Bibliographies thématiques / ETV4

Littérature scientifique sur le sujet « ETV4 »

Auteur : Grafiati
Publié le 10 mars 2023

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Articles de revues sur le sujet "ETV4"

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Eo, Jinwon, Kyuyong Han, Kenneth M Murphy, Haengseok Song et Hyunjung Jade Lim. « Etv5, an ETS transcription factor, is expressed in granulosa and cumulus cells and serves as a transcriptional regulator of the cyclooxygenase-2 ». Journal of Endocrinology 198, no 2 (20 mai 2008) : 281–90. http://dx.doi.org/10.1677/joe-08-0142.

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Etv4, Etv1, and Etv5 are members of Etv4 subfamily of E26 transformation-specific (Ets) transcription factors that are known to influence a host of biological processes. We previously showed that Etv5, expressed in Sertoli cells, plays a crucial role in maintaining spermatogonial stem cell niche in the mouse testis. However, it is not yet known whether Etv4 family members are expressed in the ovary or play any role in ovarian functions. Here, we show that Etv5 and Etv4 are expressed in mouse ovaries in granulosa and cumulus cells during folliculogenesis. Both Etv5 and Etv4 mRNAs are also detected in cumulus–oocyte complexes (COCs) and denuded oocytes. Notably, Etv4 is highly expressed in the cumulus cells of ovulated COCs at 16-h post-human chorionic gonadotropin. Cyclooxygenase-2 (PTGS2), a rate-limiting enzyme for prostaglandin synthesis, is critical for oocyte maturation and ovulation. Since several putative Ets-binding sites are present in the PTGS2 promoter, we examined whether Etv5 influences Ptgs2 transcriptional activity. Indeed, we found that addition of Etv5 increases the transcriptional activity of the 3.2-kb mouse Ptgs2 promoter by 2.5-fold in luciferase reporter assays. Collectively, the results show that Etv4 and Etv5 are expressed in granulosa and cumulus cells during folliculogenesis and ovulation, suggesting that they influence cellular events in the ovary by regulating downstream genes such as Ptgs2.
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Newton, Kim, Debra L. Dugger, Arundhati Sengupta-Ghosh, Ronald E. Ferrando, Felix Chu, Janet Tao, Wendy Lam et al. « Ubiquitin ligase COP1 coordinates transcriptional programs that control cell type specification in the developing mouse brain ». Proceedings of the National Academy of Sciences 115, no 44 (15 octobre 2018) : 11244–49. http://dx.doi.org/10.1073/pnas.1805033115.

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The E3 ubiquitin ligase CRL4COP1/DET1 is active in the absence of ERK signaling, modifying the transcription factors ETV1, ETV4, ETV5, and c-JUN with polyubiquitin that targets them for proteasomal degradation. Here we show that this posttranslational regulatory mechanism is active in neurons, with ETV5 and c-JUN accumulating within minutes of ERK activation. Mice with constitutive photomorphogenesis 1 (Cop1) deleted in neural stem cells showed abnormally elevated expression of ETV1, ETV4, ETV5, and c-JUN in the developing brain and spinal cord. Expression of c-JUN target genes Vimentin and Gfap was increased, whereas ETV5 and c-JUN both contributed to an expanded number of cells expressing genes associated with gliogenesis, including Olig1, Olig2, and Sox10. The mice had subtle morphological abnormalities in the cerebral cortex, hippocampus, and cerebellum by embryonic day 18 and died soon after birth. Elevated c-JUN, ETV5, and ETV1 contributed to the perinatal lethality, as several Cop1-deficient mice also lacking c-Jun and Etv5, or lacking Etv5 and heterozygous for Etv1, were viable.
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Dissanayake, Kumara, Rachel Toth, Jamie Blakey, Olof Olsson, David G. Campbell, Alan R. Prescott et Carol MacKintosh. « ERK/p90RSK/14-3-3 signalling has an impact on expression of PEA3 Ets transcription factors via the transcriptional repressor capicúa ». Biochemical Journal 433, no 3 (14 janvier 2011) : 515–25. http://dx.doi.org/10.1042/bj20101562.

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Compounds that inhibit signalling upstream of ERK (extracellular-signal-regulated kinase) are promising anticancer therapies, motivating research to define how this pathway promotes cancers. In the present study, we show that human capicúa represses mRNA expression for PEA3 (polyoma enhancer activator 3) Ets transcription factors ETV1, ETV4 and ETV5 (ETV is Ets translocation variant), and this repression is relieved by multisite controls of capicúa by ERK, p90RSK (p90 ribosomal S6 kinase) and 14-3-3 proteins. Specifically, 14-3-3 binds to p90RSK-phosphorylated Ser173 of capicúa thereby modulating DNA binding to its HMG (high-mobility group) box, whereas ERK phosphorylations prevent binding of a C-terminal NLS (nuclear localization sequence) to importin α4 (KPNA3). ETV1, ETV4 and ETV5 mRNA levels in melanoma cells are elevated by siRNA (small interfering RNA) knockdown of capicúa, and decreased by inhibiting ERK and/or expressing a form of capicúa that cannot bind to 14-3-3 proteins. Capicúa knockdown also enhances cell migration. The findings of the present study give further mechanistic insights into why ETV1 is highly expressed in certain cancers, indicate that loss of capicúa can desensitize cells to the effects of ERK pathway inhibitors, and highlight interconnections among growth factor signalling, spinocerebellar ataxias and cancers.
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Schmerr, Martin, Sune Kobberup, Ngai Woo et Jan Jensen. « Role of Etv4 and Etv5 in pancreatic development ». Developmental Biology 356, no 1 (août 2011) : 168. http://dx.doi.org/10.1016/j.ydbio.2011.05.622.

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Babal, Yigit Koray, Basak Kandemir et Isil Aksan Kurnaz. « Gene Regulatory Network of ETS Domain Transcription Factors in Different Stages of Glioma ». Journal of Personalized Medicine 11, no 2 (17 février 2021) : 138. http://dx.doi.org/10.3390/jpm11020138.

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The ETS domain family of transcription factors is involved in a number of biological processes, and is commonly misregulated in various forms of cancer. Using microarray datasets from patients with different grades of glioma, we have analyzed the expression profiles of various ETS genes, and have identified ETV1, ELK3, ETV4, ELF4, and ETV6 as novel biomarkers for the identification of different glioma grades. We have further analyzed the gene regulatory networks of ETS transcription factors and compared them to previous microarray studies, where Elk-1-VP16 or PEA3-VP16 were overexpressed in neuroblastoma cell lines, and we identify unique and common regulatory networks for these ETS proteins.
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Currie, Simon L., Desmond K. W. Lau, Jedediah J. Doane, Frank G. Whitby, Mark Okon, Lawrence P. McIntosh et Barbara J. Graves. « Structured and disordered regions cooperatively mediate DNA-binding autoinhibition of ETS factors ETV1, ETV4 and ETV5 ». Nucleic Acids Research 45, no 5 (6 février 2017) : 2223–41. http://dx.doi.org/10.1093/nar/gkx068.

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Cooper, Christopher D. O., Joseph A. Newman, Hazel Aitkenhead, Charles K. Allerston et Opher Gileadi. « Structures of the Ets Protein DNA-binding Domains of Transcription Factors Etv1, Etv4, Etv5, and Fev ». Journal of Biological Chemistry 290, no 22 (12 avril 2015) : 13692–709. http://dx.doi.org/10.1074/jbc.m115.646737.

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Shin, Ye Ji, Jae Won Yun et Hong Sook Kim. « Portrait of Molecular Signaling and Putative Therapeutic Targets in Prostate Cancer with ETV4 Fusion ». Biomedicines 10, no 10 (20 octobre 2022) : 2650. http://dx.doi.org/10.3390/biomedicines10102650.

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Gene fusion between androgen receptor (AR) response genes and E26 transformation-specific (ETS) family members increases the gene expression of ETS family members, and promotes tumorigenesis in prostate cancer. However, the molecular features of ETV4 fusion in prostate cancer are not fully understood, and drugs targeting ETV4 fusion have not been developed. To examine key cellular signaling pathways and explore therapeutic targets and drugs for ETV4-fusion-positive prostate cancer, we analyzed RNA sequencing data and clinical information for prostate cancer. The ETV4-fusion-positive group was selected through prior study and analysis comparing ETV4-fusion-positive and -negative groups was conducted using a Pearson correlation test. We obtained 393 genes correlated with ETV4 expression. Pathway analysis was performed using over-representation analysis (ORA), and six cancer-specific molecular signaling pathways (the irinotecan pathway, metabolism, androgen receptor signaling, interferon signaling, MAPK/NF-kB signaling, and the tamoxifen pathway) were altered in the ETV4-fusion-positive group. Furthermore, a gene–drug database was used to find an actionable drug and therapeutic target for the ETV4-fusion-positive group. Here, we have identified significantly altered genes and oncogenic signaling pathways in ETV4-fusion-positive prostate cancer, and we suggest therapeutic targets and potential drugs for ETV4-fusion-positive prostate patients.
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Zhang, Xueming, Lei Si, Zhanpeng Yue, Yang Liu, Bin Guo, Ziyi Li et Dexue Li. « Expression of Ets Transcription Factors Etv4, Etv1 in Mouse Testis. » Biology of Reproduction 83, Suppl_1 (1 novembre 2010) : 517. http://dx.doi.org/10.1093/biolreprod/83.s1.517.

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Chen, Jing, Amelie T. Van der Ven, Joseph A. Newman, Asaf Vivante, Nina Mann, Hazel Aitkenhead, Shirlee Shril et al. « ETV4 Mutation in a Patient with Congenital Anomalies of the Kidney and Urinary Tract ». International Journal of Pediatrics and Child Health 4, no 2 (4 septembre 2016) : 61–71. http://dx.doi.org/10.12974/2311-8687.2016.04.02.1.

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Congenital anomalies of the kidney and urinary tract (CAKUT) are the most common reason for chronic kidney disease in children. Although more than 30 monogenic causes have been implicated in isolated forms of human CAKUT so far, the vast majority remains elusive. To identify novel monogenic causes of CAKUT we applied homozygosity mapping, together with whole exome sequencing, in a patient from consanguineous descent with isolated CAKUT. We identified a homozygous missense mutation (p.Arg415His) of the Ets Translocation Variant Gene 4 (ETV4). The transcription factor ETV4 is a downstream target of the GDNF/RET signaling pathway that plays a crucial role in kidney development. We show by means of electrophoretic mobility shift assay that the Arg415His mutant causes loss of the DNA binding affinity of ETV4 and fails to activate transcription in a cell-based luciferase reporter assay. We furthermore investigated the impact of the mutant protein on cell migration rate. Unlike wildtype ETV4, the Arg415His mutant failed to rescue cell migration defects observed in two ETV4 knock-down cell-lines. We therefore identified and functionally characterized a recessive mutation in ETV4 in a human patient with CAKUT. We hypothesize that the pathomechanism of this mutation could be via loss of the transcriptional function of ETV4, and a resulting abrogation of GDNF/RET/ETV4 signaling pathway.
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Thèses sur le sujet "ETV4"

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Fonseca, Aline Simoneti. « Assinatura de mRNA entre adenoma e adenocarcinoma colorretal ». Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/17/17135/tde-18122014-095654/.

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O câncer colorretal está entre as principais neoplasias malignas sendo a quarta causa de morte por câncer no mundo e a terceira no Brasil. Mutações nos genes APC, DCC, K-RAS e TP53 foram originalmente associadas com a progressão do câncer colorretal (CCR) esporádico. Entretanto, estudos de genoma completo e exoma têm revelado outros genes relacionados com o CCR. Como consequência dessas mutações, um conjunto de genes alteram sua expressão modulando vias gênicas em cada estágio da progressão tumoral. Nesse sentido, há um grande esforço para definir assinaturas gênicas que auxiliem na classificação dos tumores quanto ao diagnóstico e prognóstico dos pacientes. Portanto, o objetivo deste projeto foi analisar a expressão gênica em escala genômica de amostras de adenoma e adenocarcinoma colorretal visando identificar novos marcadores genéticos ligados a transição adenoma-adenocarcinoma. Para isso, dez amostras pareadas de adenoma e adenocarcinoma do mesmo paciente foram submetidas à análise de expressão gênica pela técnica de microarranjos. Análises de bioinformática, revelaram uma assinatura de 689 genes diferencialmente expressos (fold-change>2, p<0.05), que permitiram a classificação genética entre o adenoma e o adenocarcinoma. Oitos genes (IL6, IL8, OSM, SFRP4, ETV4, ESM1, SIM2 e RETNLB) foram escolhidos para validação com base na sua função e valor de expressão no tecido tumoral. A análise in silico dos genes hiperexpressos realizada no programa MetaCore (análise de dados e vias gênicas) destacou diversas vias gênicas ligadas à tumorigênese, incluindo as de adesão celular e Transição Epitélio-Mesenquimal (TEM), importantes na fase avaçada da progressão tumoral. O gene ETV4 foi selecionado para realização dos ensaios funcionais em virtude de seus altos níveis de expressão nas dez amostras de adenocarcinoma e participação nos mecanismos de proliferação celular e no TEM. Ensaios in vitro de siRNA para o gene ETV4 resultou na diminuição da proliferação celular e no potencial clonogênico da linhagem HT29. Adicionalmente, foram investigadas mutações nos genes APC, K-RAS e TP53, nas amostras pareadas de adenoma, adenocarcinoma, tecido normal e sangue periférico dos dez pacientes. Todos os pacientes apresentaram mutação germinativas nos três genes. No entanto, apenas os genes K-RAS (40%) e TP53 (30%) apresentaram mutações somáticas e patogênicas, exclusivamente nos adenocarcinomas. Esses resultados demonstraram que, na nossa coorte, mutações nos genes TP53 e K-RAS podem estar contribuindo para a progressão em uma parcela do câncer colorretal do tipo esporádico. Em resumo, o presente estudo aponta que o gene ETV4 pode contribuir para ativar o mecanismo de proliferação celular em adenocarcinoma colorretal. Além disso, o estudo demonstra a importância da combinação da análise de mutação com o perfil de expressão para melhor compreensão da base molecular do câncer colorretal.
Colorectal cancer is among the main malignant neoplasia, it is the fourth leading cause of death in the world and the third in Brazil. Mutations in APC, DCC, KRAS and TP53 genes have been originally associated with the progression of sporadic colorectal cancer (CRC). However genome wide and exome studies have revealed other genes related to CRC. As a consequence of these mutations, a set of genes alters their expression modulating gene pathways in every stage of tumor progression. In this regard, there is great effort to define gene signatures that help to classify tumors in relation to patients diagnosis and prognosis. Therefore, the objective of this project was to analyze gene expression in genomic scale of colorectal adenoma and adenocarcinoma samples aiming to identify new genetic markers linked to adenoma- adenocarcinoma transition. For this purpose, ten paired adenoma and adenocarcinoma samples of the same patient were subjected to gene expression analysis by microarrays technique. Bioinformatics analyses revealed a signature of 689 genes differentially expressed (fold-change>2, p<0.05), which allowed the genetic classification between adenoma and adenocarcinoma. Eight genes (IL6, IL8, OSM, SFRP4, ETV4, ESM1, SIM2 and RETNLB) were chosen for validation based on their function and expression value in tumor tissue. In silico analysis of hyperexpressed genes, done in the program MetaCore (data analysis and gene pathways), highlighted diverse gene pathways linked to tumorigenesis, including the ones of cell adhesion and Epithelial-Mesenchymal Transition (EMT), important in the advanced phase of tumor progression. ETV4 gene was selected for functional assays due to its high expression levels in the ten samples of adenocarcinoma and due to its participation in cell proliferation mechanisms and in EMT. In vitro siRNA assays for ETV4 gene resulted in the decrease of cell proliferation and in the clonogenic potential of HT29 line. In addition, mutations in APC, KRAS and TP53 genes were investigated in paired samples of adenoma, adenocarcinoma, normal tissue, and peripheral blood from ten patients. All patients showed germline mutations in the three genes. However, only KRAS (40%) and TP53 (30%) genes showed somatic and pathogenic mutations, exclusively in adenocarcinomas. These results demonstrated that, in our cohort, mutations in TP53 and KRAS genes might be contributing to progression in a portion of sporadic-type colorectal cancer. In summary, the present study points out that ETV4 gene might contribute to activate cell proliferation mechanism in colorectal adenocarcinoma. Moreover, the study demonstrates the importance of combining the mutation analysis with expression profile in order to better understanding the molecular basis of colorectal cancer.
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Dumortier, Mandy. « Étude du rôle des facteurs de transcription ETV4 et ETV1 de la famille ETS dans le processus tumoral de cancers hormono-dépendants : le cancer du sein, la progression métastatique du cancer de la prostate ». Thesis, Lille 1, 2017. http://www.theses.fr/2017LIL10181.

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Les facteurs ETV1, 4, 5 sont souvent associée au développement de cancers. Le 1èr projet porte sur ETV4 et MMP13 en tant que gène cible et relais potentiel de l’effet pro-tumorigène d’ETV4 dans la tumorigenèse mammaire. ETV4 est surexprimé dans le cancer du sein et est associé à un mauvais pronostic, mais les événements impliqués sont encore peu connus. ETV4 contrôle l’expression de nombreux gènes comme MMP13. Cette étude a permis de montrer que MMP13 est un gène cible d’ETV4. En effet, la surexpression de MMP13 contribue aux effets pro-tumorigène et l’inhibition de MMP13 dans un contexte de surexpression de ETV4 diminue son impact. Enfin, l’étude effectuée dans la cohorte de patiente associe la surexpression d’ETV4 et de MMP13 à un cancer de mauvais pronostic. Le 2ème projet porte sur l’implication d’ETV1 dans la progression métastatique du cancer de la prostate (CaP). Les fusions de gènes impliquant les facteurs ERG et ETV1 sont présentes dans ≈50% et 10% des cas respectivement, ETV1 est présent à 50% sous sa forme pleine longueur et à 50% sous une forme tronquée. Les études ne présageant pas de différences entre les fusions ERG et ETV1. Dans ce contexte, mon 2ème sujet d’étude porte sur la recherche de l’implication du facteur ETV1 (pleine longueur ou tronquée) dans la formation des métastases du CaP et la recherche de gènes cibles impliqués, le tout en comparaison avec les données sur ERG. Cette étude nous a permis de mettre en évidence une différence en terme d’agressivité entre les 2 formes d’ETV1 in vitro et in vivo. Cependant la fusion étant peut représentée, les résultats récolté dans la cohorte ne peuvent permettre de confirmer cette différence d’agressivité
ETV1, 4, 5 transcription factor are overexpress in various cancer. The first part is focus in MMP13 like target gene, potentially implicated in the mammary tumorigenesis induced by ETV4. Thus we show, the regulation of MMP13 expression by ETV4. Next we show that ETV4 promotes the mammary tumorigenesis and that MMP13 is a relay. In fact, the overexpression of MMP13 is implicate in pro-tumorigenesis effect and the repression of MMP13 in context of ETV4 overexpression decreases this effect. This approach was completed by the injection of cells in mice and show MMP13 mediate the pro-tomorigene effect of ETV4. We analysed expression of MMP13 and ETV4 in primary breast tumors and show the overexpression concomintant of ETV4 and MMP13 are associated with a poor prognosis. The second part of our study is about the ETV1 factor, in the progression of metastasis of prostate cancer (PCa) and the research of involved target genes. Gene fusion involving ERG and ETV1 and their overexpression are frequent in PCa and occur in 50% and 10% of cases respectively. To understand the role of ETV1, in comparison with available data on ERG, differents PCa cells overexpress or repress ETV1 were used. We have shown that the ETV1 factor enhance tumorigenesis capacities PCa cell lines and her truncated form has opposite effects. ETV1 full-lenght (FL) induces more bones metastasis formation than her truncated form. The expression of ETV1, and his truncated form was study in PCa samples. We confirmed the pro-tumorigenic statute of ETV1 factor in PCa and we defined differences beetwen FL and truncated length and complet the comprehension of the ETV1 function in the formation of bones metastasis of PCa
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Cavazzola, Luciane Rostirola. « Análise da expressão do mRNA das enzimas timidina fosforilase e uridina fosforilase 1 e 2 e dos fatores de transcrição PDEF e ETV4 em tumores de próstata e de rim ». Pontifícia Universidade Católica do Rio Grande do Sul, 2014. http://hdl.handle.net/10923/6884.

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Prostate cancer is the most important urological tumor and the second most common in men. The incidence and mortality of this multifactorial disease are varied and take into account behavioral factors and genetic predisposition. The main predisposing factors are age, race and family history. Among the various histological subtypes, the acinar adenocarcinoma is the most common. The classification of this tumor, from transrectal ultrasonography and biopsy needle, is made for degrees of Gleason score and TNM classification that provides for tumor staging. The prostatic carcinoma has a propensity to metastasize and is regulated by various molecular signaling pathways through genes, proteins, enzymes, receptors and transcription factors. The RCC is the third most common urological tumor. The wide variation in incidence correlates with the geographical area. Risk factors can be various as smoking, genetic diseases and genetic alterations. The vast majority of cases occur in adults and in the renal parenchyma, and comprise five histological subtypes, the clear and sporadic cells being the most common. The histological differentiation is made by Fuhrman grade and staging by TNM classification. As the clinical manifestations are varied, most patients are diagnosed incidentally and by ultrasonography. The enzymes thymidine phosphorylase and uridine phosphorylase 1 and 2 as well as the transcription factors PDEF and ETV4 are reported as components of pathways leading to tumorigenesis and / or metastasis. The objective of this work is to analyze these enzymes and transcription factors and their correlation with clinical and pathological variables in prostate and kidney cancers as well as in bening tissue, by RT-PCR in real time. In prostate cancer, the geometric mean of the relative expression of transcription factors PDEF and ETV were greater in the tumor than in the benign tissues These factors also had a significant correlation between them in tumor tissue and benign tissue. The geometric mean of relative expression of the enzyme thymidine phosphorylase and uridine phosphorylase 1 strongly and significantly correlated between them in benign and in malignant prostate samples. The geometric mean of relative expression of thymidine phosphorylase also correlated moderately and significantly with the ETV4 in benign tissues. The geometric mean of relative expression of uridine phosphorylase in tumor T3 was significantly lower than in T1 and T2 prostate tumors. Kidney carcinoma TNM Classification strongly and significantly correlated with the relative expression of the enzyme thymidine phosphorylase and negatively correlated very strong and significantly with the enzyme uridine phosphorylase. The relative expression of the transcription factor ETV4 correlated negatively and significantly stronger with the TNM classification, and correlated with strength and significance with the relative expression of uridine phosphorylase in tumor tissues of the kidney.
O câncer de próstata é o mais importante tumor urológico e o segundo mais frequente no homem. As taxas de incidência e de mortalidade desta doença multifatorial são muito variadas e leva em conta fatores comportamentais e prédisposição genética. Os principais fatores predisponentes são idade avançada, raça e história familiar. Dentre os vários subtipos histológicos, o adenocarcinoma acinar é o mais frequente. A classificação deste tumor, a partir da ultra-sonografia transretal com biópsia por agulha, é feita pelos graus de escore de Gleason e pela Classificação TNM que fornece o estadiamento do tumor. O carcinoma de próstata, além de ter grande propensão em formar metástases, é regulado por várias vias moleculares de sinalização por meio de genes, proteínas, enzimas, receptores e fatores de transcrição.O carcinoma de células renais é o terceiro mais comum tumor urológico. A grande variação na taxa de incidência se correlaciona com a área geográfica. Os fatores de risco podem ser vários como tabagismo, doenças genéticas e alterações gênicas. A grande maioria dos casos ocorre em adultos no parênquima renal e, além de compreender cinco subtipos histológicos, o de células claras e esporádico é o mais frequente. A diferenciação histológica é feita pelo grau de Fuhrman e o estadiamento pela Classificação TNM. Como as manifestações clínicas são variadas, a maioria dos pacientes são diagnosticados incidentalmente e por ultra-sonografia. As enzimas timidina fosforilase e uridina fosforilase 1 e 2, bem como os fatores de transcrição PDEF e ETV4, são relatados como componentes das vias que levam à tumorigênese e/ou a metastização. O objetivo deste trabalho é analizar estas enzimas e fatores de transcrição, correlacionando-as com variáveis clínicas e patológicas nos tumores de próstata e de rim, bem como nos tecidos adjacentes a estes tumores, pela técnica de RT-PCR em tempo real. No câncer de próstata, a média geométrica da expressão relativa dos fatores de transcrição PDEF e ETV4 entre os tecidos benignos e tumorais, apresentaram correlação significativa com uma maior expressão relativa no tumor quando comparado ao seu benigno. Estes fatores também apresentaram uma correlação significativa entre eles no tecido tumoral e no tecido benigno. As médias geométricas da expressão relativa das enzimas timidina fosforilase e uridina fosforilase 1 se correlacionaram fortemente e significativamente entre os tecidos benignos e tumorais da próstata. A média geométrica da expressão relativa da timidina fosforilase também se correlacionou de forma moderada e significativa com a do ETV4, entre os tecidos benignos. A média geométrica da expressão relativa da uridina fosforilase nos tumores T3 foi significativamente menor do que nos tumores T1 e T2 da próstata. No carcinoma de rim a Classificação TNM se correlacionou fortemente e significativamente com a expressão relativa da enzima timidina fosforilase, e se correlacionou de forma negativa, muito forte e significativamente com a enzima uridina fosforilase. A expressão relativa do fator de transcrição ETV4 se correlacionou de forma negativa, forte e significativamente com a Classificação TNM, e se correlacionou de forma forte e significativamente com a expressão relativa de uridina fosforilase nos tecidos tumorais de rim.
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Cavazzola, Luciane Rostirola. « An?lise da express?o do mRNA das enzimas timidina fosforilase e uridina fosforilase 1 e 2 e dos fatores de transcri??o PDEF e ETV4 em tumores de pr?stata e de rim ». Pontif?cia Universidade Cat?lica do Rio Grande do Sul, 2014. http://tede2.pucrs.br/tede2/handle/tede/1788.

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Prostate cancer is the most important urological tumor and the second most common in men. The incidence and mortality of this multifactorial disease are varied and take into account behavioral factors and genetic predisposition. The main predisposing factors are age, race and family history. Among the various histological subtypes, the acinar adenocarcinoma is the most common. The classification of this tumor, from transrectal ultrasonography and biopsy needle, is made for degrees of Gleason score and TNM classification that provides for tumor staging. The prostatic carcinoma has a propensity to metastasize and is regulated by various molecular signaling pathways through genes, proteins, enzymes, receptors and transcription factors. The RCC is the third most common urological tumor. The wide variation in incidence correlates with the geographical area. Risk factors can be various as smoking, genetic diseases and genetic alterations. The vast majority of cases occur in adults and in the renal parenchyma, and comprise five histological subtypes, the clear and sporadic cells being the most common. The histological differentiation is made by Fuhrman grade and staging by TNM classification. As the clinical manifestations are varied, most patients are diagnosed incidentally and by ultrasonography. The enzymes thymidine phosphorylase and uridine phosphorylase 1 and 2 as well as the transcription factors PDEF and ETV4 are reported as components of pathways leading to tumorigenesis and / or metastasis. The objective of this work is to analyze these enzymes and transcription factors and their correlation with clinical and pathological variables in prostate and kidney cancers as well as in bening tissue, by RT-PCR in real time. In prostate cancer, the geometric mean of the relative expression of transcription factors PDEF and ETV were greater in the tumor than in the benign tissues These factors also had a significant correlation between them in tumor tissue and benign tissue. The geometric mean of relative expression of the enzyme thymidine phosphorylase and uridine phosphorylase 1 strongly and significantly correlated between them in benign and in malignant prostate samples. The geometric mean of relative expression of thymidine phosphorylase also correlated moderately and significantly with the ETV4 in benign tissues. The geometric mean of relative expression of uridine phosphorylase in tumor T3 was significantly lower than in T1 and T2 prostate tumors. Kidney carcinoma TNM Classification strongly and significantly correlated with the relative expression of the enzyme thymidine phosphorylase and negatively correlated very strong and significantly with the enzyme uridine phosphorylase. The relative expression of the transcription factor ETV4 correlated negatively and significantly stronger with the TNM classification, and correlated with strength and significance with the relative expression of uridine phosphorylase in tumor tissues of the kidney.
O c?ncer de pr?stata ? o mais importante tumor urol?gico e o segundo mais frequente no homem. As taxas de incid?ncia e de mortalidade desta doen?a multifatorial s?o muito variadas e leva em conta fatores comportamentais e pr?-disposi??o gen?tica. Os principais fatores predisponentes s?o idade avan?ada, ra?a e hist?ria familiar. Dentre os v?rios subtipos histol?gicos, o adenocarcinoma acinar ? o mais frequente. A classifica??o deste tumor, a partir da ultra-sonografia transretal com bi?psia por agulha, ? feita pelos graus de escore de Gleason e pela Classifica??o TNM que fornece o estadiamento do tumor. O carcinoma de pr?stata, al?m de ter grande propens?o em formar met?stases, ? regulado por v?rias vias moleculares de sinaliza??o por meio de genes, prote?nas, enzimas, receptores e fatores de transcri??o. O carcinoma de c?lulas renais ? o terceiro mais comum tumor urol?gico. A grande varia??o na taxa de incid?ncia se correlaciona com a ?rea geogr?fica. Os fatores de risco podem ser v?rios como tabagismo, doen?as gen?ticas e altera??es g?nicas. A grande maioria dos casos ocorre em adultos no par?nquima renal e, al?m de compreender cinco subtipos histol?gicos, o de c?lulas claras e espor?dico ? o mais frequente. A diferencia??o histol?gica ? feita pelo grau de Fuhrman e o estadiamento pela Classifica??o TNM. Como as manifesta??es cl?nicas s?o variadas, a maioria dos pacientes s?o diagnosticados incidentalmente e por ultra-sonografia. As enzimas timidina fosforilase e uridina fosforilase 1 e 2, bem como os fatores de transcri??o PDEF e ETV4, s?o relatados como componentes das vias que levam ? tumorig?nese e/ou a metastiza??o. O objetivo deste trabalho ? analizar estas enzimas e fatores de transcri??o, correlacionando-as com vari?veis cl?nicas e patol?gicas nos tumores de pr?stata e de rim, bem como nos tecidos adjacentes a estes tumores, pela t?cnica de RT-PCR em tempo real. No c?ncer de pr?stata, a m?dia geom?trica da express?o relativa dos fatores de transcri??o PDEF e ETV4 entre os tecidos benignos e tumorais, apresentaram correla??o significativa com uma maior express?o relativa no tumor quando comparado ao seu benigno. Estes fatores tamb?m apresentaram uma correla??o significativa entre eles no tecido tumoral e no tecido benigno. As m?dias geom?tricas da express?o relativa das enzimas timidina fosforilase e uridina fosforilase 1 se correlacionaram fortemente e significativamente entre os tecidos benignos e tumorais da pr?stata. A m?dia geom?trica da express?o relativa da timidina fosforilase tamb?m se correlacionou de forma moderada e significativa com a do ETV4, entre os tecidos benignos. A m?dia geom?trica da express?o relativa da uridina fosforilase nos tumores T3 foi significativamente menor do que nos tumores T1 e T2 da pr?stata. No carcinoma de rim a Classifica??o TNM se correlacionou fortemente e significativamente com a express?o relativa da enzima timidina fosforilase, e se correlacionou de forma negativa, muito forte e significativamente com a enzima uridina fosforilase. A express?o relativa do fator de transcri??o ETV4 se correlacionou de forma negativa, forte e significativamente com a Classifica??o TNM, e se correlacionou de forma forte e significativamente com a express?o relativa de uridina fosforilase nos tecidos tumorais de rim.
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Huang-Hobbs, Helen. « Dissecting the mechanism of ETV6 polymerization ». Thesis, University of British Columbia, 2013. http://hdl.handle.net/2429/45691.

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ETV6 (or TEL), a member of the ETS family of eukaryotic transcription factors, normally functions as a transcriptional repressor and putative tumor suppressor. ETV6 is modular, containing a SAM (or PNT) domain and a DNA-binding ETS domain joined by a flexible linker sequence. The ETV6 SAM domain self-associates in a head-to-tail fashion, forming helical polymers proposed to generate extended repressive complexes at target DNA sites. ETV6 is also frequently involved in chromosomal translocations yielding unregulated chimeric oncoproteins with the SAM domain fused to the catalytic domain of a tyrosine receptor kinase such as NTRK3. Cellular transformation likely results from SAM domain-mediated polymerization and constitutive activation of the kinase domain. In the case of the ETV6- NTRK3 fusion (EN), this transformation is linked to congenital fibrosarcomas. Our goal is to investigate via mutations within its SAM domain, the thermodynamic and dynamic mechanisms underlying the altered transformation properties of ETV6-NTRK3. These studies have been carried out using monomeric variants of the isolated SAM domains with "head" or "tail" point mutations that prevent self-association, yet allow for formation of a mixed dimer with a native binding interface. Specifically, we used a combination of NMR spectroscopy and isothermal titration calorimetry to study the effects of additional mutations on their dimerization. Consistent with its involvement in a crystallographically-observed interdomain salt bridge, mutation of Lys99 was found to weaken the association of ETV-SAM monomers in solution, and to disrupt cellular transformation by EN. This supports the role of the SAM domain self-association in the activation of ETV6-NTRK3, and helps define the mechanisms underlying cellular transformation by similar chimeric oncoproteins.
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Hart, Stephen Michael. « In vivo analysis of the ETV6-CBFA2 fusion gene ». Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.392499.

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Jomrich, Gerd, Florian Maroske, Jasmin Stieger, Matthias Preusser, Aysegül Ilhan-Mutlu, Daniel Winkler, Ivan Kristo, Matthias Paireder et Sebastian Friedrich Schoppmann. « MK2 and ETV1 Are Prognostic Factors in Esophageal Adenocarcinomas ». IVyspring International Publisher, 2018. http://dx.doi.org/10.7150/jca.22310.

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Background. Esophageal cancer is ranked in the top ten of diagnosed tumors worldwide. Even though improvements in survival could be noticed over the last years, prognosis remains poor. ETS translocation variant 1 (ETV1) is a member of a family of transcription factors and is phosphorylated by mitogen-activated protein kinase (MAPK)-activated protein kinase 2 (MK2). Aim of this study was to evaluate the prognostic role of MK2 and ETV1 in esophageal cancer. Methods. Consecutive patients that underwent surgical resection at the department of surgery at the Medical University of Vienna between 1991 and 2012 were included into this study. After microscopic analysis, tissue micro arrays (TMAs) were created and immunohistochemistry was performed with antibodies against MK2 and ETV1. Results. 323 patients were included in this study. Clinical data was achieved from a prospective patient data base. Nuclear overexpression of MK2 was observed in 143 (44.3%) cases for nuclear staining and in 142 (44.0%) cases a cytoplasmic overexpression of MK2 was observed. Nuclear and cytoplasmic ETV1 overexpression was detected in 20 cases (6.2%) and 30 cases (9.3%), respectively. In univariate survival analysis, cMK2 and nETV1 were found to be significantly associated with patients' overall survival. Whereas overexpression of cMK2 was associated with shorter, nETV1 was associated with longer overall survival. In multivariate survival analysis, both cMK2 and nETV1 were found to be independent prognostic factors for the subgroup of EAC as well. Discussion. Expression of MK2 and ETV1 are prognostic factors in patients, with esophageal adenocarcinoma.
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Kaulfuß, Katja [Verfasser]. « Identifizierung von Zielgenen des chimären Transkriptionsfaktors ETV6/RUNX1 / Katja Kaulfuß ». Berlin : Freie Universität Berlin, 2018. http://d-nb.info/1196805180/34.

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Favier, Marie. « Les thrombopénies héréditaires rares : implications des gènes ETV6, ITGA2B, ITGB3 ». Thesis, Aix-Marseille, 2017. http://www.theses.fr/2017AIXM0559.

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L’identification des gènes impliqués dans les thrombopénies apporte des éléments importants pour la compréhension des voies de régulation de la production et des fonctions des plaquettes voire de l’hématopoïèse. Notre laboratoire a développé une stratégie d’identification de gènes à l’origine de thrombopénies sans hypothèse a priori par séquençage d’exomes. Cette stratégie a permis de mettre en évidence des mutations touchant les gènes ETV6, ITGA2B et ITGB3.Les thrombopénies à volume plaquettaire normal sont particulièrement importantes à détecter en raison d’un risque d’évolution vers une pathologie onco-hématologique. L’origine génétique de cette catégorie de thrombopénie s’est pendant longtemps limitée aux mutations du gène runx1. Le travail que j’ai effectué au cours de ma thèse a contribué à impliquer le gène etv6 dans ce groupe de thrombopénies.Concernant le gène etv6 6 familles ont présenté des mutations pathogènes. Toutes ces mutations sont à l’origine d’une perte de l’activité répressive du gène et un nombre élevé de cellules CD34+ circulant dans le sang révélant le rôle d’ETV6 dans la prédisposition onco-hématologique. De plus la mégacaryopoïèse présente deux principales anomalies. Elles associent une augmentation du nombre de colonies progéniteurs mégacaryocytaires à une formation de proplaquettes réduites. Concernant les gènes itga2b et itgb3 3 familles ont été étudiées.Des défauts quantitatifs ou qualitatifs du récepteur αIIbβ3 conduisant à sa perte de fonction se retrouvent dans la thrombasthénie de Glanzmann (GT) caractérisée par une thrombopathie mais un nombre de plaquettes et une morphologie normale
The identification of the genes involved in thrombocytopenia provides important elements for understanding the pathways of regulation of the production and functions of platelets or even hematopoiesis. Our laboratory has developed a strategy for identifying genes causing thrombocytopenia without a priori hypothesis by sequencing exomes. This strategy has been applied to families with autosomal dominant thrombocytopenia and has demonstrated mutations in the genes etv6, ​​itga2b and itgb3. Normal platelet thrombocytopenia are particularly important to detect because of the risk of developing onco-hematological pathology. The genetic origin of this category of thrombocytopenia has long been limited to mutations in the runx1 gene. More recently, mutations on the ankrd26 promoter have been reported. The work I did during my thesis helped to involve the etv6 gene in this group of thrombocytopenia. Concerning this gene six families have pathogenic mutations. All these mutations are the cause of a loss of the repressive activity of the gene and a high number of CD34+ cells circulating in the blood revealing the role of ETV6 in the onco-hematological predisposition. In addition, megakaryopoiesis has two main anomalies. They associate an increase in the number of megakaryocytic progenitor colonies with the formation of reduced proplatelets.Concerning the itga2b and itgb3 genes, 3 families were studied. These genes encode the αIIbβ3 integrin. Integrin αIIbβ3 is a platelet receptor for fibrinogen and Von Willebrand factor, and plays a crucial role in thrombosis and hemostasis
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Craig, Michael P. « Transcriptional Regulation of Developmental and Tumor-Induced Angiogenesis by Etv2 and Fli1b ». University of Cincinnati / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1427982504.

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Livres sur le sujet "ETV4"

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Suman. Snēha : ETV dhārāvāhikaku skrīnplērūpaṃ. Haidarābād : Uṣōdayā Pablikēṣans, 1997.

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(Greece), Hellēnikē Trapeza Viomēchanikēs Anaptyxeōs. Hē drastēriotēta tēs ETVA to etos 1985. [Athēna] : Hē Trapeza, 1985.

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Frank, N. Magid Associates Inc. Executive Summary of Findings : Prepared for ETVC Limited(Survey Research). [Uk] : Frank N Magid Associates, 1991.

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Gokhale, L. N. The use of ETV in India and Japan. Pune, India : L.N. Gokhale, 1986.

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), National Risk Management Research Laboratory (U S. Environmental technology verification (ETV) program case studies : Demonstrating program outcomes. Cincinnati, OH : National Risk Management Research Laboratory, Office of Research and Development, U.S. Environmental Protection Agency, 2006.

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Der Europäische Verbund territorialer Zusammenarbeit (ETVZ) : Neue Chancen für die Europaregion Tirol-Südtirol-Trentino. Wien : Braumüller, 2011.

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1945-, Kurfürst Ulrich, dir. Solid sample analysis : Direct and slurry sampling using GF-AAS and ETV-ICP. Berlin : Springer, 1998.

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Curabay, Şensu. 20. kuruluş yılında Anadolu Üniversitesi açiköğretim sistemi ve Açıköğretim Fakültesi eğitim televizyonu, ETV. Eskişehir [Turkey] : Anadolu Üniversitesi, 2002.

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Bibliothèqye publique d'information. (23 et 24 octobre 2002). Les 25 ans de la BPI : Encyclopédisme, actualité, libre-accès : actes du colloque international organisé par la Bibliothèqye publique d'information, au Centre Pompidou, les 23 et24 octobre 2002. Paris : Editions de la Bibliothèque publique d'information, 2003.

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George, Papandreou Andreas, Papanagiōtou Kōstas, Sallas Michalēs G et Hellēnikē Trapeza Viomēchanikēs Anaptyxeōs (Greece), dir. Themeliōsē tou ergostasiou tēs Hellēnikēs Viomēchanias Alouminas stē Thisvē/Voiōtias stis 27 Oktōvriou 1987 : Homilies tou Prōthypourgou Andrea Papandreou, tou Anaplērōtē-Hypourgou V.E.T. Kōsta Papanagiōtou, tou Dioikētē tēs ETVA Michalē G. Salla. Athēna : Hellēnikē Trapeza Viomēchanikēs Anaptyxeōs, 1987.

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Chapitres de livres sur le sujet "ETV4"

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Bohlander, Stefan K. « ETV6 ». Dans Encyclopedia of Cancer, 1343–46. Berlin, Heidelberg : Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_2035.

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Sundaresh, Aishwarya, et Owen Williams. « Mechanism of ETV6-RUNX1 Leukemia ». Dans Advances in Experimental Medicine and Biology, 201–16. Singapore : Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-3233-2_13.

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Aramendía Marzo, Maite, Martín Resano et Frank Vanhaecke. « ETV-ICPMS for Analysis of Polymers ». Dans Mass Spectrometry Handbook, 1061–77. Hoboken, NJ, USA : John Wiley & Sons, Inc., 2012. http://dx.doi.org/10.1002/9781118180730.ch44.

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Ford, Anthony M., et Mel Greaves. « ETV6-RUNX1 + Acute Lymphoblastic Leukaemia in Identical Twins ». Dans Advances in Experimental Medicine and Biology, 217–28. Singapore : Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-3233-2_14.

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Dezena, Roberto Alexandre. « General Principles of Endoscopic Third Ventriculostomy (ETV) ». Dans Endoscopic Third Ventriculostomy, 67–79. Cham : Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-28657-6_5.

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Dezena, Roberto Alexandre. « Surgical Technique of Endoscopic Third Ventriculostomy (ETV) ». Dans Endoscopic Third Ventriculostomy, 81–91. Cham : Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-28657-6_6.

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Ruggeri, Tommaso, et Masaru Sugiyama. « Shock Wave in a Polyatomic Gas Analyzed by ET14 ». Dans Classical and Relativistic Rational Extended Thermodynamics of Gases, 389–407. Cham : Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-59144-1_17.

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Lo, William B., et Abhaya V. Kulkarni. « Endoscopic Third Ventriculostomy with Choroid Plexus Cauterization (ETV–CPC) Versus CSF Shunting ». Dans Cerebrospinal Fluid Disorders, 317–29. Cham : Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-97928-1_18.

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Verrept, Peter, Sylvie Boonen, Luc Moens et Richard Dams. « Solid Sampling by Electrothermal Vaporization-Inductively Coupled Plasma-Atomic Emission and -Mass Spectrometry (ETV-ICP-AES/-MS) ». Dans Solid Sample Analysis, 191–246. Berlin, Heidelberg : Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-662-03716-4_4.

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Samandouras, George. « Shunts and endoscopic third ventriculostomy ». Dans The Neurosurgeon's Handbook, 696–702. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780198570677.003.0572.

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Actes de conférences sur le sujet "ETV4"

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Kunju, Lakshmi P., Shannon Carskadon, Ritu Bhalla, Javed Siddiqui, Scott A. Tomlins, Arul M. Chinnaiyan et Nallasivam Palanisamy. « Abstract 4216 : Novel RNAIn situhybridization method for the detection of ETV1, ETV4 and ETV5 rearrangements in prostate cancer. » Dans Proceedings : AACR 104th Annual Meeting 2013 ; Apr 6-10, 2013 ; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-4216.

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Tyagi, Nikhil, Sanjeev K. Srivastava, Arun Bhardwaj, Sumit Arora, William E. Grizzle, Laurie B. Owen, Ajay P. Singh et Seema Singh. « Abstract 2011 : ETV4 promotes pancreatic cancer progression and metastasis ». Dans Proceedings : AACR Annual Meeting 2014 ; April 5-9, 2014 ; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-2011.

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Kim, E. « PO-111 Capicua suppresses hepatocellular carcinoma progression by controlling ETV4-MMP1 axis ». Dans Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.152.

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Srivastava, Sanjeev K., Nikhil Tyagi, Gurpreet Kaur, Sumit Arora, Arun Bhardwaj, William E. Grizzle, Ajay P. Singh et Seema Singh. « Abstract 3120 : Evidence supporting a role of ETV4 in pancreatic cancer pathogenesis. » Dans Proceedings : AACR 104th Annual Meeting 2013 ; Apr 6-10, 2013 ; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-3120.

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Butler, Miriam S., Michael Hsing, Mani Roshan Moniri, Desmond Lau, Paul Yen, Ari Kim, Scott Lien et al. « Abstract 1648 : Targeting ETS factor ETV4 as a novel therapeutic for the management of breast and prostate cancer ». Dans Proceedings : AACR 106th Annual Meeting 2015 ; April 18-22, 2015 ; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-1648.

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Shah, Amip, Chandrakant D. Patel et Cullen Bash. « Designing Environmentally Sustainable Computer Systems Using Networks of Exergo-Thermo-Volume Building Blocks ». Dans ASME 2009 InterPACK Conference collocated with the ASME 2009 Summer Heat Transfer Conference and the ASME 2009 3rd International Conference on Energy Sustainability. ASMEDC, 2009. http://dx.doi.org/10.1115/interpack2009-89037.

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As regulation and competition drives the creation of environmentally sustainable systems, cradle-to-cradle life-cycle assessment (LCA) methodologies are becoming increasingly commonplace. However, existing LCA techniques are often laborious and costly to implement. Moreover, while LCA provides great insight into the impact of a given product or service, the translation of LCA outputs into iterative design inputs is not straightforward. A tighter linkage between product design and LCA methods is desired. In this paper, we propose creating such a linkage through the method of “exergo-thermo-volumes”. Specifically, we consider the design of an enterprise server with multiple heat dissipating components. Each of these heat dissipating components can be represented as an exergo-thermo-volume (ETV). Simultaneously, the cooling solution that removes heat from each of these components is also treated as an ETV. We show that the optimal system design can be determined through superposition of each of these ETVs with appropriately coupled boundary conditions. The resulting ETV representation of discretized heat sources and companioned cooling solutions essentially leads to the creation of an ETV network, which can then be optimized for the minimum sustainability footprint. We find that the optimal solution predicted by the exergo-thermo-volume approach matches those that would be predicted intuitively based on general design-for-environment and thermal management practices, but — using the current approach — we are also able to quantitatively show the difference between the optimal and sub-optimal choices. We conclude by demonstrating the applicability of the exergo-thermo-volume approach for the sustainable design of an enterprise server.
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Chica-Parrado, Maria Rosario, Julio Montes-Torres, Cynthia Robles-Podadera, Martina Alvarez, Jose Jerez, Luis Vicioso, Lidia Pérez-Villa et al. « Abstract P1-10-26 : Gene expression levels of DTX3, CACNA1G, IL11, ETV4 and TSPAN7 selected by LASSO penalty regression could predict pCR after neoadjuvant chemotherapy in breast cancer tumors ». Dans Abstracts : 2019 San Antonio Breast Cancer Symposium ; December 10-14, 2019 ; San Antonio, Texas. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.sabcs19-p1-10-26.

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Terada, Minoru. « ETV ». Dans the 10th annual SIGCSE conference. New York, New York, USA : ACM Press, 2005. http://dx.doi.org/10.1145/1067445.1067480.

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Xagoraris, Zafiris, et George Soulis. « The new geographic information system in ETVA VI.PE. » Dans Fourth International Conference on Remote Sensing and Geoinformation of the Environment, sous la direction de Kyriacos Themistocleous, Diofantos G. Hadjimitsis, Silas Michaelides et Giorgos Papadavid. SPIE, 2016. http://dx.doi.org/10.1117/12.2240856.

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Uemura, Suguru, Daiichiro Hasegawa, Akemi Shono, Khin Kyae Mon Thwin, Nanako Nino, Satoru Takafuji, Takeshi Mori et al. « Abstract A11 : A pediatric ETV6-ABL1-positive acute lymphoblastic leukemia case with ETV6-ABL1-independent resistance to tyrosine kinase inhibitor ». Dans Abstracts : AACR Special Conference : Pediatric Cancer Research : From Basic Science to the Clinic ; December 3-6, 2017 ; Atlanta, Georgia. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.pedca17-a11.

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Rapports d'organisations sur le sujet "ETV4"

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Morrissey, Colm. Small Molecule Inhibitors of ERG and ETV1 in Prostate Cancer. Fort Belvoir, VA : Defense Technical Information Center, septembre 2014. http://dx.doi.org/10.21236/ada613409.

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Morrissey, Colm. Small Molecule Inhibitors of ERG and ETV1 in Prostate Cancer. Fort Belvoir, VA : Defense Technical Information Center, septembre 2013. http://dx.doi.org/10.21236/ada593129.

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Orkin, Stuart H. Exploring the Mechanisms of Pathogenesis in Prostate Cancer Involving TMPRSS2-ERG (Or ETV1) Gene Rearrangement. Fort Belvoir, VA : Defense Technical Information Center, janvier 2008. http://dx.doi.org/10.21236/ada491425.

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Orkin, Stuart H. Exploring the Mechanisms of Pathogenesis in Prostate Cancer Involving TMPRSS2-ERG (Or ETV1) Gene Rearrangement. Fort Belvoir, VA : Defense Technical Information Center, janvier 2009. http://dx.doi.org/10.21236/ada501163.

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Detcheva, Albena K., Jürgen Hassler, Lidia Ivanova, Caroline Hommel et Thomas Vogt. ETV-ICP-OES Determination of Essential, Non-essential and Toxic Elements in Seven Bulgarian Herbs. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, avril 2019. http://dx.doi.org/10.7546/crabs.2019.04.05.

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Fisher, Robert J. Environmental Technology Verification Coatings and Coating Equipment Program (ETV CCEP). High Transfer Efficiency Spray Equipment - Generic Verification Protocol (Revision 0). Fort Belvoir, VA : Defense Technical Information Center, septembre 2006. http://dx.doi.org/10.21236/ada470549.

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Fisher, Robert J. Environmental Technology Verification Coatings and Coating Equipment Program (ETV CCEP). Final Technology Applications Group TAGNITE - Testing and Quality Assurance Plan (T/QAP). Fort Belvoir, VA : Defense Technical Information Center, juillet 2006. http://dx.doi.org/10.21236/ada459899.

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[Environmental Hazards Assessment Program annual report, June 1992--June 1993]. South Carolina ETV Socratic Dialog II. Office of Scientific and Technical Information (OSTI), juin 1993. http://dx.doi.org/10.2172/10109121.

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