate the expression of genes MYC, MYCN and TERT in tumor fragments of pediatric medulloblastoma and correlate gene expression profiles with clinical parameters. Analysis of gene expression was performed by quantitative PCR real time in 37 tumor samples and correlated with clinical and pathological data. All 37 samples overexpressed MYCN gene (p= 0.001), 95% and 84% of the samples overexpressed TERT and MYC, respectively (p<0.0001). Twenty nine (78%) of all samples had concomitant high expression of MYC, MYCN and TERT genes together. Seventeen (59%) were high-risk classification, 10 (34%) were metastatic (M+) stage, two (7%) were anaplastic or largecell/ anaplastic subtype, eight (28%) of patients relapsed, beyond thirteen (45%) suffered partial surgical resection. and fourteen (48%) died. We found correlation between MYC, MYCN and TERT expression (p<0.0001). The identification of a subgroup with concomitant overexpression of the three investigated genes suggests the possibility of using more than one aspect of molecular indicative of unfavorable prognosis that characterizes the group with poor outcome. However, in future this may be enhanced by targeted therapy for the product TERT as proposed in some neoplasms. The identification of molecular events in the medulloblastoma categorization aims to help at-risk groups moving towards individualized medicine.
TEDE
BV UNIFESP: Teses e dissertações
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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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Östergren, Tiolina. "Identification of MYCN and SOX9 target genes and a study of drug treatment effects in medulloblastoma." Thesis, Uppsala universitet, Institutionen för biologisk grundutbildning, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-262085.

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Medulloblastoma (MB) is the most common malignant brain tumor affecting children. The transcription factors MYCN and SOX9 are associated with initiation, maintenance and recurrence of MB and are also connected to more aggressive tumors. In this study, a ChIP was performed to isolate DNA from genes that are transcriptionally regulated by these proteins. Identification of these target genes will reveal new potential drug targets and help us better understand the functions of MYCN and SOX9. The ChIP was not fully optimized during this project and the target genes were not sent for sequencing and identified. To study the connection between SOX9 and recurrence, cells with different levels of SOX9 were treated with drugs, after which cell viability was measured. No significant difference in resistance could be measured. Change in expression level of MYCN, SOX9 and other relevant genes after drug treatment was also studied. The results show an increase in SOX9 and HES1, suggesting that these genes are involved in tumor recurrence.
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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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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 Sarian
Tese (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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Lee, Sun Young. "The search for Myc-family genes in lepidopteran insects, strategies and applications." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq62172.pdf.

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Ibson, Julia Mary. "Structure and expression of myc genes in human small cell lung cancer." Thesis, University of Cambridge, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.330254.

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Souza, Ana Carolina Mamana Fernandes de. "Comparação das técnicas de PCR em tempo real e PCR para o estudo dos genes MYCN, DDX1 e NAG em pacientes portadores de neuroblastoma." Universidade de São Paulo, 2007. http://www.teses.usp.br/teses/disponiveis/5/5136/tde-21062007-141525/.

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O neuroblastoma é o tumor sólido extra-cranial mais comum e mortal da infância, sendo o tempo de sobrevida nos casos mais agressivos ainda muito curto. Uma das esperanças nesses casos é que os estudos moleculares possam fornecer informações sobre os genes ou as vias moleculares que governam a patogênese dos neuroblastomas. Pois, há poucos genes como o MYCN, que foi descrito por estar diretamente ligado ao neuroblastoma. A amplificação deste oncogene ocorre em pouco mais de 25% dos neuroblastomas e é considerada como o mais importante marcador de prognóstico nestes tumores, sendo fortemente relacionada aos estádios avançados da doença e falha no tratamento. Outros genes do amplicon do MYCN, incluindo o DDX1 \"DEAD box polypeptide 1 gene\" e o NAG \"neuroblastoma-amplified gene\", estão sendo observados por se apresentarem co-amplificados com o MYCN. Entretanto, a importância deste fenômeno no prognóstico ainda é desconhecida. Os objetivos deste trabalho foram determinar qual o melhor método para estudar a amplificação dos genes MYCN, DDX1 e NAG, além de esclarecer a importância da coamplificação dos genes DDX1 e NAG no prognóstico. Procedimento: O número de cópias dos genes MYCN, DDX1 e NAG foi determinado por PCR em Tempo Real e PCR convencional em 100 neuroblastomas primários. Os dados da PCR em Tempo Real foram analisados por quantificação absoluta e relativa. Os resultados da PCR convencional foram analisados por eletroforese em gel de agarose, medindo a intensidade das bandas formadas no gel no sistema Kodak. A relevância da amplificação gênica como marcador de prognóstico foi avaliada em 74 pacientes, dos quais nós obtivemos o acompanhamento clínico. Resultados: Nos 74 casos estudados, ambos os métodos demonstraram que a amplificação do MYCN estava associada com os estádios mais avançados da doença. A análise das curvas de sobrevida livre de progressão confirmou que pacientes com ausência de amplificação do MYCN apresentavam maior tempo de sobrevida. Nós também analisamos a amplificação do DDX1 nas mesmas amostras incluindo aquelas com ausência de amplificação de MYCN. Não foi encontrada nenhuma relação entre a co-amplificação com idade ao diagnóstico ou tempo de sobrevida. Conclusões: Os métodos aplicados para calcular o número de cópias dos genes na PCR em Tempo Real mostraram-se equivalentes. A PCR em Tempo Real apresentou maior acurácia nos resultados quando comparada à PCR convencional. A análise da sobrevida não demonstrou relação entre a amplificação dos genes DDX1 e/ou NAG com piora no prognóstico.
Neuroblastoma is the most common and deadly extra-cranial solid childhood tumor. Survival rates for aggressive neuroblastomas are still disappointingly low. One of the hopes is that molecular studies will provide insights into the genes and molecular pathways that govern neuroblastoma pathogenesis. However, at present only a few genes as MYCN have been directly linked to neuroblastoma. MYCN oncogene amplification, occurring in up to 25% of neuroblastomas, has been considered the most important prognostic factor, strongly correlating to advanced stage disease and treatment failure. Another genes in the MYCN amplicon, including the DEAD box polypeptide 1 (DDX1) gene, and neuroblastoma-amplified gene (NAG gene), have been found to be frequently co-amplified with MYCN in NB. But the prognostic significance of the coamplification remains unclear. The aims of this study were to evaluate which is the best method to study the gene amplification of those three genes MYCN, DDX1 and NAG, as well as clarify the prognostic significance of the co-amplification or DDX1 and NAG with MYCN. Procedure: The gene copy numbers of MYCN, DDX1, and NAG were determined by the real-time quantitative polymerase chain reaction and conventional polymerase chain reaction in 100 primary NBs. Real-Time data were analyzed by absolute and relative quantification. For conventional PCR, samples were electrophoresed on a 2% agarose gel and the intensity of each band evaluated by Kodak image software. To evaluate of the prognostic significance of the gene amplification we had only 74 cases in witch we could analyze the follow-up. Results: In all 74 cases, both methods demonstrated that MYCN amplification was associated mainly with advanced cancer stages, and the analysis of overall survival confirmed that patients without MYCN amplification had a cumulative survival significantly higher than patients with oncogene amplification. We also studied DDX1 and NAG amplification for all NB samples even that without MYCN amplification. No relationship between any gene co-amplification status and disease stage, age at diagnosis, or overall survival was found. Conclusions: The two methods used to calculate gene copy number for Real Time PCR assay shown to be equivalent. Real Time PCR assay shown to be more accurate to study gene amplification than conventional PCR assay. Survival analysis pointed out that DDX1 and/or NAG amplification has no additional adverse effect on prognosis.
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Books on the topic "Myc Genes"

1

Perry, Claire Louise. A search for novel MHC-encoded IDDM susceptibility genes using oriental haplotypes. Birmingham: University of Birmingham, 1997.

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The Myc Gene Methods And Protocols. Humana Press Inc., 2013.

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Soucie, Erinn Louisa. Myc and apoptosis: Identifying key regulators and target genes. 2004.

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Eisenman, Robert N., and Chi V. Dang. MYC and the Pathway to Cancer. Cold Spring Harbor Laboratory Press, 2014.

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Potter, M. C-myc In B-cell Neoplasia: 14TH WORKSHOP ON MECHANISMS IN B-CELL NEOPLASIA (Current Topics in Microbiology & Immunology). Edited by M. Potter. SPRINGER-VERLAG, 1997.

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Michael, Browning, and McMichael Andrew J, eds. HLA and MHC: Genes, molecules and function. Oxford: BIOS Scientific, 1996.

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Yang, Wei-Cheng. Sequence Analysis of MHC Class II Genes in Cetaceans. INTECH Open Access Publisher, 2012.

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Browning, Michael. HLA AND MHC GENES MOLECULES AND FUNCTIONS (Human Molecular Genetics). Routledge, 1996.

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Browning, Michael, and Andrew McMichael. HLA and MHC: Genes, Molecules and Function (Human Molecular Genetics Series). Academic Pr, 1999.

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Aptsiauri, Natalia, Angel Miguel Garcia-Lora, and Teresa Cabrera. MHC Class I Antigens In Malignant Cells: Immune Escape And Response To Immunotherapy. Springer, 2013.

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Book chapters on the topic "Myc Genes"

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Dang, Chi V., and Linda A. Lee. "Retroviruses, Cancer Genes, and Tumor Suppressor Genes." In c-Myc Function in Neoplasia, 37–64. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-22681-0_2.

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Shim, H., B. C. Lewis, C. Dolde, Q. Li, C. S. Wu, Y. S. Chun, and C. V. Dang. "Myc Target Genes in Neoplastic Tranformation." In Current Topics in Microbiology and Immunology, 181–90. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60801-8_18.

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Grandori, Carla. "A High-Throughput siRNA Screening Platform to Identify MYC-Synthetic Lethal Genes as Candidate Therapeutic Targets." In The Myc Gene, 187–200. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-429-6_12.

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Kato, Gregory J., Daniel S. Wechsler, and Chi V. Dang. "DNA binding by the Myc oncoproteins." In Oncogenes and Tumor Suppressor Genes in Human Malignancies, 313–25. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-3088-6_16.

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Dean, M., J. Cleveland, H. Y. Kim, J. Campisi, R. A. Levine, J. N. Ihle, and U. Rapp. "Deregulation of the c-myc and N-myc Genes in Transformed Cells." In Current Topics in Microbiology and Immunology, 216–22. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-74006-0_29.

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Dang, Chi V., and Linda A. Lee. "Myc Target Genes in Cell Proliferation and Programmed Cell Death." In c-Myc Function in Neoplasia, 171–92. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-22681-0_10.

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Dildrop, R., K. Zimmerman, R. A. DePinho, G. D. Yancopoulos, A. Tesfaye, and F. W. Alt. "Differential Expression of myc-family Genes During Development: Normal and Deregulated N-myc Expression in Transgenic Mice." In Current Topics in Microbiology and Immunology, 100–109. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-74006-0_14.

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Papas, T. S., N. C. Kan, D. K. Watson, J. A. Lautenberger, C. Flordellis, K. P. Samuel, U. G. Rovigatti, M. C. Psallidopoulos, R. Ascione, and P. H. Duesberg. "Myc, a Genetic Element that is Shared by a Cellular Gene (proto-myc) and by viruses with one (MC29) or two (MH2) onc genes." In RNA Tumor Viruses, Oncogenes, Human Cancer and AIDS: On the Frontiers of Understanding, 1–13. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2583-3_1.

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Kerr, D. J., J. A. Plumb, G. C. Wishart, M. Z. Khan, R. I. Freshney, and D. A. Spandidos. "The Effect of H-ras and C-myc Oncogene Transfection on the Response of Lung Epithelial Cells to Growth Factors and Cytotoxic Drugs." In The Superfamily of ras-Related Genes, 285–94. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-6018-6_31.

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Zaritskey, A., I. Stuif, T. Bykova, A. Sominskaya, N. Anikina, and B. Afanasiev. "Coexpression of mdr-1 and myc Genes in Relation to Prognosis in Acute Leukemia Patients." In Acute Leukemias VI, 593–98. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60377-8_93.

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Conference papers on the topic "Myc Genes"

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"In silico analysis of the R2R3-Myb, bHLH-Myc and WDR proathocyanidins regulatory genes in Gossypium genus." In SYSTEMS BIOLOGY AND BIOINFORMATICS (SBB-2020). Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences., 2020. http://dx.doi.org/10.18699/sbb-2020-23.

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Picard, Daniel J., Limei Zhou, Yaqi Hu, Meihua Li, David Shih, Duncan Stearns, Susan Cohn, et al. "Abstract 3109: Myc confers aggressive medulloblastoma phenotypes by regulating cell migration and adhesion genes." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-3109.

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Sato, Fuyuki, and Yasueru Muragaki. "Abstract 3355: Clock genes DEC1 and BMAL1 regulate the expression of stem cell marker genes Sox2 and c-Myc in cervical cancer." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-3355.

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Anderson, Philip D., Sydika A. McKissic, Monica Logan, Meejeon Roh, Omar Franco, Jie Wang, Irina Doubinskaia, et al. "Abstract 2983: Nkx3.1 and c-Myc co-regulate shared target genes involved in prostate cancer." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2983.

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Ji, Hongkai, George Wu, Xiangcan Zhan, Alexandra Nolan, Cheryl Koh, Angelo De Marzo, Jinshui Fan, et al. "Abstract 928: Species and cell type independent core MYC target genes in cancer and stem cells." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-928.

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Zhang, Kai, Hien Dang, and Anna Barry. "Abstract 2483: NELFE modulates chromatin accessibility to amplify the transcription of MYC-associated genes in hepatocellular carcinoma." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-2483.

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Dudek, Hank, Kathleen Wortham, Rokhand Arvan, Anee Shah, Bo Ying, Wendy Cyr, Hailin Yang, et al. "Abstract B222: Dicer substrate siRNAs to MYC, B-catenin, and other target genes effectively induce in vivo target gene knockdown and tumor inhibition." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-b222.

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Hook, Kenneth E., Adam Pavlicek, Scott J. Garza, Maruja E. Lira, Keith Ching, Julie Kan, Sreesha P. Srinivasa, and James G. Christensen. "Abstract 2615: Amplification and/or high expression of Myc family genes sensitizes tumor cells to aurora kinase inhibitors." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-2615.

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Pal, Bidisha, Wael Tasabehji, Sandhya Sorra, Joyeeta Talukdar, and Bikul Das. "Abstract 4297: MYC HIF-2 alpha embryonic stemness genes mediate a transcriptional network to maintain asymmetric self-renewal in oral cancer." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-4297.

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Bhadury, Joydeep, Lisa M. Nilsson, Muralidharan Veppil Somsundar, Lydia C. Green, Ulrich B. Keller, Kevin G. McLure, and Jonas A. Nilsson. "Abstract B26: BET and HDAC inhibitors induce similar genes and biological effects and synergize to kill in Myc-induced murine lymphoma." In Abstracts: AACR Special Conference on Myc: From Biology to Therapy; January 7-10, 2015; La Jolla, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1557-3125.myc15-b26.

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Reports on the topic "Myc Genes"

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Pillai, Shiv S. MHC Genes and Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2000. http://dx.doi.org/10.21236/ada394028.

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Sheen, Joon-Ho. A Gene Amplification Phenotype in c-Myc-Induced Mammary Tumors Cells. Fort Belvoir, VA: Defense Technical Information Center, July 2001. http://dx.doi.org/10.21236/ada396567.

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Sheen, Joon-Ho. A Gene Amplification Phenotype in c-Myc-Induced Mammary Tumors Cells. Fort Belvoir, VA: Defense Technical Information Center, July 2000. http://dx.doi.org/10.21236/ada390716.

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Melkoumian, Zaroui. Regulation of C-myc Gene Expression by Potassium Channel Blocker Quindine in MCF-7 Human Breast Cancer Cell Line. Fort Belvoir, VA: Defense Technical Information Center, July 2000. http://dx.doi.org/10.21236/ada384096.

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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). Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.7097.

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Harrison, Maria J., and Matthew E. Hudson. Identification of genes that regulate phosphate acquisition and plant performance during arbuscular my corrhizal symbiosis in medicago truncatula and brachypodium distachyon. Office of Scientific and Technical Information (OSTI), November 2015. http://dx.doi.org/10.2172/1226798.

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