Relevant bibliographies by topics / Sarcoma Ewing

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Sarcoma Ewing'

Author: Grafiati
Published: 4 June 2021
Last updated: 4 February 2022

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Journal articles on the topic "Sarcoma Ewing"

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Ramaswamy, Anant, Bharat Rekhi, Sameer Bakhshi, Sachin Hingmire, and Manish Agarwal. "Indian data on bone and soft tissue sarcomas: A summary of published study results." South Asian Journal of Cancer 05, no. 03 (July 2016): 138–45. http://dx.doi.org/10.4103/2278-330x.187587.

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AbstractBone sarcomas are rare tumors, approximating 0.2% of all cancers, with osteosarcoma (OGS), chondrosarcoma, and Ewing sarcoma being the most common cancers in this subset. The formation of disease management groups/clinics focused on sarcomas has resulted in better understanding and management of these uncommon tumors. Multiple large-scale retrospective data from Tata Memorial Hospital (TMH) and All India Institute of Medical Sciences have reported outcomes comparable to Western data in the field of OGS and Ewing sarcoma, with interesting prognostic factors identified for further evaluation. Soft tissue sarcomas are a rare heterogeneous group of tumors, more than 50 different tumor entities. The common subtypes identified in India include Ewing sarcoma and synovial sarcoma. Valuable work regarding brachytherapy has been done by radiation oncologists from the TMH, especially in pediatric patients.
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Ulusan, S., Z. Koc, E. Tuba Canpolat, and T. Çolakoglu. "Radiological findings of primary retroperitoneal ewing sarcoma." Acta Radiologica 48, no. 7 (September 2007): 814–18. http://dx.doi.org/10.1080/02841850701408244.

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Ewing sarcomas are most commonly located in bone, while extraskeletal involvement of the retroperitoneum is extremely rare. We describe the radiologic and pathological findings in an adult patient with retroperitoneal extraskeletal Ewing sarcoma.
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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.
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Świtaj, Tomasz, and Paulina Jagodzińska-Mucha. "Ewing sarcoma." Oncology in Clinical Practice 14, no. 6 (March 15, 2019): 392–98. http://dx.doi.org/10.5603/ocp.2018.0052.

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Szabo, Brittany, and Justin Gambini. "Ewing Sarcoma." JBJS Journal of Orthopaedics for Physician Assistants 8, no. 2 (2020): e0004-e0004. http://dx.doi.org/10.2106/jbjs.jopa.20.00004.

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Mankin, Henry J. "Ewing sarcoma." Current Opinion in Orthopedics 11, no. 6 (December 2000): 479–85. http://dx.doi.org/10.1097/00001433-200012000-00010.

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Casado, M., E. Rollán, S. Guardado, N. Gascón, A. Mañas, M. Cabeza, and J. Pérez-Regadera. "Ewing sarcoma." Reports of Practical Oncology & Radiotherapy 18 (June 2013): S200. http://dx.doi.org/10.1016/j.rpor.2013.03.154.

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Ju, Hee Young. "Ewing Sarcoma." Clinical Pediatric Hematology-Oncology 26, no. 1 (April 30, 2019): 27–34. http://dx.doi.org/10.15264/cpho.2019.26.1.27.

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Choi, Eun-Young K., Jerad M. Gardner, David R. Lucas, Jonathan B. McHugh, and Rajiv M. Patel. "Ewing sarcoma." Seminars in Diagnostic Pathology 31, no. 1 (January 2014): 39–47. http://dx.doi.org/10.1053/j.semdp.2014.01.002.

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Ben-Ami, Tal, Elisha Waldman, Wygoda Marc, Michael Weintraub, Shoshana Revel-Vilk, and Iris Fried. "Ewing Sarcoma." Journal of Pediatric Hematology/Oncology 38, no. 1 (January 2016): 38–42. http://dx.doi.org/10.1097/mph.0000000000000456.

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Dissertations / Theses on the topic "Sarcoma Ewing"

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Branford, White Harriet A. "Heterogeneity in Ewing sarcoma." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:7af59b69-e68f-41af-b5f0-8a7d278f6fd7.

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Ewing sarcoma, an aggressive primary bone and soft tissue tumour is characterised by the expression of the chimeric transcription factor EWS-FLI1 in 90% of patients. This alters expression of many genes including activation of the Insulin Growth Factor (IGF) pathway via IGFBP3 supression. Phase I/II trials with an IGF-1 inhibitor have demonstrated tumour regression in a modest number of Ewing sarcoma patients. The aim of this thesis was to identify mechanisms contributing to the heterogeneity of resistance in Ewing sarcoma following inhibition with OSI-906, a dual kinase inhibitor of IGF-1 (IGF-1R) and Insulin (IR) receptors. The hypothesis was that mechanisms of resistance relate to heterogeneity of responses to signalling pathway activation and inhibition. Through selection, disruption of the pathway would identify subpopulations of cells both sensitive and resistant in their response allowing for interrogation of resistance mechanisms. A genome wide approach was taken to model the resistance profile of cell lines. Through developing a method of unbiased quantification, a panel of validated Ewing sarcoma cell lines (EuroBoNet) were imaged and segmented to assess the responses of biomarkers on signalling pathway activation. Heterogeneity was confirmed between cell lines. The application to diagnostic biopsies led to the identification of prognostic classifiers and cellular subpopulations with clinical prognostic significance. The distribution of Ki67 was found to be predictive of survival and cells with lower levels of CD99 in the cytoplasm were most discriminative. Parallel sequencing strategies (RNA-seq, whole exome sequencing, and aCGH/ SNP array) for genome-wide screening was carried out for point mutations, copy number changes and rearrangements. Systematic detection was used to characterise genomic rearrangements and functional validation performed. Resistant clones, formed via ENU mutagenesis of cell lines, were sequenced in order to demonstrate the resistance profile of OSI-906. In summary heterogeneity of Ewing sarcoma at the genomic and proteomic level can influence the signalling dependency of tumours and response to inhibitors. Genomic and proteomic profiling of tumour cells may be relevant to future developments of novel therapies.
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Vallurupalli, Mounica. "Identifying Targetable Liabilities in Ewing Sarcoma." Thesis, Harvard University, 2014. http://etds.lib.harvard.edu/hms/admin/view/62.

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Background: Despite multi-modality therapy, the majority of patients with metastatic or recurrent Ewing sarcoma (ES), the second most common pediatric bone malignancy, will die of their disease. ES tumors express aberrantly activated ETS transcription factors through translocations that fuse the EWS gene to ETS family genes FLI1 or ERG. The aberrant activation of ETS transcription factors promotes malignant transformation and proliferation. While, FLI1 or ERG cannot be readily targeted, there is an opportunity to deploy functional genomics screens, to develop novel therapeutic approaches by identifying targetable liabilities in EWS/FLI1 dependent tumors. Materials and Methods: We performed a near whole-genome pooled shRNA screen in a panel of five EWS/FLI1 dependent Ewing sarcoma cell lines and one EWS/ERG cell line to identify essential genes. Essential genes were defined as those genes whose loss resulted in reduced viability selectively in ES cells compared to non-Ewing cancer cell lines. Essential hits were subsequently validated with genomic knockdown and chemical inhibition in vitro, followed by validation of the on-target effect of chemical inhibition. Next, we determined the in vivo effects of small-molecule inhibition on survival and tumor growth in NOD scid gamma (NSG) mice with established subcutaneous ES xenografts. Results: Top hits in our screen that could be readily targeted by small-molecule inhibitors, and thus have potential for rapid clinical validation, were selected for further investigation. These hits included IKBKE, CCND1 and CDK4. IKBKΕ, a non-canonical IKK with an oncogenic role in breast cancer, was one of the top kinase hits in the screen. IKBKΕ shares significant homology to TBK1, another non-canonical IKK that is essential in k-RAS dependent lung cancer. We validated IKBKE through small-molecule inhibition of IKBKE/TBK1 and shRNA based knockdown. Ewing sarcoma cell lines are sensitive to low micromolar concentrations of two IKBKE/TBK1 inhibitors (CYT387 and MRT67307). Additionally, in a panel of ES cell lines, knockdown of IKBKE resulted in decreased growth and impaired colony formation. These observations, paired with impairment of NF-κB nuclear localization following CYT387 treatment suggests that non-canonical IKK mediated signaling may be essential in Ewing sarcoma. We further validated these results through inhibition of IKBKE/TBK1 in in vivo xenograft models treated with 100 mg/kg/day of CYT387. Treatment over the course of twenty-nine days resulted in a significant increase in survival (p-value = 0.0231) and a significant decrease (p-value = 0.036) in tumor size after fifteen days of treatment. CDK4 and CCND1 are highly expressed in Ewing sarcoma as compared to other tumor types. shRNA mediated knockdown of CDK4 and CCND1 resulted in impaired viability and anchorage independent growth. Furthermore, treatment of Ewing sarcoma cell lines with a highly selective CDK4/6 inhibitor, LEE011, resulted in decreased viability (IC50 range of 0.26-18.06 μM), potent G1 arrest in six of eight EWS/FLI1 containing Ewing sarcoma lines tested and apoptosis in a panel of four highly sensitive lines. Administration of 75 mg/kg/day and 250 mg/kg/day of LEE011 in NSG mice with Ewing xenografts resulted in significant impairment of tumor growth, (p-value <0.001 for both treatment arms), as compared to vehicle control. Conclusions: These studies suggest a role for the targeting of IKBKE and CDK 4/6 in Ewing sarcoma, findings with immediate clinical relevance for patients with this malignancy, because small-molecule inhibitors of these proteins have already entered clinical trial for other disease indications.
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Saulnier, Olivier. "Deciphering the splicing landscape of Ewing sarcoma." Thesis, Sorbonne Paris Cité, 2018. http://www.theses.fr/2018USPCC268.

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Certains cancers peuvent être caractérisés par un facteur de transcription aberrant. C’est le cas du sarcome d’Ewing qui est caractérisé par une translocation chromosomique générant une protéine de fusion appelée EWSR1-ETS. Ces protéines de fusion ont principalement été étudiées en tant que facteur de transcription car elles ont la capacité de se fixer sur des séquences de type répétition de GGAA dans le génome et d’activer la transcription de nombreux gènes. Les fusions EWSR1-ETS ont aussi la capacité de recruter les protéines du complexe du remodelage de la chromatine afin d’augmenter l’accessibilité aux régions riches en répétition de GGAA et donc promouvoir un programme transcriptionnel aberrant. Cette propriété dépend majoritairement de la partie EWSR1 et de son domaine de faible complexité qui lui permet, notamment, d’interagir avec de nombreuses protéines. Les fusions EWSR1-ETS ont aussi été impliquées dans la régulation de l’épissage alternatif ; mais à ce jour cette fonction reste peu décrite et est principalement attribuée à la partie EWSR1. Cependant, il a récemment été montré que la protéine ERG (qui est très homologue à FLI1) contrôle la stabilité des ARN messagers. Ces observations nous ont mené à tester le rôle potentiel de ERG (et par conséquent de FLI1) dans l’épissage alternatif afin de mieux décrire les mécanismes impliqués dans la régulation de l’épissage alternatif induite par les protéines de fusion EWSR1-ETS dans le sarcome d’Ewing. Ce travail a permis d’identifier une nouvelle fonction des protéines de la sous-famille ERG (ERG, FLI1 et FEV) dans la régulation de l’épissage alternatif. Nous avons montré que les protéines ERG interagissent avec RBFOX2, un régulateur de l’épissage et que ERG et RBFOX2 induisent une régulation de l’épissage similaire suggérant, ainsi, un mécanisme de collaboration. Nos résultats démontrent que ERG interagit avec RBFOX2 par son extrémité C-terminale. De manière intéressante, ce domaine est retenu dans les fusions EWSR1-ETS. Nous avons donc confirmé que les fusions EWSR1-ETS étaient aussi capable d’interagir avec RBFOX2 et d’induire un programme d’épissage alternatif commun. Cependant, au contraire de la collaboration observée pour ERG et RBFOX2, nous avons montré que les fusions EWSR1-FLI1 ont un rôle opposé sur le programme d’épissage de RBFOX2. Nous avons également montré que EWS-FLI1 induisait l’épissage alternative du gène ADD3 ce qui a pour conséquence la répression du phénotype mésenchymateux des cellules du sarcome d’Ewing. Notre travail a permis d’identifier de nouveaux mécanismes afin de mieux comprendre comment la dérégulation de l’épissage alternatif par des facteurs de transcriptions oncogéniques influent sur la biologie du sarcome d’Ewing
Cancer can be characterized by abnormal fusion transcription factors. These transcription factors may have gain of function, neomorphic DNA binding properties or aberrant transcriptional activity. This is the case for Ewing sarcoma, which is characterized by a chromosomal translocation EWSR1-ETS. Ewing sarcoma fusion oncoproteins have been mostly studied as aberrant transcription factors due to their ability to specifically bind GGAA repeat sequences and to activate de novo enhancers. In addition, its ability to recruit chromatin-remodeling proteins, to induce chromatin opening and to drive an aberrant transcriptional program is a neomorphic property of the EWSR1 moiety that depends on its low complexity domain. EWSR1-ETS fusions have recently been implicated in alternative splicing regulation but to date this function is mainly attributed to the EWSR1 part. However, ERG protein, a member of the ETS transcription factor family, has been lately shown to control post-transcriptional processes such as mRNA stability. Considering these observations, we decided to challenge this view by studying ERG as a bona fide splicing regulator. This work highlights a new function of ERG subfamily proteins (ERG, FLI1 and FEV) in alternative splicing regulation. We have shown that ERG proteins interact with the master splicing regulator RBFOX2 to similarly regulate a common splicing program. We demonstrated that this new function is mediated via protein-protein interaction through the C-terminal domain of ERG. Because this domain remains in EWSR1-ETS fusions, we demonstrated that EWSR1-FLI1 protein is still able to bind RBFOX2 as expected. In addition, EWSR1-FLI1 induces massive changes of the splicing landscape of Ewing sarcoma and regulates an RBFOX2-dependent splicing program. However, in contrast to the collaborative effect observed for ERG, we found that EWSR1-FLI1 antagonizes RBFOX2-splicing function by repressing RBFOX2 binding to its pre-mRNAs targets. Importantly, we have found that mis-splicing of ADD3 by EWS-FLI1 leads to the repression of the mesenchymal phenotype of Ewing sarcoma cells. Our study provides direct evidence to understand how splicing dysregulation by an oncogenic transcription factor impacts on Ewing sarcoma biology
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Donahue, Andrew, and Abigail Cruz. "Ewing-like Sarcoma – Hiding in PA view." Digital Commons @ East Tennessee State University, 2019. https://dc.etsu.edu/asrf/2019/schedule/102.

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Ewing-like sarcomas (ELS) are a heterogenous group of neoplasms that typically occur in the bone and soft tissue of pediatric and young adult patients. ELS share various degrees of morphological, immunohistochemical, molecular, and clinical similarity with Ewing sarcomas. However, these tumors lack the pathognomonic molecular hallmark of Ewing sarcoma, which is defined as translocation between a gene of the RNA-binding TET family (EWSR1 or FUS) with a gene of the ETS-transcription family (FLI1, ERG, ETV1, ETV4, or FEV). Accurate classification and distinction from classical Ewing sarcomas is important for patient management. A subset of ELS harboring the BCOR-CCNB3 fusion has been described recently – the majority of which that have been reported to date are bone-based tumors, though there have been cases of discrete soft tissue-based tumors. We herein present a case of ELS harboring the BCOR-CCNB3 translocation occurring in a pediatric patient presenting with a large abdominal mass discovered on chest CT after failed outpatient treatment for pneumonia with effusion. This patient was a 14-year-old Caucasian boy with a past medical history significant for obesity and three episodes of pneumonia since 6-years-old. Imaging showed a large heterogeneous mass at the posterior left upper quadrant of the abdomen protruding through the posterior aspect of the left hemidiaphragm causing atelectasis. The mass abuts the inferior leftward aspect of the descending thoracic aorta and also protrudes between the 11th and 12th posterior lateral left rib. Pathology revealed this mass to be an Ewing-like sarcoma with a BCOR-CCNB3 fusion. Patient was treated with chemotherapy and radiation. This case demonstrates the importance of determining an accurate diagnosis to provide specific management.
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Becker, Ricardo Gehrke. "Controle local nos tumores da família Ewing: resultados do primeiro estudo do grupo colaborativo brasileiro (EWING I)." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2016. http://hdl.handle.net/10183/164733.

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O sarcoma de Ewing é uma neoplasia maligna agressiva que acomete ossos e tecidos moles com maior frequência em crianças e adolescentes. O tratamento consta de quimioterapia de indução, seguida pelo controle local da doença (cirurgia, cirurgia associada à radioterapia, ou apenas radioterapia), e quimioterapia de consolidação. A introdução da quimioterapia possibilitou aumento significativo na sobrevida dos pacientes nas últimas décadas. Por outro lado, o impacto da modalidade de controle local ainda não está bem estabelecido. Estudos observacionais têm demonstrado superioridade do tratamento cirúrgico em relação à radioterapia isolada, no entanto, são limitados os estudos prospectivos que confirmam esta diferença. O objetivo deste estudo é avaliar o impacto da modalidade de tratamento local nos desfechos oncológicos, bem como descrever o perfil clínico-epidemiológico de portadores de sarcoma de Ewing ósseo não-metastático. Os dados foram coletados em 15 instituições no período entre 2003 e 2010 e fazem parte do primeiro estudo do Grupo Colaborativo Brasileiro para Tratamento dos Tumores da Família Ewing (EWING I). Dos 73 pacientes incluídos, 47 foram tratados com cirurgia isolada, 13 receberam cirurgia associada à radioterapia, e 13 apenas radioterapia. O seguimento médio foi de 4,5 anos (2,3 até 6,7 anos) e a sobrevida geral e livre de eventos foi de 63,3 e 62,1 por cento em 5 anos, respectivamente. A falha do tratamento local foi de 0 (zero) por cento para a modalidade de cirurgia associada à radioterapia, 6,5 por cento para cirurgia isolada, e 10 por cento para radioterapia (p=0,5). A sobrevida dos pacientes submetidos à radioterapia isolada foi significativamente inferior à sobrevida dos tratados com cirurgia e com cirurgia associada a radioterapia (30,8 versus 71,7 versus 64,1 por cento, respectivamente). Concluiu-se que não houve diferença em termos de falha local de acordo com a modalidade de tratamento empregada, no entanto houve diferença significativa em termos de sobrevida. Apesar dos resultados cirúrgicos superiores, a radioterapia isolada ainda apresenta papel fundamental no tratamento de casos selecionados.
Ewing sarcoma is a small round cell malignancy of bone and soft tissue that usually occurs in children and adolescents. Current treatment includes induction chemotherapy, local control of the primary tumor (surgery, surgery plus radiotherapy, or radiotherapy) and consolidation chemotherapy. The introduction of chemotherapy has improved significantly the oncologic outcomes in Ewing sarcoma. On the other hand, the impact of the local control modality has not been established. Surgery alone or in combination with radiation has traditionally been considered a good choice for resectable ES, while unresectable tumors have been treated with definitive radiotherapy. Despite the results from a few trials and observational studies, there is no consistent knowledge about the local control modality in ES outcomes. The present study aims to evaluate the impact of the local control modality in the oncologic outcomes, as well as to describe the clinical features of the patients with localized Ewing sarcoma of the bone. The data were collected between 2003 and 2010 in 15 hospitals and were part of the first Brazilian Collaborative Group for the Treatment of the Ewing Sarcoma Family Tumors (EWING 1). From 73 patients (median age 12.8 years old), 47 were treated with surgery, 13 with surgery plus radiotherapy, and 13 with definitive radiotherapy. Median follow up was 4.5 years (2.3 to 6.7 years) and the overall and event-free survival 63.3 and 62.1 percent in 5 years, respectively. The local control failure was 0 percent for surgery plus radiotherapy, 6.5 percent for surgery, and 10 percent for radiotherapy (p=.5). The survival of the patients treated with radiotherapy was significantly worse than those treated with surgery and surgery plus radiotherapy (30.8 versus 71.7 versus 64.1 percent, respectively). In conclusion, there was no significant difference in local failure according to the modality of treatment, but there was significant difference in survival rates. Despite the better outcomes in individuals treated with surgery, the radiotherapy modality has still an important role in selected patients.
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Lagares, Tena Laura María. "Caveolina-1 en la progresión metastásica del Sarcoma de Ewing." Doctoral thesis, Universitat de Barcelona, 2013. http://hdl.handle.net/10803/145475.

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El sarcoma de Ewing (SE) es el segundo tumor óseo maligno infantil más frecuente y presenta una alta incidencia de enfermedad metastásica. Este tipo de tumores presentan una translocación génica característica que da origen a una proteína de fusión, normalmente EWS/FLI1. Esta proteína de fusión actúa como factor de transcripción aberrante, regulando la expresión de diferentes genes implicados en la iniciación, mantenimiento y progresión del tumor. Nuestro grupo describió como uno de estos genes diana a caveolina 1 (CAV1), describiendo además su papel determinante en el fenotipo maligno del SE, en la tumorigénesis, en la angiogénesis y en la resistencia a apoptosis inducida por quimioterapia. Para investigar el papel concreto de CAV1 en el proceso metastásico de este sarcoma, se creó un modelo de baja expresión de CAV1 en líneas celulares de SE y se determinaron cambios en su capacidad migratoria, invasiva y metastásica. En los ensayos in vitro se halló una menor capacidad migratoria de las células con silenciamiento de CAV1 y una reducción en la expresión de metaloproteinasa 9 (MMP-9) y en la actividad de MMP-2, ambas MMPs implicadas en el proceso de invasión. La regulación de la actividad de MMP-2 parece estar relacionada con la posible regulación que ejerce CAV1 en la función de la MMP de membrana tipo 1 (MT1-MMP), proteína fundamental para la activación de MMP-2. Por otro lado, en este estudio se propone que CAV1 promueve la expresión de MMP-9 transcripcionalmente a través de la regulación de la activación de la vía de señalización de ERK1/2 (Extracellular signal-regulated kinase 1/2). En nuestro modelo, ERK1/2 activo translocaría al núcleo donde activaría los factores de transcripción responsables de la activación del promotor de MMP-9. Por otro lado, la fosforilación de RSK2 (Ribosomal S6 kinase 2) por parte de ERK1/2 en el citoplasma, produciría la activación de RSK2 que a su vez activaría la proteína ribosomal rpS6, uno de los responsables de la iniciación de la traducción, por lo que también podría estar influyendo a la producción de MMP-9 a este nivel. Según nuestros resultados, CAV1 estaría influyendo en la capacidad migratoria de las células de SE mediante dos mecanismos: 1) a través de la activación de la vía de ERK1/2 y 2) mediante la unión a diferentes proteínas con dominio SH2 a través de la fosforilación de CAV1 en la tirosina 14. ERK1/2 influye en la regulación de la capacidad migratoria de una forma de pendiente o independiente de RSK1. Además, en los ensayos de metástasis experimental in vivo las células con inhibición de CAV1 presentaron una menor incidencia de metástasis pulmonar, hecho que correlacionó con una disminución en la expresión de SPARC (Secreted protein acidic and rich in cysteine), una proteína de adhesión importante en procesos metastásicos. En resumen, nuestros resultados evidencian la importancia de CAV1 en el proceso metastásico del SE.
Ewing’s sarcoma (ES) is the second most common bone tumor in childhood and occurs with a high incidence of metastatic disease. Such tumors have a characteristic gene translocation that gives rise to a fusion protein, most commonly EWS/FLI1. This fusion protein acts as an aberrant transcription factor regulating the expression of different target genes involved in the initiation, maintenance and progression of the tumor. Our group described caveolin 1 (CAV1) as one of these target genes, describing its role in the malignant phenotype, tumorigenicity and resistance to chemotherapy-induced apoptosis of ES cell lines. To investigate the specific role of CAV1 in the metastatic process of this sarcoma, we established a model of low expression of CAV1 in cell lines of ES. Then, we measured changes in their migratory capacity, invasiveness and metastatic potential. In vitro, we found a lower migratory capability of CAV1 knockdown cells and a reduction in MMP-9 expression and MMP-2 activity. The regulation of MMP-2 activity seems to be related to the possible regulation that CAV1 exerts on the function of MT1- MMP, an essential protein for the activation of MMP-2. On the other hand, we suggest that CAV1 promotes the expression of MMP-9, both transcriptionaly and post-transcriptionaly, through regulating ERK1/2 signaling pathway. In our model, activated ERK1/2 would translocate to the nucleus where it would activate the transcription factors responsible for MMP-9 promoter activation. At the cytoplasm, activated ERK1/2 would phosphorylate and activate RSK2, which, in turn, would promote rpS6 activation, leading to protein translation initiation. Our results indicate that CAV1 is regulating migratory capability of ES cells by two different mechanisms; 1) through ERK1/2 pathway activation, 2) by linking several proteins bearing SH2 domains trough phosphorylated Tyr14 of CAV1. ERK1/2 seems to regulate cell migration in both RSK1-dependent and independent manner. In addition, experimental metastasis assays in vivo showed that, CAV1 knockdown cells had a lower incidence of pulmonary metastasis, a fact that correlated with a decrease in the expression of SPARC, a major adhesion protein in metastatic processes. In summary, our results demonstrate the importance of CAV1 in the metastatic process on ES tumors.
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Jonker, Anneliene. "Synthetic Lethality and Metabolism in Ewing Sarcoma : Knowledge Through Silence." Thesis, Paris 11, 2014. http://www.theses.fr/2014PA11T039/document.

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Le sarcome de Ewing est la seconde tumeur pédiatrique de l’os la plus fréquente. Elle est caractérisée par une translocation chromosomique résultant à la fusion de EWSR1 avec un membre de la famille ETS. Chez 85% des patients, cette fusion conduit à l’expression de la protéine chimérique EWS-FLI1 qui est l’oncogène majeur de ce sarcome. Ce dernier agit principalement par son action transcriptionelle sur des cibles qui lui sont propres. Au niveau thérapeutique, le sarcome d’Ewing est traité par chimiothérapie, chirurgie locale et par radiothérapie. La survie à long terme des patients est de l’ordre de 70%, mais beaucoup plus basse pour les patients métastatiques et quasi nulle lors d’une récidive. Parmi maintes caractéristiques, certains cancers présentent une dérégulation énergétique. L’influence d’EWS-FLI1 sur cet aspect n’a fait l’objet d’aucune étude dans le contexte du sarcome d’Ewing. Nous avons donc étudié par profilage métabolomique des cellules de sarcome d’Ewing en présence ou en absence d’EWS-FLI1. En comparant ces deux conditions, des modulations du profil énergétique relatif au cycle de Krebs, des précurseurs de le glycosylation ainsi que des métabolites de la voie de la méthionine et du tryptophane ont été observés. En parallèle, grâce à un crible de banque de shRNAs réalisé dans des conditions expérimentales similaires à l’étude métabolomique (lignée d’Ewing avec ou sans EWS-FLI1), nous avons pu identifier des gènes présentant des caractéristiques « synthétique létales », c'est-à-dire tuant uniquement les cellules du sarcome d’Ewing en présence de son oncogène
Ewing sarcoma, the second most commonly occurring pediatric bone tumor, is most often characterized by a chromosomal translocation between EWSR1 and FLI1. The gene fusion EWS-FLI1 accounts for 85% of all Ewing sarcoma and is considered the major oncogene and master regulator of Ewing sarcoma. EWS-FLI1 is a transcriptional modulator of targets, both directly and indirectly. Ewing sarcoma is aggressively treated with chemotherapy, localized surgery and radiation and has an overall survival of about 70%, however, survival for metastasis or relapsed cases remains low. One of the cancer hallmarks, metabolic deregulation, is most likely partly dependent on EWS-FLI1 in Ewing sarcoma cells. In order to get a better understanding of Ewing sarcoma biology and oncogenesis, it might be of high interest to investigate the influence of EWS-FLI1 in Ewing sarcoma cells. We therefore performed a global metabolic profiling of Ewing sarcoma cells with or without inhibition of EWS-FLI1. Several changes in the energy metabolism were observed throughout this study; the observed changes were consistent with an energy profile that moved from a cancer cell energy metabolism towards the energy metabolism of a more normal cell upon EWS-FLI1 inhibition, primarily based on the TCA cycle. Levels of TCA intermediates, glycosylation precursors, methionine pathway metabolites and amino acids, especially changes in the tryptophan metabolic pathway, were altered upon EWS-FLI1 inhibition. Parallel to this study, we performed a high-throughput synthetic lethality screen, in order to not only identify essential genes for cell survival and proliferation, but also to identify new synthetic lethal targets that could specifically target Ewing sarcoma cells carrying the EWS-FLI1 fusion gene
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Dionísio, Fernando Carrasco Ferreira. "Avaliação da reprodutibilidade intra e interobservador da segmentação manual de sarcomas ósseos em imagens de ressonância magnética." Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/17/17158/tde-10042018-165710/.

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Os sarcomas ósseos representam uma proporção significativa de tumores na faixa etária pediátrica, ainda apresentando um quadro desafiador devido a sua significativa taxa de morbimortalidade. Pesquisas para o desenvolvimento de novas modalidades terapêuticas e para o desenvolvimento de métodos que identifiquem características da doença que possam permitir melhor estratificação dos pacientes através de dados clinicamente relevantes para individualizar as condutas clínicas são necessárias. Dentro deste contexto surge o conceito de radiômica, que visa extrair dados clinicamente relevantes a partir de imagens médicas. Entretanto, para colocar a radiômica em prática, é necessário selecionar, nas imagens médicas, as áreas de interesse referentes às patologias estudadas, e este processo se denomina segmentação. O objetivo primário deste estudo foi avaliar a reprodutibilidade intra e inter-observador da segmentação manual de sarcomas ósseos em imagens de ressonância magnética (RM). Como objetivo secundário, foi avaliada a capacidade da segmentação semiautomática em reduzir o tempo necessário para segmentação, mantendo similaridade com a segmentação manual. O estudo foi realizado de forma retrospectiva com inclusão de pacientes com diagnóstico de osteossarcoma ou sarcoma de Ewing confirmado por estudo histopatológico e que tivessem imagens de RM realizadas no Hospital Universitário de nossa Instituição realizadas previamente a qualquer intervenção terapêutica. Três médicos radiologistas, de forma independente e às cegas em relação as demais segmentações e em relação ao resultado histopatológico, realizaram a segmentação manual dos contornos destes tumores utilizando o software 3DSlicer, permitindo que fosse realizada avaliação da reprodutibilidade interobservador. Um dos radiologistas realizou uma segunda segmentação manual dos mesmos casos, possibilitando a avaliação da reprodutibilidade intraobservador, e, ainda, uma terceira segmentação foi realizada, utilizando metodologia semiautomática, disponível no software mencionado. Para a análise estatística, foi utilizado o coeficiente de similaridade de Dice (DICE), a distância Hausdorff (DH), comparações de volumes e análises dos intervalos de tempo necessários para realização das segmentações. Os parâmetros avaliados demonstraram haver boa reprodutibilidade intraobservador, com DICE variando entre 0,83 a 0,97; e distância Hausdorff variando entre 3,37 a 28,73 mm. Também foi demonstrada boa reprodutibilidade interobservador com DICE variando entre 0,73 a 0,97; e distância Hausdorff variando entre 3,93 a 33,40 mm. A segmentação semiautomática demonstrou boa similaridade em relação à segmentação manual (DICE variando entre 0,71 a 0,96 e DH variando entre 5,38 a 31,54 mm), havendo redução significativa do tempo necessário para segmentação. Entre todas as situações comparadas, os volumes não apresentaram diferenças estatisticamente significativas (p-valor>0,05).
Bone sarcomas represent a significant proportion of tumors in the pediatric age group and they still are a challenge due to their significant morbidity and mortality rates. Reseaches are important for the development of new therapeutic modalities and for the development of methods that identify features that allow better stratification of the patients with theses diseases for individualization of their treatments. In this context emerges the concept of radiomics, which is the process of extraction of clinically relevant data from medical images. It is important to segment the areas of interest im medical images for the pratice of this process. The primary objective of this study was to evaluate the intra- and interobserver reproducibility of manual segmentation of bone sarcomas on magnetic resonance imaging (MRI). As a secondary objective, it was evaluated if the semiautomatic segmentation could be similar to manual segmentation and if the semiautomatic method could reduce the time required for segmentation. The study was performed retrospectively with the inclusion of patients with osteosarcoma or Ewing sarcoma confirmed by histopathological study and who had MRI performed at the University Hospital of our Institution prior to any therapeutic intervention. Three radiologists, independently and blindly in relation to the other segmentations and in relation to the histopathological results, performed the manual segmentation of the contours of these tumors using 3DSlicer software, allowing an interobserver reproducibility evaluation. One of the radiologists performed a second manual segmentation of the same cases, allowing the evaluation of intraobserver reproducibility. A third segmentation was performed, using semi-automatic methodology, available in the mentioned software. For the statistical analysis, Dice similarity coefficient (DICE), Hausdorff distance (DH), comparisons between volumes and time intervals for segmentations were used. The parameters evaluated demonstrated a good intraobserver reproducibility, with DICE ranging from 0.83 to 0.97 and Hausdorff distance ranging from 3.37 to 28.73 mm. Good interobserver reproducibility was also demonstrated with DICE ranging from 0.73 to 0.97 and Hausdorff distance ranging from 3.93 to 33.40 mm. Semiautomatic segmentation demonstrated good similarity to manual segmentation (DICE ranging from 0.71 to 0.96 and HD ranging from 5.38 to 31.54mm), and there was significant reduction in the time required for segmentation. Among all the situations compared, the volumes did not present significant statistical differences (p-value> 0.05).
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Figuerola, Bou Elisabet. "Polycomb and KDM6A Roles in the Epigenetic Dynamics of Ewing Sarcoma Tumorigenesis." Doctoral thesis, Universitat de Barcelona, 2019. http://hdl.handle.net/10803/668710.

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Ewing sarcoma (ES) is a highly aggressive tumour of the bone and soft tissue that typically affects children, adolescents, and young adults. The fusion protein EWSR1‐FLI1 is the main genetic alteration found that acts as a pioneer factor during early ES tumorigenesis. EWSR1– FLI1 binds GGAA microsatellites causing remodelling of enhancers and genome reprogramming. Among the proteins cooperating with EWSR1‐FLI1 at enhancers, our group has described that the Polycomb subunit RING1B co‐localizes genome‐wide and promotes oncogene recruitment and transcriptional activation of key enhancer genes. In this thesis, we show that RING1B is a critical factor for ES tumour growth and, together with other E3 ubiquitin ligases, is deregulated by the neddylation pathway inhibitor MLN4924 (pevonedistat). Treatment of ES cell lines with the inhibitor promotes RING1B loss from EWSR1‐FLI1–activated targets as well as eviction of EWSR1‐FLI1, thereby deregulating gene expression. Lack of neddylation caused by the drug appears to be the mechanism behind the in vitro and in vivo degradation of RING1B. We also study how introduction of EWSR1‐FLI1 to a putative cell‐of‐origin deregulates distribution of the histone repressive mark H3K27me3. Although the global levels of this histone modification are maintained, we observe a perturbed distribution. Specifically, gain or loss of H3K27me3 occurs in some EWSR1‐FLI1–repressed or –activated regions, respectively, which coincide with enrichment of its writer, EZH2, and its eraser, KDM6A, in a transformed ES cell line. Finally, we demonstrate that targeting the tumorigenic distribution of H3K27me3 by combined inhibition of EZH2 (with GSK126) and KDM6A (with GSKJ4) causes a synergic cytotoxic response in ES cell lines. Altogether, our data provide further insight into the epigenetic mechanisms underlying EWSR1‐FLI1–mediated transformation and reveal new targets for future clinical trials.
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Horbach, Leonardo. "Avaliação de alvos moleculares envolvidos na resistência tumoral de sarcoma de Ewing." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2017. http://hdl.handle.net/10183/171020.

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O Sarcoma de Ewing (ES) é um raro tumor de ossos e tecidos moles com uma característica translocação cromossomal, a fusão EWS/FLI-1, que atua sobre diversos processos oncogênicos. O desenvolvimento da resistência à quimioterapia é comum no tumor e continua como uma das principais causas na falha do tratamento. O objetivo desse estudo foi avaliar a expressão de genes após a indução de resistência em linhagens celulares de ES. Foi selecionado um conjunto de genes (CCAR1, TUBA1A, POLDIP2, SMARCA4 e SMARCB1) a partir da mineração da literatura em resistência tumoral para duas drogas utilizadas na terapia de ES, doxorrubicina e vincristina. Descrevemos a expressão de cada gene selecionado antes e após as linhagens SK-ES-1 serem submetidas a um protocolo de indução de resistência para ambos os fármacos, que obteve êxito ao induzir as células à resistência. A expressão relativa dos níveis de mRNA foi avaliada e foi encontrada em maior expressão para os genes SMARCA4, SMARCB1 e POLDIP2, e em menor expressão para os genes TUBA1A e CCAR1, quando comparadas às linhagens de controle não-resistentes de cada quimioterápico. Os resultados sugerem o envolvimento de mecanismos de reparo de dano ao DNA, remodelamento de cromatina via SWI/SNF, atividade de microtúbulos e atividade spliceossomal nos processos de resistência quimioterápica em ES.
Ewing Sarcoma (ES) is a rare bone and soft tissue tumor with a characteristic chromosomal translocation, the fusion protein EWS/FLI-1, that drives several oncogenic processes. The development of resistance to chemotherapy is common and remains as the main cause of treatment failure. The goal of this study was to evaluate the expression of selected genes in ES cell lines after induction of resistance. A set of genes (CCAR1, TUBA1A, POLDIP2, SMARCA4 and SMARCB1) was data mined from tumoral resistance literature for two drugs used in ES therapy, doxorubicin and vincristine. We describe the expression of each selected gene before and after SK-ES-1 cell lines were exposed to a drug resistance inducing protocol for doxorubicin and vincristine. Cell lines were successfully induced to be resistant to doxorubicin and vincristine. The relative mRNA expression levels were upregulated for genes SMARCA4, SMARCB1 and POLDIP2 and downregulated for genes TUBA1A and CCAR1, when comparing resistant and non-resistant ES cell lines for each drug. The results suggest involvement of repair pathways, SWI/SNF chromatin remodeling, microtubule and spliceosomal activity processes in drug resistance mechanisms in ES.
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Books on the topic "Sarcoma Ewing"

1

Cidre-Aranaz, Florencia, and Thomas G. P. Grünewald, eds. Ewing Sarcoma. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1020-6.

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Littrell, Jennifer Hites. Ewing Sarcoma: My Journey. Westbow Press, 2018.

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Littrell, Jennifer Hites. Ewing Sarcoma: My Journey. Westbow Press, 2018.

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Aranaz, Florencia Cidre, and Thomas Gruenewald. Ewing Sarcoma: Methods and Protocols. Humana Press, 2020.

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Mirabello, Lisa, Rochelle E. Curtis, and Sharon A. Savage. Bone Cancers. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0042.

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Cancers arising from bone or cartilage account for about 0.2% of malignant neoplasms. They are histologically heterogeneous with multiple rare subtypes. Osteosarcoma and Ewing sarcoma occur primarily in children and young adults, whereas other bone cancers occur in older individuals. As a group, bone cancers have few known environmental risk factors, the exception being a strong association between therapeutic radiation and increased risk of osteosarcoma. The genetic etiology is also better understood in osteosarcoma, although there have been limited studies in other types of bone cancers. This chapter reviews the worldwide incidence of more common types of primary bone cancers, patterns in survival over time, and the associated environmental and genetic risk factors.
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Sharon, Oosthoek, ed. Kate's story. [Edmonton]: Oz New Media, 1995.

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Book chapters on the topic "Sarcoma Ewing"

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Lin, Patrick P., Cynthia E. Herzog, Ashleigh Guadagnolo, and Shreyaskumar Patel. "Ewing Sarcoma." In Bone Sarcoma, 99–116. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-5194-5_6.

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Liu, Dongyou. "Ewing Sarcoma." In Tumors and Cancers, 71–76. Boca Raton : Taylor & Francis, 2018. | Series: Pocket guides to biomedical sciences | “A CRC title, part of the Taylor & Francis imprint, a member of the Taylor & Francis Group, the academic division of T&F Informa plc.”: CRC Press, 2017. http://dx.doi.org/10.1201/9781315120553-13.

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Kovar, Heinrich. "Ewing Sarcoma." In Encyclopedia of Cancer, 1349–52. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_2042.

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Indelicato, Daniel, and Robert B. Marcus. "Ewing Sarcoma." In Decision Making in Radiation Oncology, 1073–88. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16333-3_22.

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Gupta, Apar. "Ewing Sarcoma." In PET/MR Imaging, 9–11. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-65106-4_4.

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Franchi, Alessandro. "Ewing Sarcoma." In Encyclopedia of Pathology, 107–10. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-41894-6_5000.

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Amrith, Shantha, Stephanie Ming Young, Eric Ting, Bingcheng Wu, Min En Nga, and Gangadhara Sundar. "Ewing Sarcoma." In Ocular Adnexal Lesions, 305–9. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-3798-7_59.

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Dragun, Anthony E., Paul J. Schilling, Tod W. Speer, Feng-Ming Kong, Jingbo Wang, Hedvig Hricak, Oguz Akin, et al. "Ewing Sarcoma." In Encyclopedia of Radiation Oncology, 237–45. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-540-85516-3_301.

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Matthay, Katherine K. "Ewing sarcoma." In Evidence-Based Pediatric Oncology, 25–33. Oxford: John Wiley & Sons, Ltd, 2013. http://dx.doi.org/10.1002/9781118625309.ch3.

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Franchi, Alessandro. "Ewing Sarcoma." In Encyclopedia of Pathology, 1–3. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-28845-1_5000-1.

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Conference papers on the topic "Sarcoma Ewing"

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Martin, M., K. Pennington, and P. Escalante. "Ewing Sarcoma of the Mediastinum." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a6955.

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He, Di, Johnni Hansen, Noah Federman, Jorn Olsen, Beate Ritz, and Julia E. Heck. "Abstract 5778: Hernia and Ewing sarcoma." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-5778.

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Triche, Timothy J., Jon Nagy, Hyung Kang, Chris Denny, and Sheetal Bajaj Mitra. "Abstract A28: Targeted therapy of Ewing sarcoma." In Abstracts: Advances in Sarcomas: From Basic Science to Clinical Translation; May 16-19, 2017; Philadelphia, PA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1557-3265.sarcomas17-a28.

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Kayarthodi, Shubhalaxmi, Yasuo Fujimura, Kunchala Rungsrisuriyachai, Jinbo Fang, Veena Rao, and Shyam P. Reddy. "Abstract 2035: Anti-epileptic drug targets Ewing sarcoma." In 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.am2013-2035.

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Alimbetov, Dauren, Yidong Chen, Peter Houghton, and Raushan Kurmasheva. "Abstract A23: Novel approaches to Ewing sarcoma therapy." In Abstracts: AACR Special Conference on the Advances in Pediatric Cancer Research; September 17-20, 2019; Montreal, QC, Canada. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.pedca19-a23.

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Jawhar, Wajih, Paul Waterhouse, Rama Khokha, Takeaki Ishii, Robert Turcotte, Nada Jabado, and Livia Garzia. "Abstract A64: Functional genomics of metastatic Ewing sarcoma." In Abstracts: AACR Special Conference on the Advances in Pediatric Cancer Research; September 17-20, 2019; Montreal, QC, Canada. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.pedca19-a64.

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Zaveri, Tanish, and Mukesh Zaveri. "Region Based Image Fusion for Detection of Ewing Sarcoma." In 2009 Seventh International Conference on Advances in Pattern Recognition (ICAPR). IEEE, 2009. http://dx.doi.org/10.1109/icapr.2009.33.

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Crompton, Brian, Chip Stewart, Amaro Taylor-Weiner, Gabriela Alexa, Kyle Kurek, Monica Calicchio, Adam Kiezun, et al. "Abstract 999: The genomic landscape of pediatric Ewing sarcoma." In 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.am2014-999.

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Mutz, Cornelia N., Raphaela Schwentner, Maximilian O. Kauer, Jozef Ban, Dave N. T. Aryee, Sophie Erhardt, Dietmar Fuchs, Andreas Heitger, and Heinrich Kovar. "Abstract 1162: Investigating the NAD metabolome in Ewing Sarcoma." In 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.am2015-1162.

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Goss, Kelli, Stacia Koppenhafer, Kathryn Harmoney, and David Gordon. "Abstract 1955: Targeting ribonucleotide reductase (RNR) in Ewing sarcoma." 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.am2017-1955.

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