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Academic literature on the topic 'Fusions ETS'

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Published: 7 July 2024
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Journal articles on the topic "Fusions ETS":

1

Smith, Jenny L., Rhonda E. Ries, Yi-Cheng Wang, Amanda R. Leonti, Todd A. Alonzo, Alan S. Gamis, Richard Aplenc, et al. "ETS Family Transcription Factor Fusions in Childhood AML: Distinct Expression Networks and Clinical Implications." Blood 138, Supplement 1 (November 5, 2021): 2356. http://dx.doi.org/10.1182/blood-2021-148894.

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Abstract The ETS family of genes encode transcription factors (TFs) containing the ETS DNA binding domain, which have roles in cellular growth and development, including embryonic hematopoiesis. Dysregulation of these genes is associated with malignant transformation and tumorigenesis. In childhood acute myeloid leukemia (AML), the MNX1-ETV6 t(7;12)(q36;p13) and FUS-ERG t(16;21)(p11;q22) fusions are associated with adverse outcome. However, the biological and clinical implications of other ETS oncofusions in pediatric AML remain unknown. We identified 62 ETS gene fusions in 1,473 primary diagnostic AML samples (4.2%) using whole transcriptome RNA-sequencing and karyotype data. Four ETS family genes were identified to be involved in fusions with various partner genes: ETV6, ERG, FEV, and FLI1. Fusions with ETV6 were the most abundant (58%, 36/62) while FEV and FLI1 were the least; 21 fusion partners were identified where many function as TFs and co-activators (Figure 1A). MNX1-ETV6 (N=16) is enriched in infants (87.5% < 3 years, p < 0.001, Figure 1B), consistent with previous reports. ETV6 fusions with various partners (ETV6-Other, N=20) were likewise enriched in infants (50% < 3 years) and were significantly younger than patients without ETS fusions (median age: 3.0 vs 9.6 years, p = 0.025). FUS-ERG (N=10), HNRNPH1-ERG (N=8), and ETS fusions with various partners (ETS-Other, N=8) were primarily identified in patients 5-18 years old. Outcomes for patients with ETS fusions was determined after censoring for stem cell transplantation. Patients with ETS fusions as a collective group had adverse outcome with an EFS of 17.7% vs 39.9% (p = 0.047, Figure 1C), similar to high-risk cases in the reference group (22%), suggesting that patients with any ETS fusion may be considered high risk. Evaluation of outcomes by individual fusion groups at 3 years from diagnosis demonstrated an EFS of 0% for HNRNPH1-ERG, 18.0% for FUS-ERG, 14.2% for ETV6-Other, 20.8% for ETS-Other, and 28.4% for those with MNX1-ETV6. Twenty-one patients (37.5%) with ETS family fusions received stem cell transplant (SCT) in first complete remission, including HNRNPH1-ERG (N=5), FUS-ERG (N=3), ETV6-Other (N=5), ETS-Other (N=2), and MNX1-ETV6 (N=6). For these SCT recipients, OS at 3 years after transplant was 60.2%. We investigated whether ETS family fusions might have similar transcriptome profiles. Unsupervised uniform manifold approximation and projection (UMAP) on RNA-seq gene expression data followed by Leiden clustering found that individual fusions clustered in the same 3D space. More importantly, ETS fusion groups clustered closely to one another, indicating a shared transcriptional profile (Figure 1D, circle). Next, ETS fusion groups were each independently compared to the reference cohort (N=1421) using differential expression (DE) analysis. Intersection of DE genes revealed 17 overexpressed genes common to ETS fusions and 9/17 (52%) were also dysregulated when contrasting ETS cohorts to healthy normal marrows' transcriptome (N=68, Figure 1E). The minimal set of dysregulated genes included an adhesion molecule EDIL3, a prostaglandin (PG) enzyme HPGD, and a tyrosine phosphatase PTP4A3, which is strongly associated with progression in lymphoblastic leukemia and multiple myeloma. EDIL3 was reported to be overexpressed in MNX1-ETV6 and we found this molecule is a common feature of ETS fusions and their cellular dysregulation. The minimal set of 9 genes were further investigated using protein interaction networks defined from Pathway Commons v11. FUS-ERG and HNRNPH1-ERG both had significantly (adj. p < 0.001) activated HPGD networks; PG-E synthase and > 10 PG metabolism genes were upregulated. PG metabolism has important roles in regulating hematopoietic stem and progenitor (HSPC) functions and PG-E2 was shown to increase HSPC survival. ETV6-MXN1, ETV6-Other, and FUS-ERG had activated PTP4A3 networks and its expression was associated with sensitivity to BET inhibitors (BETi) in myeloma. They also exhibited increased activity of an ERG network with the overexpression of upstream regulators CBFA2T3 and GATA, and downstream targets like VWF and ZBTB16. Overall, we show that ETS fusions are uniformly high risk and share dysregulated cell adhesion (EDIL3) and transcriptional networks for ERG, HPGD, and PTP4A3, which provide opportunities for further research into the metabolome and therapeutics (BETi) in these fusions. Figure 1 Figure 1. Disclosures Shaw: T-Cell and/or Gene Therapy for Cancer: Patents & Royalties.
2

Barbi de Moura, Michelle, Fadel S. Alyaqoub, Gargi D. Basu, David W. Hall, Jess R. Hoag, Janine R. LoBello, Frederick L. Baehner, Snehal Govind Thakkar, and Steven Canfield. "Erythroblast transformation-specific transcription factor fusions in prostate cancer." Journal of Clinical Oncology 41, no. 6_suppl (February 20, 2023): 224. http://dx.doi.org/10.1200/jco.2023.41.6_suppl.224.

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224 Background: Common drivers in advanced prostate cancer (PC) involve fusions of the 3’ DNA binding domain-containing region of an Erythroblast Transformation Specific (ETS) transcription factor gene with a 5’ region of another gene, often one that is androgen-regulated. Previous work indicates that PCs harboring TMPRSS2:ERG fusions are more dependent on androgen signaling, and men with such tumors may, therefore, be more responsive to the effects of androgen deprivation therapy than men lacking this fusion. In this study, we examined the frequency of fusions involving ETS-family genes, including TMPRSS2:ERG, and determined how often such fusions would be missed if detection relied solely on DNA sequencing. Methods: To identify fusions and compare DNA-only versus DNA plus RNA sequencing, we utilized the Oncomap ExTra genomic profiling assay. This assay performs whole-exome, whole-transcriptome DNA and RNA sequencing of tumor and matched normal samples to identify somatic alterations in tumors. Single-nucleotide variants, indels, copy number alterations, alternative transcripts, and gene fusions are all detected. We specifically searched for fusions involving ETS transcription factor genes ERG and ETV1- 7. Results: A total of 512 PC patient samples assayed between April 2018 and July 2022 were included in the analysis; 226 ETS fusions were present in 223 (43.6%) patients; 3 patients carried two fusions. There were 196 ERG fusions including 185 (36.1%) patients having the familiar TMPRSS2: ERG fusion and 8 (1.6%) patients with a SLC45A3: ERG fusion, which is known to be associated with particularly poor prognosis. ETV1, 4, and 5 fusions were found in 29 (5.7%) patients and involved 12 different 5’ partner genes, the most common of which were SLC45A3 (6 fusions) and CANT1 (4 fusions). The two partner genes were on the same chromosome in 192 fusions, with 190 requiring a single deletion to create the fusion and 2 requiring a single inversion. For the 34 fusions involving genes on different chromosomes, a single translocation would be sufficient to produce the fusion gene in 23 cases; in 11 cases more than one structural rearrangement would be required. A total of 66 (29.6%) fusions were not detected in the DNA sequencing data, including 40 (21.6%) TMPRSS2: ERG fusions. In addition, 16 fusions were detected only in the DNA data, as RNA could not be sequenced, including 13 TMPRSS2: ERG fusions. Conclusions: In addition to TMPRSS2: ERG, the Oncomap ExTra assay identified several low frequency ETS fusions, all of which could be used to assist patients and physicians to select appropriate treatments. The identification of ETS fusions appears to be limited when using only DNA sequencing. Oncomap ExTra RNA analysis identified 66 additional fusions, representing almost 30% of those present, not identified by whole-exome DNA sequencing, suggesting RNA plus DNA assays detect fusions more reliably than DNA-only assays.
3

Staege, Martin S., and Daniela Max. "Genetics and Epigenetics of the TET-ETS Translocation Network." Genetics & Epigenetics 2 (January 2009): GEG.S2815. http://dx.doi.org/10.4137/geg.s2815.

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In the present paper we review the translocation network involving TET and ETS family members with special focus on the Ewing family of tumors. FUS (fusion, involved in t(12;16) in malignant liposarcoma = TLS, Translocated in liposarcoma), EWSR1 (Ewing sarcoma breakpoint region 1) and TAF15 (TATA box-binding protein-associated factor, 68-KD) are the three human members of the TET family of RNA binding proteins. In addition, two EWSR1 pseudogenes are present in the human genome. TET family members are involved in several oncogenic gene fusions. Five of the 18 known fusion partners belong to the E26 (E twenty-six, ETS) family of transcription factors. Gene fusions between TET or ETS family members and other fusion partners link these gene fusions to a large network of oncogenic gene rearrangements.
4

Wei, Ting, Ji Lu, Tao Ma, Haojie Huang, Jean-Pierre Kocher, and Liguo Wang. "Re-Evaluate Fusion Genes in Prostate Cancer." Cancer Informatics 20 (January 2021): 117693512110275. http://dx.doi.org/10.1177/11769351211027592.

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Background: Thousands of gene fusions have been reported in prostate cancer, but their authenticity, incidence, and tumor specificity have not been thoroughly evaluated, nor have their genomic characteristics been carefully explored. Methods: We developed FusionVet to dedicatedly validate known fusion genes using RNA-seq alignments. Using FusionVet, we re-assessed 2727 gene fusions reported from 36 studies using the RNA-seq data generated by The Cancer Genome Atlas (TCGA). We also explored their genomic characteristics and interrogated the transcriptomic and DNA methylomic consequences of the E26 transformation-specific (ETS) fusions. Results: We found that nearly two-thirds of reported fusions are intra-chromosomal, and 80% of them were formed between 2 protein-coding genes. Although most (76%) genes were fused to only 1 partner, we observed many fusion hub genes that have multiple fusion partners, including ETS family genes, androgen receptor signaling pathway genes, tumor suppressor genes, and proto-oncogenes. More than 90% of the reported fusions cannot be validated by TCGA RNA-seq data. For those fusions that can be validated, 5% were detected from tumor and normal samples with similar frequencies, and only 4% (120 fusions) were tumor-specific. The occurrences of ERG, ETV1, and ETV4 fusions were mutually exclusive, and their fusion statuses were tightly associated with overexpressions. Besides, we found ERG fusions were significantly co-occurred with PTEN deletion but mutually exclusive with common genomic alterations such as SPOP mutation and FOXA1 mutation. Conclusions: Most of the reported fusion genes cannot be validated by TCGA samples. The ETS family and androgen response genes were significantly enriched in prostate cancer–specific fusion genes. Transcription activity was significantly repressed, and the DNA methylation was significantly increased in samples carrying ERG fusion.
5

Gasi Tandefelt, Delila, Joost Boormans, Karin Hermans, and Jan Trapman. "ETS fusion genes in prostate cancer." Endocrine-Related Cancer 21, no. 3 (March 20, 2014): R143—R152. http://dx.doi.org/10.1530/erc-13-0390.

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Prostate cancer is very common in elderly men in developed countries. Unravelling the molecular and biological processes that contribute to tumor development and progressive growth, including its heterogeneity, is a challenging task. The fusion of the genes ERG and TMPRSS2 is the most frequent genomic alteration in prostate cancer. ERG is an oncogene that encodes a member of the family of ETS transcription factors. At lower frequency, other members of this gene family are also rearranged and overexpressed in prostate cancer. TMPRSS2 is an androgen-regulated gene that is preferentially expressed in the prostate. Most of the less frequent ETS fusion partners are also androgen-regulated and prostate-specific. During the last few years, novel concepts of the process of gene fusion have emerged, and initial experimental results explaining the function of the ETS genes ERG and ETV1 in prostate cancer have been published. In this review, we focus on the most relevant ETS gene fusions and summarize the current knowledge of the role of ETS transcription factors in prostate cancer. Finally, we discuss the clinical relevance of TMRPSS2–ERG and other ETS gene fusions in prostate cancer.
6

Anderson, Nathaniel D., Richard de Borja, Matthew D. Young, Fabio Fuligni, Andrej Rosic, Nicola D. Roberts, Simon Hajjar, et al. "Rearrangement bursts generate canonical gene fusions in bone and soft tissue tumors." Science 361, no. 6405 (August 30, 2018): eaam8419. http://dx.doi.org/10.1126/science.aam8419.

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Sarcomas are cancers of the bone and soft tissue often defined by gene fusions. Ewing sarcoma involves fusions between EWSR1, a gene encoding an RNA binding protein, and E26 transformation-specific (ETS) transcription factors. We explored how and when EWSR1-ETS fusions arise by studying the whole genomes of Ewing sarcomas. In 52 of 124 (42%) of tumors, the fusion gene arises by a sudden burst of complex, loop-like rearrangements, a process called chromoplexy, rather than by simple reciprocal translocations. These loops always contained the disease-defining fusion at the center, but they disrupted multiple additional genes. The loops occurred preferentially in early replicating and transcriptionally active genomic regions. Similar loops forming canonical fusions were found in three other sarcoma types. Chromoplexy-generated fusions appear to be associated with an aggressive form of Ewing sarcoma. These loops arise early, giving rise to both primary and relapse Ewing sarcoma tumors, which can continue to evolve in parallel.
7

Buteyn, Nathaniel J., Connor Burke, Eve Gardner, Vincent J. Sartori, Rhonda E. Ries, Todd A. Alonzo, Soheil Meshinchi, and Timothy Triche. "Reclassification of ETS Family Transcription Factor Fusions in Pediatric AML Based on Molecular Drivers." Blood 142, Supplement 1 (November 28, 2023): 4298. http://dx.doi.org/10.1182/blood-2023-189474.

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Pediatric Acute Myeloid Leukemia (pAML) patients with a fusion involving an E26 transformation-specific (ETS) transcription factor have traditionally been considered high-risk. The most common fusions include ETV6::MNX1 t(7;12)(q36;p13) and FUS::ERG t(16;21)(p11;q22), yet primary fusion alone has proven incapable of predicting response to treatment. Indeed, within the 60 pAML patients with ETS fusions from the Children's Oncology Group (COG) trials AAML0531 and AAML1031, there were 25 unique fusions and diverse outcomes between patients who did share a primary fusion. A molecular based reclassification of ETS fused pAML could prove beneficial in the development of novel therapeutic additions to standard induction. Here, using genetic and RNAseq data from over 1,400 pediatric patients from AAML0531 and AAML1031, we reclassified ETS patients based on oncogenic transcriptional profiles as well as access to hematopoietic stem cell transplant (HSCT) ( Figure 1A). (19/60) patients presented with an enhanced MYC transcriptional signature (p-val < 0.00) independent of fusion partners [EP300::ETV6, ETV6::CCND3, ETV6::FAM133B, ETV6::FOXO1, ETV6::INO80D, ETV6::LMBR1, ETV6::MNX1, EWSR1::FEV, FLI1::IFIT2, FUS::ERG, FUS::FEV, FUS::FLI1]. Median event-free survival (EFS) was 293.5 days; median overall survival (OS) was 620.5 days. Notably, 100% (19/19) of patients with a MYC-driven signature relapsed; of the six patients who received HCST, five died within 3 years of diagnosis. Preliminary in vitro data in ETS cell lines with an enhanced MYC transcriptional signature (YNH-1, TSU-1621) suggests that the BET bromodomain inhibitor JQ1 may dampen MYC and induce anti-proliferative effects. (7/60) patients were defined by an EZH2-driven “immune-cold” signature characterized by global loss of immune receptors. Patients presented at diagnosis with significantly elevated EZH2 and low levels of MHC I and II receptors typically observed at relapse; additionally, there was significant downregulation in T cell and natural killer cell ligands and a 100% failure rate for HSCT. Median EFS was 255 days and median OS was 339 days. We have previously discussed the mechanism of leukemogenesis as well as proposed therapeutic interventions for this subset (Buteyn, ASH 2021). (34/60) patients did not possess either a MYC-driven or EZH2-driven signature. These “other” ETS were instead defined by whether or not the patient underwent HCST. (21/34) patients did not receive HCST and had median EFS and OS of 429 and 1194 days, respectively. The relapsed or refractory rate in this population was still 75%; (8/14) of R/R patients were deceased within three years. The remaining (13/60) ETS patients did receive HSCT in first remission. (11/13) are still alive and at a rate higher than the general pAML population post-HSCT (62.6%). Despite a survival rate at approximately 85%, ‘Other ETS +HSCT’ patients were all still categorized as ‘High Risk’ at the end of AAML1031. Overall, reclassification based on molecular drivers appears to not only be more accurate in predicting relapse and final outcome, but also in proposing novel agents for pAML patients who overwhelmingly do not respond to standard regimens. Reinvigoration of immune recognition by inhibition of EZH2 and/or inhibition of MYC-driven proliferation via BET inhibitors may prove an essential step in setting the stage for successful HSCT for a significant portion of pAML ETS patients.
8

Lawlor, E. R., J. A. Mathers, T. Bainbridge, D. E. Horsman, A. Kawai, J. H. Healey, A. G. Huvos, J. A. Bridge, M. Ladanyi, and P. H. Sorensen. "Peripheral primitive neuroectodermal tumors in adults: documentation by molecular analysis." Journal of Clinical Oncology 16, no. 3 (March 1998): 1150–57. http://dx.doi.org/10.1200/jco.1998.16.3.1150.

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PURPOSE The Ewing tumor (ET) family of peripheral primitive neuroectodermal tumors (pPNETs) are primitive small round-cell tumors (SRCTs) of the bone and soft tissue that occur predominantly in children and adolescents. However, pPNETs only rarely enter the differential diagnosis of bone and soft tissue SRCTs in adults. Recently, gene fusions between the EWS gene and different members of the ETS transcription factor family have been shown to occur in virtually all pPNETs and thus constitute a pathognomonic marker for this tumor subclass. The aim of the present study was to document EWS/ETS fusion gene expression in suspected pPNETs of adults as objective evidence for the existence of this tumor family in older patients. PATIENTS AND METHODS The three contributing molecular diagnostic laboratories retrospectively compiled a cohort of all SRCT cases in which EWS/ETS gene fusions had been shown by molecular analysis. This cohort was surveyed for cases that occurred in patients aged 40 years or older, which were then analyzed for their clinical and pathologic features. RESULTS Nine patients between 40 and 65 years of age were found to have tumors positive for EWS/ETS gene fusions. Standard histopathologic and clinical features of these cases, other than age, were similar to those of childhood pPNETs. Patients were initiated on appropriate therapy after molecular analysis confirmed the diagnosis of pPNET. CONCLUSION Identification of an EWS/ETS gene fusion is useful in providing objective evidence of the diagnosis of pPNET in patients over the age of 40 years. This diagnosis should be considered in adults who present with bone and soft tissue SRCTs and appropriate biopsy specimens should be collected for molecular analysis at the time of diagnosis.
9

Downing, Nicholas F., Kaitlyn M. Mills, and Peter C. Hollenhorst. "Abstract 3033: Oncogenic ETS transcription factors avoid repression by EZH2 and FOXO1 in prostate cancer and Ewing sarcoma." Cancer Research 84, no. 6_Supplement (March 22, 2024): 3033. http://dx.doi.org/10.1158/1538-7445.am2024-3033.

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Abstract ETS transcription factors play roles throughout development, aiding in hematopoiesis, blood vessel formation and cell fate. The ETS family is composed of 28 members, all of which share an ETS DNA-binding domain. Chromosomal rearrangements that lead to the overexpression of specific ETS promote oncogenic transformation and tumor development. More than half of prostate tumors are driven by aberrant expression of an ETS protein. Our lab has demonstrated that oncogenic ETS form essential interactions with a ubiquitous RNA-binding protein, EWS, to promote prostate tumorigenesis. A similar mechanism exists in Ewing sarcoma (ES). ES tumors are driven by the expression EWS/ETS fusion proteins. This project focuses on the similarities and differences between oncogenic ETS in prostate cancer and EWS/ETS fusions in Ewing sarcoma. We compared biological functions of the most common oncogenic ETS in prostate cancer, ERG, and the most common fusion in ES, EWS/FLI1. Both ERG and EWS/FLI1 promoted migration and clonogenic survival in normal prostate epithelial cell lines, RWPE1 and PNT2. These data suggest that the EWS-ERG complex and EWS/FLI1 fusion protein can function similarly in prostate cells. Knockdown of endogenous EWS/FLI1 in the ES cell line, A673, reduced anchorage-independent colony formation in soft agar. Rescue with exogenous EWS/FLI1 or EWS/ERG restored colony formation relative to control. Wildtype ERG was unable to rescue colony formation in A673. This suggests that ERG and EWS/FLI1 function differently in A673 cells. Pulldown assays from A673 lysates reveal that ERG interacts with EZH2 and FOXO1. Our lab has established that ERG acts as a transcriptional repressor through the formation of an ERG-EZH2-PRC2 complex. Others demonstrate that FOXO1 represses ERG activity by reducing its recruitment to the target sites. Both the N-terminal truncation of ERG and phosphorylation of ERG at S96 disrupted these interactions and rescued anchorage independent growth in A673 ES cells. These data suggest that EWS/ETS fusions avoid transcriptional repression in Ewing tumors due to loss of the N-terminus of the ETS protein. Citation Format: Nicholas F. Downing, Kaitlyn M. Mills, Peter C. Hollenhorst. Oncogenic ETS transcription factors avoid repression by EZH2 and FOXO1 in prostate cancer and Ewing sarcoma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 3033.
10

Clark, Jeremy P., and Colin S. Cooper. "ETS gene fusions in prostate cancer." Nature Reviews Urology 6, no. 8 (August 2009): 429–39. http://dx.doi.org/10.1038/nrurol.2009.127.

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Dissertations / Theses on the topic "Fusions ETS":

1

Carouge, Élisa. "Récepteur MET et fusions ETS : co-acteurs dans la progression du cancer de la prostate." Electronic Thesis or Diss., Université de Lille (2022-....), 2024. https://pepite-depot.univ-lille.fr/ToutIDP/EDBSL/2024/2024ULILS005.pdf.

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Le cancer de la prostate (CaP) a l'incidence la plus élevée parmi les cancers masculins dans les pays européens et américains. Dans les stades avancés de la maladie, le développement des métastases (osseuses dans 80% des cas) entraîne un taux de mortalité important. Le récepteur MET et les fusions de gènes ETS avec un promoteur hormono-dépendant sont des acteurs importants dans la progression du cancer de la prostate. Parmi les membres de la famille de facteurs de transcription ETS, ERG est retrouvé dans 60% des cas des fusions et ETV1 dans 10% des cas. MET est un récepteur à activité tyrosine kinase exprimé dans les stades avancés de la maladie, dans les tumeurs hormono-résistantes et les métastases osseuses. Les fusions ERG et ETV1 sont retrouvées tout au long de la maladie, allant des stades d'initiation jusqu'aux stades métastatiques. De façon intéressante, il existe de nombreux liens fonctionnels entre MET et ERG/ETV1 suggérant leur appartenance à la même voie de régulation. Le but de notre étude est de comprendre le rôle individuel du récepteur MET et des fusions ETS ainsi que leur collaboration dans la progression du CaP.Pour ce faire, nous avons mis en place des modèles cellulaires de CaP hormono-indépendants dans lesquels l'expression et l'activité du récepteur MET sont effectives et pour lesquels une surexpression de ERG ou ETV1 a été induite via une infection rétrovirale. Ces modèles ont été utilisés pour réaliser des tests phénotypiques de prolifération, migration ou encore invasion, une analyse transcriptomique comparative (RNAseq) et des tests in vivo chez des souris humanisées exprimant l'HGF humain.Les résultats que nous avons obtenus montrent que les facteurs de transcription ERG et ETV1 induisent des capacités migratoires et invasives plus importantes in vitro et que l'activation de la voie de signalisation du récepteur amplifie les effets. In vivo, ERG et ETV1 entraînent des volumes tumoraux plus importants après injection des cellules en sous-cutanée et l'application d'un traitement par un inhibiteur spécifique de MET réverse ces effets. Finalement, la réalisation d'une analyse transcriptomique, comparant les différents modèles, a permis d'identifier des gènes différentiellement exprimés selon la surexpression de ERG, de ETV1 et/ou de l'activation de la voie MET, gènes cibles signature pouvant potentiellement être impliqués dans la progression tumorale.Ainsi, les données obtenues montrent pour la première fois une collaboration entre le récepteur MET et les facteurs ERG/ETV1 pour induire des caractéristiques plus agressives dans des modèles de CaP. A terme, le projet vise à identifier des signatures moléculaires de cette coopération afin de mettre en lumière des outils de pronostic, diagnostic ou encore de thérapie ciblée
Prostate cancer (PCa) has the highest incidence of all male cancers in Europe and the USA. In the advanced stages of the disease, the development of metastases (bone metastases in 80% of cases) leads to a high mortality rate. MET receptor and ETS gene fusions with a hormone-dependent promoter are important actors in the progression of prostate cancer. Among the members of the ETS family of transcription factors, ERG is found in 60% of fusions and ETV1 in 10%. MET is a tyrosine kinase receptor expressed in the advanced stages of the disease, in hormone-resistant tumours and in bone metastases. ERG and ETV1 fusions are found throughout the disease, from initiation to metastatic stages. Interestingly, there are many functional links between MET and ERG/ETV1, suggesting that they belong to the same regulatory pathway. The aim of our study is to understand the individual roles of MET receptor and ETS fusions and their collaboration in PCa progression.To this end, we built hormone-independent CaP cellular models in which MET receptor expression and activity are effective and ERG or ETV1 overexpression has been induced via retroviral infection. These models were used to perform phenotypic tests of proliferation, migration and invasion, comparative transcriptomic analysis (RNAseq) and in vivo tests in humanised mice expressing human HGF. The results we obtained show that the transcription factors ERG and ETV1 induce greater migratory and invasive capacities in vitro and that activation of the receptor signalling pathway amplifies the effects. In vivo, ERG and ETV1 induce larger tumour volumes after subcutaneous injection of the cells, and treatment with a specific MET inhibitor reverses these effects. Finally, a transcriptomic analysis comparing the different models, permits to identify genes differentially expressed according to overexpression of ERG, ETV1 and/or activation of MET pathway, signature target genes potentially involved in tumour progression.The data obtained show, for the first time, a collaboration between MET receptor and ERG/ETV1 factors to induce more aggressive characteristics in PCa models. The project aims to identify the molecular signatures of this cooperation in order to highlight prognostic, diagnostic and targeted therapy tools
2

Hughes, Katelyn. "Gene fusions in cancer: Classification of fusion events and regulation patterns of fusion pathway neighbors." Digital WPI, 2016. https://digitalcommons.wpi.edu/etd-theses/764.

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Cancer is a leading cause of death worldwide, resulting in an estimated 1.6 million mortalities and 600,000 new cases in the US alone in 2015. Gene fusions, hybrid genes formed from two originally separated genes, are known drivers of cancer. However, gene fusions have also been found in healthy cells due to routine errors in replication. This project aims to understand the role of gene fusion in cancer. Specifically, we seek to achieve two goals. First, we would like to develop a computational method that predicts if a gene fusion event is associated with the cancer or healthy sample. Second, we would like to use this information to determine and characterize molecular mechanisms behind the gene fusion events. Recent studies have attempted to address these problems, but without explicit consideration of the fact that there are overlapping fusion events in both cancer and healthy cells. Here, we address this problem using FUsion Enriched Learning of CANcer Mutations (FUELCAN), a semi-supervised model, which classifies all overlapping fusion events as unlabeled to start. The model is trained using the known cancer and healthy samples and tested using the unlabeled dataset. Unlabeled data is classified as associated with healthy or cancer samples and the top 20 data points are put back into the training set. The process continues until all have been appropriately classified. Three datasets were analyzed from Acute Lymphoblastic Leukemia (ALL), breast cancer and colorectal cancer. We obtained similar results for both supervised and semi-supervised classification. To improve our model, we assessed the functional landscape of gene fusion events and observed that the pathway neighbors of both gene fusion partners are differentially expressed in each cancer dataset. The significant neighbors are also shown to have direct connections to cancer pathways and functions, indicating that these gene fusions are important for cancer development. Future directions include applying the acquired transcriptomic knowledge to our machine learning algorithm, counting transcription factors and kinases within the gene fusion events and their neighbors and assessing the differences between upstream and downstream effects within the pathway neighbors.
3

Zartova, Irina. "Mesonic fusion - pion and eta meson production in light ion nuclear fusion reactions." Doctoral thesis, Stockholms universitet, Fysikum, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-39875.

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The present thesis describes two experiments performed in the storage ring CELSIUS at The Svedberg Laboratory in Uppsala. In the first experiment the importance of three - nucleon clustering in the six - nucelon system was investigated. The total cross section for the production of the ground state and the 3.56 MeV second excited state of 6Li in the 3He(3He,6Li)π+ reaction has been measured at two beam energies, 261.1 and 262.5 MeV, corresponding to center - of - mass energies 1.2 and 1.9 MeV above the production threshold for the 3.56 MeV state. For the ground state the result was 347 ± 84 ± 42 and 92 ± 84 ± 11 nb respectively. The result for the 3.56 MeV state, 104 ± 23 ± 12 and 56 ± 35 ± 7 nb respectively, is compared to the result of a previous study where the 3.56 MeV state was populated in the d(4He,6Li)π0 reaction. In the second experiment a clean sample of 5×105 eta mesons was prepared by means of the d(p,3He)η reaction. Eta production was tagged by the precise determination of the kinetic energy of the associated 3He ions. In the subsequent decay of eta mesons, channels with lepton - anti - lepton pairs were studied in the WASA detector. In a separate study properties of the WASA deuterium pellet target were investigated and in particular the effects on the beam of the beam - target interactions. In both sets of experiments the fused nuclear system was detected by means of a zero - degree spectrometer with a semiconductor detector telescope. Choosing the detectors to match the rather different requirements, precise information regarding the identity and the momentum of the detected ions could be obtained in both cases.
4

Bisset, Louise Clair. "Fluorescence of a DNA-binding protein." Thesis, University of Newcastle Upon Tyne, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.320129.

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White, David Maurice. "Pedagogical Fusion." VCU Scholars Compass, 2007. http://scholarscompass.vcu.edu/etd/993.

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During the five semesters that I have been at VCU I have learned a great deal from the courses that I have been enrolled in but I have learned the most through my experiences as a Teaching Assistant. These experiences have been so valuable because of the wide range of subject areas in which I have been involved and the diverse instructors that I have assisted. Although I hesitate to use the word "problem" I feel that there is a tendency in teacher training for a student to latch onto one professor and model their teaching practices after that one mentor. While this is not always a bad thing I feel that it can lead some students down a dead-end path of self-exploration and individualization of their personal teaching style. I feel that I have been given a rare and invaluable opportunity in that I have been permitted to assist so many different teachers in such a wide array of subjects. In this thesis, I propose to examine the widely varied experiences that I have had here at VCU as a Teacher and Teaching Assistant. I will look at the teaching styles that I have witnessed, the methodologies and approaches of each course, and most importantly I will put forth my personal teaching philosophy that I have developed from my experiences here at VCU.
6

Leclercq, Guillaume. "L'imposition directe des fusions intracommunautaires dans lesquelles une société française à l'IS est impliquée." Poitiers, 2000. http://www.theses.fr/2000POIT3023.

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BOUREUX, ANTHONY. "Etude des proprietes oncogeniques des proteines de fusion resultant de translocations chromosomiques impliquant des membres de la famille ets." Paris 11, 1999. http://www.theses.fr/1999PA112063.

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Les membres de la famille ets sont des facteurs de transcription impliques dans differents processus oncogeniques chez l'homme. Le travail de cette these concerne l'etude des proprietes de deux types de proteines de fusion impliquant des membres de la famille ets. Le premier aspect de ce travail a consiste a etudier les proprietes transactivatrices et transformantes de la proteine ews-fli1 caracteristique des tumeurs d'ewing. L'etude du domaine ews de ews-fli1 permet de mettre en evidence plusieurs correlations entre ces deux proprietes. De plus, l'analyse de differents mutants de la region fli1 et ews-fli1 montre que l'association du domaine ets et du domaine carboxy-terminal de fli1 est requise pour les proprietes transformantes de ews-fli1. Ceci semble suggerer que la transformation cellulaire par ews-fli1 soit dependante de cooperations intra-moleculaires et inter-moleculaires avec d'autres facteurs de transcription. Le deuxieme aspect concerne l'etude des proprietes fonctionnelles des proteines de fusion, impliquees dans differentes leucemies et dans lesquelles tel est fusionnee au pdgfr ou a jak2. La proteine tel-jak2, recemment identifiee, presente les memes proprietes que la proteine tel-pdgfr. Elles forment, in vivo, des homo-oligomeres, qui permet l'activation constitutive de l'activite tyrosine kinase intrinseque de jak2 ou de pdgfr. De plus, ces proteines permettent la survie et la proliferation des cellules baf/3 de maniere independante de l'interleukine 3. L'analyse des voies de signalisation dans les cellules baf/3 exprimant les proteines de fusion tel-jak2 ou tel-pdgfr montre une activation constitutive de la proteine kinase jnk1. Cependant, cette activation semble requise seulement pour la proliferation des cellules baf/3 sous controle de la proteine tel-pdgfr. L'ensemble de ces resultats permet de comprendre et de mieux apprehender le mecanisme d'action des proteines de fusions impliquant des proteines ets.
8

Lowden, Mia Rochelle Ahmed Shawn. "Genesis of end-to-end chromosome fusions." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2008. http://dc.lib.unc.edu/u?/etd,2227.

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Thesis (Ph. D.)--University of North Carolina at Chapel Hill, 2008.
Title from electronic title page (viewed Jun. 26, 2009). "... in partial fulfillment of requirements for the degree of Doctor of Philosophy in the Department of Biology." Discipline: Biology; Department/School: Biology.
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Pradhan, Pushkar S. "Multiresolution based, multisensor, multispectral image fusion." Diss., Mississippi State : Mississippi State University, 2005. http://library.msstate.edu/etd/show.asp?etd=etd-07082005-140541.

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Xu, Jin. "Understanding the molecular determinants of prostate tumorigenesis: androgen receptor's requirement for histone deacetylases and the role of recurrent ETS fusion." Diss., Restricted to subscribing institutions, 2008. http://proquest.umi.com/pqdweb?did=1563274481&sid=5&Fmt=2&clientId=48051&RQT=309&VName=PQD.

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Books on the topic "Fusions ETS":

1

Quintin, Yves P. Les fusions-acquisitions aux USA. Bruxelles: Bruylant, 2005.

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Webster, Tim. NetObjects Fusion handbook. Indianapolis, Ind: Hayden Books, 1996.

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EPS Conference on Controlled Fusion and Plasma Physics (21st 1994 Montpellier, France). Invited and contributed papers presented at the 21st EPS Conference on Controlled Fusion and Plasma Physics: Montpellier, France, 27 June-1 July, 1994. [Lausanne]: CRPP, Ecole polytechnique fédérale de Lausanne, 1994.

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EPS Conference on Controlled Fusion and Plasma Physics (21st 1994 Montpellier, France). 21st EPS Conference on Controlled Fusion and Plasma Physics: Montpellier, 27 June-1 July 1994 : contributed papers. Edited by Joffrin E, Platz P, Stott P. E, and European Physical Society. [Geneva]: European Physical Society, 1994.

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Jarvis, Janie. Family fusion: Bonding, sharing, and learning in a hostile world. Roswell, Ga: Lorica Pub., 2003.

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Dietrich, Rometsch, and Wessels Wolfgang, eds. The European Union and member states: Towards institutional fusion? Manchester: Manchester University Press, 1996.

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Beuter, Bruno Hubertus. Ubi non est ordo, ibi est con fusio: Konflikte und Konfliktlösungen im Leben und im Werk des Nikolaus von Kues. Frankfurt am Main: Peter Lang, 2007.

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Malka, Richard. L'ordre de Cice ron: Mis en examen. Grenoble: Gle nat, 2006.

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Tanil, Gamze. Europeanization, integration and identity: A social constructivist fusion perspective on Norway. New York: Routledge, 2012.

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G, Carlos D. Mesa. Presidentes de Bolivia: Entre urnas y fusiles : el poder ejecutivo, los ministros de estado. 2nd ed. La Paz: Editorial Gisbert, 1990.

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Book chapters on the topic "Fusions ETS":

1

Dobi, Albert, Taduru Sreenath, and Shiv Srivastava. "Androgen-Dependent Oncogenic Activation of ETS Transcription Factors by Recurrent Gene Fusions in Prostate Cancer: Biological and Clinical Implications." In Androgen-Responsive Genes in Prostate Cancer, 307–28. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6182-1_19.

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de Alava, Enrique, and Santiago Ramón y Cajal. "EWS-FLI (ets) Fusion Transcripts." In Encyclopedia of Cancer, 1–5. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_2046-3.

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de Alava, Enrique, and Santiago Ramón y Cajal. "EWS-FLI (ets) Fusion Transcripts." In Encyclopedia of Cancer, 1659–62. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-46875-3_2046.

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de Alava, Enrique, and Santiago Ramon y. Cajal. "EWS-FLI (ets) Fusion Transcripts." In Encyclopedia of Cancer, 1352–55. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_2046.

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Brenner, J. Chad, Arul M. Chinnaiyan, and Scott A. Tomlins. "ETS Fusion Genes in Prostate Cancer." In Prostate Cancer, 139–83. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6828-8_5.

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Gasi, Delila, and Jan Trapman. "Androgen Regulation of ETS Gene Fusion Transcripts in Prostate Cancer." In Methods in Molecular Biology, 335–48. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-243-4_19.

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Demangeat, J.-L., and M. Steinbach. "Complémentarité entre la scintigraphie myocardique et le coroscanner (fusion)." In Imagerie en coupes du coeur et des vaisseaux, 201–4. Paris: Springer Paris, 2011. http://dx.doi.org/10.1007/978-2-8178-0154-4_18.

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Rodríguez Gutiérrez, Oliva. "Los aditus en los teatros romanos hispanos: entre valores estructurales y simbólicos." In Les théâtres antiques et leurs entrées, 159–87. Lyon: MOM Éditions, 2024. http://dx.doi.org/10.4000/11qrp.

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Las provincias hispanas cuentan con buen número de teatros conocidos, algunos de ellos objeto de nuevas investigaciones en los últimos años, que han permitido actualizar y renovar el panorama del conocimiento general sobre este tipo de espacios y su funcionamiento. En todos los casos, son edificios construidos en época imperial, lo que hace que respondan a un modelo arquitectónico ya bien definido, donde graderío y cuerpo escénico se fusionan y a la vez se articulan a través del aditus, que adopta complejas y creativas soluciones estructurales. Pero, a su vez, los teatros hispanos forman plenamente parte del paisaje urbano, debiendo reflexionar en su papel ideológico y religioso. En él, sin duda, los itinera se destacan como fundamentales pasillos ceremoniales, lectura esta que ayuda a comprender mejor muchas de las evidencias arqueológicas que han llegado hasta nosotros.
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Hazan, J., and M. Bamberger. "Corrosion and Protection (Conversion Coating and Plasma Electrolytic Oxidation) of Ti6Al4V Processed by Powder Bed Fusion—Additive Manufacturing. EIS Study." In TMS 2020 149th Annual Meeting & Exhibition Supplemental Proceedings, 1317–27. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-36296-6_122.

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Fliegauf, M., J. Burger, R. Claus, M. Stock, F. Otto, and M. Lübbert. "Inducible AML1/ET0 Expression in U-937 Myeloid Cells: a Model to Identify Genes Targeted by the Leukemia-Specific Fusion Protein." In Haematology and Blood Transfusion Hämatologie und Bluttransfusion, 28–33. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-59358-1_8.

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Conference papers on the topic "Fusions ETS":

1

Saulnier, Olivier, Katia Guerdi, Marie-Ming Aynaud, Alina Chakraborty, Josephine Pineau, Christina O. Grady, Martin Dutertre, Franck Dequiedt, and Olivier Delattre. "Abstract LB-323: A novel function of ETS transcription factors in alternative splicing is altered in oncogenic FET-ETS fusions." 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-lb-323.

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Han, Sumin, Chad Brenner, Aaron Sabolch, Kari Wilder-Romans, Karen Knudsen, Theodore Lawrence, Arul Chinnaiyan, and Felix Feng. "Abstract 1463: PARP inhibition reverses radiation resistance conferred by ETS fusions 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.am2012-1463.

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Mani, Ram S., Scott A. Tomlins, Chad J. Brenner, Lei Wang, Matthew Iyer, Jindan Yu, Qi Cao, et al. "Abstract 2155: The origins and functional consequences of ETS gene fusions in prostate cancer." 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.am2011-2155.

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Schwentner, Raphaela, Sven Bilke, Max Kauer, Gunhild Jug, Robert L. Walker, Paul S. Meltzer, and Heinrich Kovar. "Abstract 2198: A functional ETS/E2F module in cancers expressing ETS fusion genes." 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.am2012-2198.

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Sarbishei, O., A. Roshan Fekr, M. Janidarmian, B. Nahill, and K. Radecka. "A minimum MSE sensor fusion algorithm with tolerance to multiple faults." In 2013 18th IEEE European Test Symposium (ETS). IEEE, 2013. http://dx.doi.org/10.1109/ets.2013.6569380.

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Kareddula, Aparna, Whitney Petrosky, Irina Tereshchenko, Daniel Medina, Hana Aviv, Eric Singer, Robert S. DiPaola, and Kim M. Hirshfield. "Abstract 5883: CHD1 as regulator of cell adhesion in Ets fusion negative prostate cancer." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-5883.

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Morsalin, Sharif, Chunshu Yang, Jinbo Fang, Yasuo Fujimura, Shubhalaxmi Kayarthodi, Huali Xu, Ujwala Gunnal, et al. "Abstract B21: Functional Role of ETS/ETV1-Fusion Proteins in Prostate Cancer and Other Cancers." In Abstracts: Ninth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; September 25-28, 2016; Fort Lauderdale, FL. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7755.disp16-b21.

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Mracek, Stepan, Jan Vana, Martin Drahansky, Radim Dvorak, and Svetlana N. Yanushkevich. "Thermal Face Recognition: A Fusion Approach." In 2012 Third International Conference on Emerging Security Technologies (EST). IEEE, 2012. http://dx.doi.org/10.1109/est.2012.24.

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Khemmar, Redouane, Fabien Bonardi, Jean-Yves Ertaud, and Xavier Savatier. "Biometrie authentication platform-based multisensor fusion." In 2017 Seventh International Conference on Emerging Security Technologies (EST). IEEE, 2017. http://dx.doi.org/10.1109/est.2017.8090422.

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Zhao, Xiaofeng, Hua Jiang, and Liyan Jiao. "A Data Fusion Based Intrusion Detection Model." In 2009 First International Workshop on Education Technology and Computer Science. IEEE, 2009. http://dx.doi.org/10.1109/etcs.2009.232.

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Reports on the topic "Fusions ETS":

1

Pollack, Jonathan R. Achilles Heel of ETS Fusions. Fort Belvoir, VA: Defense Technical Information Center, July 2010. http://dx.doi.org/10.21236/ada540242.

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Li, Zhe, Douglas Linn, and Xin Zhang. Genomewide Search of Oncogenic Pathways Cooperating With ETS Fusions in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2014. http://dx.doi.org/10.21236/ada615422.

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Li, Zhe, Douglas Linn, and Xin Zhang. Genome-wide Search of Oncogenic Pathways Cooperating with ETS Fusions in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2013. http://dx.doi.org/10.21236/ada586039.

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Feng, Felix. ETS Gene Fusions as Predictive Biomarkers of Resistance to Radiation Therapy for Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2014. http://dx.doi.org/10.21236/ada614486.

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Feng, Felix. ETS Gene Fusions as Predictive Biomarkers of Resistance to Radiation Therapy for Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2012. http://dx.doi.org/10.21236/ada570983.

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Feng, Felix. ETS Gene Fusions as Predictive Biomarkers of Resistance to Radiation Therapy for Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2013. http://dx.doi.org/10.21236/ada592099.

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Boyer, Marcel. Commentaires sur la politique de la concurrence et les marchés du travail. CIRANO, February 2022. http://dx.doi.org/10.54932/jxfq4798.

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Traditionnellement, les préoccupations liées au travail ne constituent pas un enjeu majeur lors de l’examen de la politique de la concurrence, mais l’approche préconisée à l’égard des accords de fixation des salaires, de non-débauchage et de non-mobilité entre les entreprises est l’une des principales raisons qui expliquent l’attention portée récemment par le Parlement à la politique de la concurrence et aux marchés du travail. Les principaux intervenants des milieux universitaires et politiques ont demandé une mise en application plus rigoureuse en ce qui concerne le pouvoir des monopsones/oligopsones sur les marchés du travail, par exemple lors de l’évaluation des fusions et des acquisitions, ainsi qu’en ce qui concerne le pouvoir de marché associé à la représentation des travailleurs (syndicats) et à l’accréditation professionnelle à titre d’obstacles à l’entrée sur le marché du travail. L’objectif ici est de recenser les nombreux défis et pièges dans l’évaluation de l’intensité de la concurrence sur les marchés du travail, tant au niveau de l’offre que de la demande, de même que dans la recherche de recours, s’il y a lieu.
8

Delgado, Lucas Esteban, and Axel Rivas. Graduate XXI: Un mapa del futuro: Cincuenta innovaciones educativas en América Latina. Inter-American Development Bank, April 2016. http://dx.doi.org/10.18235/0006193.

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Este documento es una guía de las innovaciones educativas que están surgiendo en América Latina a partir del uso intensivo de nuevas tecnologías. Es un mapa que hace posible avistar el futuro, o al menos ciertas tendencias que comienzan a tomar forma. Muestra un continente en transformación lleno de movimientos, emprendimientos y fusiones. Invita a los nuevos educadores a sumarse a un tiempo de cambios. Es un documento de inspiraciones.
9

Bruce. L51642 Field Nondestructive Examination of ERW Pipe Seams. Chantilly, Virginia: Pipeline Research Council International, Inc. (PRCI), June 1991. http://dx.doi.org/10.55274/r0010587.

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Electric resistance welded (ERW) pipe has been used in the natural gas transmission industry for many years. The Department of Transportation (DOT) has recently expressed interest in the integrity of the weld seam in pipelines made from ERW pipe that was manufactured prior to 1970. Specifically, the DOT has requested that natural gas transmission and hazardous liquid pipeline operators determine whether or not their pipelines that meet this description require hydrostatic proof testing. The initial concern from the DOT was for seam weld selective corrosion, although reference has since been made to growth of manufacturing discontinuities in the ERW seam. Early ERW pipe was manufactured using either direct current or low-frequency alternating current, processes that were prone to producing incomplete fusion discontinuities. These discontinuities (also referred to as cold welds, penetrators, etc.), if present in a pipeline, can grow under normal service or under upset operating conditions resulting in leaks or ruptures. There exists a need for a method that a pipeline operator could use to demonstrate the integrity of pipelines that were made from this older ERW pipe other than hydrostatic testing, which is expensive and potentially harmful to pipeline integrity. The use of a nondestructive-examination (NDE) technique would enable an operator to sample the integrity of a suspect pipeline during other routine in-service maintenance operations without the need for hydrostatic testing. The detection of incomplete fusion discontinuities is difficult if not impossible with conventional NDE techniques. The intimate mechanical contact between compressed surfaces causes a small amount of reflection and a large amount of transmission of ultrasonic signals. Recently however, several ultrasonic techniques have been introduced to study these types of discontinuities in resistance spot welds and inertia friction welds. These new techniques are based on ultrasonic spectroscopy, that is, the frequency dependence of the various ultrasonic interfacial parameters. These parameters include reflection and transmission coefficients and the frequency dependence of ultrasonic volumetric parameters (e.g., velocity and attenuation).
10

Stubrin, Lilia, Anabel Marín, Enrique Carreras, Rocío Palacín, and Lucía Mauro. Caso de estudio Don Mario: una empresa Argentina que gana el mercado global de semilla de soja. Inter-American Development Bank, March 2023. http://dx.doi.org/10.18235/0004765.

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El grupo Don Mario (GDM) es una empresa que desarrolla semillas de Argentina que se ha convertido en un jugador importante en el mercado global proveyendo el 20% de las variedades de soja que se utilizan en el mundo. La empresa exporta actualmente a más de 11 países. El crecimiento e internacionalización del grupo Don Mario es un fenómeno de enorme interés ya que se produjo en un período en el que el mercado global de semillas se concentró masivamente en unas pocas empresas internacionales a través de un proceso de fusiones y adquisiciones sin precedentes, que involucró la desaparición de cientos de empresas semilleras independientes. En este reporte discutimos los principales cambios en la demanda mundial, tecnológicos, regulatorios y de estructura de mercado que han operado y operan como oportunidades y desafíos para la expansión de Don Mario; presentaremos una serie de indicadores que describen el contexto global y local en el cual opera la empresa Don Mario; analizamos en detalle el alcance y modelo de la inserción internacional de la empresa Don Mario; explicaremos los elementos claves que explican el éxito de la firma; el uso e impacto de las políticas públicas; y los desafíos pendientes que tiene la empresa para continuar su proceso de crecimiento internacional.

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