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Cancer: Ewing's Sarcoma

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Total 35 results found since Jan 2013.

Plasma hydrogenated cationic detonation nanodiamonds efficiently deliver to human cells in culture functional siRNA targeting the Ewing sarcoma junction oncogene.
Abstract The expression of a defective gene can lead to major cell dysfunctions among which cell proliferation and tumor formation. One promising therapeutic strategy consists in silencing the defective gene using small interfering RNA (siRNA). In previous publications we showed that diamond nanocrystals (ND) of primary size 35 nm, rendered cationic by polyethyleneimine-coating, can efficiently deliver siRNA into cell, which further block the expression of EWS/FLI-1 oncogene in a Ewing sarcoma disease model. However, a therapeutic application of such nanodiamonds requires their elimination by the organism, partic...
Source: Biomaterials - February 13, 2015 Category: Materials Science Authors: Bertrand JR, Pioche-Durieu C, Ayala J, Petit T, Girard HA, Malvy CP, Le Cam E, Treussart F, Arnault JC Tags: Biomaterials Source Type: research

Abstract 3422: RNAi screening identifies FGFR4 as a modulator of growth and survival in Ewing sarcoma
Ewing sarcoma is the second most common cancer of bone and soft tissue arising in children and young adults. Standard treatment of Ewing sarcoma includes surgery, radiation, and chemotherapy largely consisting of combinations of non-targeted cytotoxic agents. Although the survival rate has improved for patients treated for localized disease, the survival rate of patients with metastatic tumor remains lower than 30%. In order to improve therapeutic options for Ewing Sarcoma, we employed a functional genomics approach based on RNA interference (RNAi) screening to identify genes whose silencing affected the proliferation and ...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Azorsa, D. O., Gonzales, I. M., Arora, S., Hagelstrom, R. T., Little, T. H., Arceci, R. J., Mousses, S. Tags: Molecular and Cellular Biology Source Type: research

PKC{iota}/Dvl2 in Wnt3a-dependent Neurite Outgrowth Cell Biology
Previously we reported that Wnt3a-dependent neurite outgrowth in Ewing sarcoma family tumor cell lines was mediated by Frizzled3, Dishevelled (Dvl), and c-Jun N-terminal kinase (Endo, Y., Beauchamp, E., Woods, D., Taylor, W. G., Toretsky, J. A., Uren, A., and Rubin, J. S. (2008) Mol. Cell. Biol. 28, 2368–2379). Subsequently, we observed that Dvl2/3 phosphorylation correlated with neurite outgrowth and that casein kinase 1δ, one of the enzymes that mediate Wnt3a-dependent Dvl phosphorylation, was required for neurite extension (Greer, Y. E., and Rubin, J. S. (2011) J. Cell Biol. 192, 993–1004). However, the functional ...
Source: Journal of Biological Chemistry - March 29, 2013 Category: Chemistry Authors: Greer, Y. E., Fields, A. P., Brown, A. M. C., Rubin, J. S. Tags: Signal Transduction Source Type: research

Abstract 479: Inhibition of the splicing of the EWS-FLI1 fusion transcript reverses EWS-FLI1 driven oncogenic expression in Ewing sarcoma
This study has implications for the treatment of ES through inhibition of proteins required for expression of the EWS-FLI1 transcript and identifies a candidate lead compound for further clinical development. Our findings may also open up strategies for treatment of other cancers driven by fusion oncogenes.Citation Format: Patrick J. Grohar, Suntae Kim, Sara Haddock, Guillermo Rangel Rivera, Matt Harlow, Nichole K. Maloney, Konrad Huppi, Kristen Gehlhaus, Magdalena Grandin, Carleen Klumpp-Thomas, Eugen Buehler, Lee J. Helman, Scott E. Martin, Natasha J. Caplen. Inhibition of the splicing of the EWS-FLI1 fusion transcript r...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Grohar, P. J., Kim, S., Haddock, S., Rangel Rivera, G., Harlow, M., Maloney, N. K., Huppi, K., Gehlhaus, K., Grandin, M., Klumpp-Thomas, C., Buehler, E., Helman, L. J., Martin, S. E., Caplen, N. J. Tags: Tumor Biology Source Type: research

GSE73092 High-throughput RNAi cell viability screen to identify selective targets for EWS-FLI1 positive Ewing sarcoma
Contributors : Kristiina Iljin ; Tao HeSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensWe have performed a high-throughput RNA interference screen to identify targets inhibiting EWS-FLI1 driven cell proliferation in Ewing sarcoma cells. EWS-FLI1 expressing A673 Ewing sarcoma cells were screened both in presence and absence of EWS-FLI1 shRNA induction with druggable siRNA library. Leucine rich repeats and WD repeat Domain containing 1 (LRWD1) targeting siRNA pool was the strongest anti-proliferative hit identified only in presence of EWS-FLI1. Validation experiments confirmed the anti-...
Source: GEO: Gene Expression Omnibus - September 16, 2018 Category: Genetics & Stem Cells Tags: Expression profiling by high throughput sequencing Homo sapiens Source Type: research

GSE120512 Transcriptome modulation by loss-of-YAP1/TAZ in SK-N-MC Ewing Sarcoma cells
Contributors : Juan Diaz-Martin ; Laura Romero-PerezSeries Type : Expression profiling by arrayOrganism : Homo sapiensYAP1 (Yes-associated protein 1) and TAZ (transcriptional coactivator with PDZ-binding motif, or WWTR1) are nucleo-cytoplasmic shuttling proteins that can function in the nucleus as transcriptional coactivators. Here we sought to evaluate which genes are regulated by endogenous levels of YAP/TAZ. We compared SK-N-MC cells transfected with a control non-targeting siRNA with cells transfected with a mix of siRNA targeting both YAP and TAZ.
Source: GEO: Gene Expression Omnibus - September 27, 2018 Category: Genetics & Stem Cells Tags: Expression profiling by array Homo sapiens Source Type: research

Systems biology of Ewing sarcoma: a network model of EWS-FLI1 effect on proliferation and apoptosis
In this study, a network linking EWS-FLI1 to cell cycle and apoptosis phenotypes was constructed through an original method of network reconstruction. Transcriptome time-series after EWS-FLI1 silencing were used to identify core modulated genes by an original scoring method based on fitting expression profile dynamics curves. Literature data mining was then used to connect these modulated genes into a network. The validity of a subpart of this network was assessed by siRNA/RT-QPCR experiments on four additional Ewing cell lines and confirmed most of the links. Based on the network and the transcriptome data, CUL1 was ident...
Source: Nucleic Acids Research - October 18, 2013 Category: Research Authors: Stoll, G., Surdez, D., Tirode, F., Laud, K., Barillot, E., Zinovyev, A., Delattre, O. Tags: Computational Biology Source Type: research

Dual targeting of EWS-FLI1 activity and the associated DNA damage response with Trabectedin and SN38 synergistically inhibits Ewing sarcoma cell growth.
CONCLUSIONS: These results provide the basis and rationale for translating this drug combination to the clinic. In addition, the study highlights an approach that utilizes a targeted agent to interfere with an oncogenic transcription factor and then exploits the resulting changes in gene expression to develop a molecularly targeted combination therapy. PMID: 24277455 [PubMed - as supplied by publisher]
Source: Clinical Cancer Research - November 25, 2013 Category: Cancer & Oncology Authors: Grohar PJ, Segars LE, Yeung C, Pommier Y, D'Incalci M, Mendoza A, Helman LJ Tags: Clin Cancer Res Source Type: research

Ewing sarcoma EWS protein regulates midzone formation by recruiting Aurora B kinase to the midzone.
Abstract Ewing sarcoma is a malignant bone cancer that primarily occurs in children and adolescents. Eighty-five percent of Ewing sarcoma is characterized by the presence of the aberrant chimeric EWS/FLI1 fusion gene. Previously, we demonstrated that an interaction between EWS/FLI1 and wild-type EWS led to the inhibition of EWS activity and mitotic dysfunction. Although defective mitosis is considered to be a critical step in cancer initiation, it is unknown how interference with EWS contributes to Ewing sarcoma formation. Here, we demonstrate that the EWS/FLI1- and EWS-knockdown cells display a high incidence of ...
Source: Cell Cycle - June 19, 2014 Category: Cytology Authors: Park H, Turkalo TK, Nelson K, Folmsbee SS, Robb C, Belford B, Azuma M Tags: Cell Cycle Source Type: research

Abstract A10: Functional characterization of Ewing's sarcoma susceptibility loci
Conclusions: In synopsis, our data indicate that the previously identified ES susceptibility regions and candidate genes may play a prominent role in ES pathobiology. Citation Format: Thomas Grunewald, Marie-Ming Aynaud, Franck Tirode, Eleni Tomazou, Didier Surdez, Thomas Rio Frio, Virginie Bernard, Virginie Raynal, Carlo Lucchesi, Gaelle Pierron, Pascale Gilardi-Hebenstreit, Patrick Charnay, Heinrich Kovar, Olivier Delattre. Functional characterization of Ewing's sarcoma susceptibility loci. [abstract]. In: Proceedings of the AACR Special Conference on Pediatric Cancer at the Crossroads: Translating Discovery into Improve...
Source: Cancer Research - October 9, 2014 Category: Cancer & Oncology Authors: Grunewald, T., Aynaud, M.-M., Tirode, F., Tomazou, E., Surdez, D., Frio, T. R., Bernard, V., Raynal, V., Lucchesi, C., Pierron, G., Gilardi-Hebenstreit, P., Charnay, P., Kovar, H., Delattre, O. Tags: Genetic Predisposition to Pediatric Cancers Source Type: research

Abstract 3989: High throughput screening highlights NFkB signaling in Ewing sarcoma
Ewing sarcoma (ES) is the second most frequent pediatric bone tumor and still remains of poor prognosis especially for metastatic patients. Genetically, ES is characterized by a chromosomal translocation between EWSR1 and ETS family members (FLI1 in 85% of cases). This leads to the expression of EWS-FLI1 chimeric oncogene transcription factor. Aiming at identifying EWS-FLI1 regulated genes with potential therapeutic targets, a genome wide method was developed to rank these potential hits by combining Ewing sarcoma transcriptome and ChIPSeq data. Accordingly, 273 selected genes were further investigated using a siRNA approa...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Surdez, D., Stoll, G., Tirode, F., Laud, K., Barillot, E., Delattre, O. Tags: Tumor Biology Source Type: research

Abstract 478: EWS/FLI1 transcription is modulated by the PI3K pathway via SP1 in Ewing sarcoma
Ewing sarcoma (ES) is the second most frequent bone cancer in childhood and it is characterized by the presence of the balanced t(11;22)(q24;q12) translocation in more than 85% of cases, generating a dysregulated transcription factor EWS/FLI1. ES belongs to small-round-blue-cell tumors and it is a very aggressive osteolytic cancer with early tendency for development of metastasis. Mostly it affects bones such as pelvis, femour and ribs but can also arise in soft tissues, mainly in adults. EWS/FLI1 is an essential oncogenic component of ES development which is necessary for tumor cell maintenance, through inappropriate regu...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Giorgi, C., Boro, A., Lopez-Garcia, L. A., Schaefer, B. W., Niggli, F. K. Tags: Tumor Biology Source Type: research

Abstract 4966: Identification of deubiquitinating enzyme USP19 as a regulator of EWS/FLI1 protein turnover in Ewing sarcoma
Ewing sarcoma belongs to the family of pediatric tumors which arise most commonly in bone. The majority of Ewing sarcoma is characterized by a balanced translocation between chromosomes 11 and 22 which encodes for the uniquely expressed fusion protein EWS/FLI1. Tumor cells are crucially dependent on expression of the fusion protein. Protein degradation is an important and highly regulated process in all cells and novel insights are beginning to be applied for cancer therapy. We aim to investigate the mechanism of turnover with the goal to diminish EWS/FLI1 protein and thereby identify novel targets for Ewing sarcoma treatm...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Gierisch, M. E., Lopez-Garcia, L. A., Pfistner, F., Niggli, F. K., Schaefer, B. W. Tags: Molecular and Cellular Biology Source Type: research

Abstract A155: Small molecule metabolic inhibitors, compound A and the derivatives specifically inhibit the cell growth of Ewing's sarcoma cells harbor EWS-FLI1 in vitro and in vivo
Conclusions: Compound A and its derivatives may be a therapeutic agent with potent antitumor activity for Ewing's sarcoma patients.Citation Format: Hiromichi Kosaka, Yasuo Watanabe, Michihiro Maemoto, Masamori Sugawara, Miwa Watanabe, Yoko Ono, Yoshisuke Nakasato, Masahiro Matsubara, Ryuichiro Nakai. Small molecule metabolic inhibitors, compound A and the derivatives specifically inhibit the cell growth of Ewing's sarcoma cells harbor EWS-FLI1 in vitro and in vivo. [abstract]. In: Proceedings of the AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; 2015 Nov 5-9; Boston, MA. Philadelphia (P...
Source: Molecular Cancer Therapeutics - January 7, 2016 Category: Cancer & Oncology Authors: Kosaka, H., Watanabe, Y., Maemoto, M., Sugawara, M., Watanabe, M., Ono, Y., Nakasato, Y., Matsubara, M., Nakai, R. Tags: Therapeutic Agents: Other: Poster Presentations - Proffered Abstracts Source Type: research

Abstract A18: Epigenetic profiling uncovers the suppressive role of caveolae in Ewing sarcoma
Ewing sarcoma (ES) is the second most common bone tumor in childhood. ES harbors a characteristic gene translocation that gives rise to a fusion protein, most commonly EWS/FLI1 (EF). Caveolin-1 (CAV1) is a direct target of EF, it is overexpressed in ES and has an oncogenic role. CAV1 and the Polymerase I and transcript release factor (PTRF) interact at the plasma membrane and are essential for caveolae formation. The methylome analysis of ES samples and cell lines revealed a hypermethylation in the N-shore islands of the PTRF promoter compared to normal cells. We hypothesize that, as ES cells have very few caveolae and do ...
Source: Cancer Research - April 3, 2016 Category: Cancer & Oncology Authors: Huertas–Martinez, J., Court, F., Rello–Varona, S., Martin, D. H., Almacellas, O., Sainz–Jaspeado, M., Garcia–Monclus, S., Lagares–Tena, L., Buȷ, R., Hontecillas–Prieto, L., Mateo–Lozano, S., Sastre, A., Azo Tags: Epigenetics Source Type: research