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Cancer: Rhabdomyosarcoma

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Total 29 results found since Jan 2013.

Susceptibility of Enterovirus-D68 to RNAi-mediated antiviral knockdown
Publication date: Available online 20 July 2019Source: Antiviral ResearchAuthor(s): Nicholas Klaiber, Michael A. McVoy, Wei ZhaoAbstractEnterovirus D68 (EV-D68) represents an emerging pathogen which has demonstrated a capacity for causing epidemic illness in pediatric and immunocompromised patients. With no effective antiviral treatment available, therapeutic interventions are currently limited to supportive care. Utilizing available genomic sequences from the 2014 B3 Epidemic EV-D68 clade and the 1962 Fermon EV-D68 strains, we performed in silico comparative genomic analysis, identifying several islands of phylogenetic co...
Source: Antiviral Therapy - July 21, 2019 Category: Virology Source Type: research

Susceptibility of Enterovirus-D68 to RNAi-mediated antiviral knockdown.
Abstract Enterovirus D68 (EV-D68) represents an emerging pathogen which has demonstrated a capacity for causing epidemic illness in pediatric and immunocompromised patients. With no effective antiviral treatment available, therapeutic interventions are currently limited to supportive care. Utilizing available genomic sequences from the 2014 B3 Epidemic EV-D68 clade and the 1962 Fermon EV-D68 strains, we performed in silico comparative genomic analysis, identifying several islands of phylogenetic conservation within the viral RNA-dependent RNA polymerase gene. The effects of transfecting short-interfering double-st...
Source: Antiviral Research - July 19, 2019 Category: Virology Authors: Klaiber N, McVoy MA, Zhao W Tags: Antiviral Res Source Type: research

Complement C5b-9 and Cancer: Mechanisms of Cell Damage, Cancer Counteractions, and Approaches for Intervention
In conclusion, osmotic burst of inflated complement-damaged cells may occur, but these bursts are most likely a consequence of metabolic collapse of the cell rather than the cause of cell death. The Complement Cell Death Mediator: A Concerted Action of Toxic Moieties Membrane pores caused by complement were first visualized by electron microscopy on red blood cell membranes as large ring structures (22). Similar lesions were viewed on E. coli cell walls (23). Over the years, ample information on the fine ultrastructure of the MAC that can activate cell death has been gathered (24) and has been recently further examined (...
Source: Frontiers in Immunology - April 9, 2019 Category: Allergy & Immunology 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

Abstract 487: Whole genome screen to identify genes targeting MYCN-driven embryonal tumors
MYCN is a driver of neuroblastoma (NB) tumorigenesis and is over-expressed in a number of tumors of embryonal origin, including rhabdomyosarcoma, medulloblastoma and diffuse intrinsic pontine gliomas. We sought to identify regulators of MYCN transcription by performing a whole genome screen (WGS) for regulators of MYCN promoter activity using a NB cell model. A plasmid containing the MYCN promoter (1.3kb upstream of MYCN TSS) fused to luciferase and stably integrated into the genome of NGP NB cells was the readout system. NGP-MYCNpluc, was selected based on MYCN luciferase activity inhibition by ATRA and HDAC inhibitors to...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Thiele, C. J., Liu, Z., Veschi, V., Buehler, E., Martin, S. Tags: Tumor Biology Source Type: research

FOXM1 expression in rhabdomyosarcoma: a novel prognostic factor and therapeutic target
This study aimed to determine the role of FOXM1 in RMS. We investigated the expression levels of FOXM1 and vascular endothelial growth factor (VEGF) and angiogenesis in a large series of RMS clinical cases using immunohistochemistry (n = 92), and we performed clinicopathologic and prognostic analyses. In vitro studies were conducted to examine the effect of FOXM1 knock-down on VEGF expression, cell proliferation, migration, and invasion in embryonal RMS (ERMS) and alveolar RMS (ARMS) cell lines, using small interference RNA (siRNA). High FOXM1 expression was significantly increased in the cases of ARMS, which has an ad...
Source: Tumor Biology - November 9, 2015 Category: Cancer & Oncology Source Type: research

MET/ERK2 pathway regulates the motility of human alveolar rhabdomyosarcoma cells.
In this study, we demonstrated the functions of MET signaling in ARMS in vitro by using three human ARMS cell lines and three human embryonal rhabdomyosarcoma (ERMS) cell lines. MET mRNA levels and MET protein expression in ARMS cell lines was higher than those in ERMS cell lines as detected by real-time quantitative PCR and western blotting, respectively. Based on cell growth and cell cycle analyses it was found that HGF stimulation did not enhance the proliferation of ERMS or ARMS cell lines. HGF-stimulated cell motility of ARMS cell lines was inhibited by U0126 (ERK1/2 inhibitor) but was only partially inhibited by PD9...
Source: Oncology Reports - November 16, 2016 Category: Cancer & Oncology Tags: Oncol Rep Source Type: research

Proteomic Profiling of Chikungunya Virus-Infected Human Muscle Cells: Reveal The Role of Cytoskeleton Network in CHIKV Replication.
Abstract Chikungunya virus (CHIKV) is an arthropod-borne, positive-sense, single-stranded RNA virus belonging to genus Alphavirus and family Togaviridae. The clinical manifestations developed upon CHIKV-infection include fever, myositis, arthralgia and maculopapular rash. Thus, the re-emergence of CHIKV has posed serious health threats worldwide. Due to the fact that myositis is induced upon CHIKV-infection, we sought to understand the dynamic proteomic regulation in SJCRH30, a human rhabdomyosarcoma cell line, to gain insights on CHIKV pathogenesis. Two-dimensional gel electrophoresis (2DE) in combination of matr...
Source: Journal of Proteomics - June 13, 2014 Category: Biochemistry Authors: Issac TH, Lee TE, Chu JJ Tags: J Proteomics Source Type: research

Abstract PR02: Negative regulation of myogenesis by Mtor: A pathway toward differentiation therapy in rhabdomyosarcoma
Rhabdomyosarcoma (RMS), the most common soft tissue sarcoma in children, is composed of skeletal myoblast-like cells that have lost the capacity to terminally differentiate. This suggests that RMS cells may contain a factor that blocks normal muscle differentiation. Because cell cycle arrest is coupled to muscle differentiation, identifying putative negative regulators of differentiation could lead to novel therapeutic approaches aimed at fostering terminal differentiation. To gain insight into the events that normally trigger the initial phase of muscle differentiation, we carried out a high content cell-based screen usin...
Source: Cancer Research - October 9, 2014 Category: Cancer & Oncology Authors: Wilson, R. A., Liu, J., Xu, L., Zheng, Y., Skapek, S. X. Tags: Developmental Biology of Pediatric Malignancies Source Type: research

Abstract 764: A role for GLI1 in the development of multidrug resistance in rhabdomyosarcoma (RMS) cells
RMS is the most common sarcoma of childhood. About 30% of patients with localized tumors will recur following treatment. The outcome for patients with recurrent RMS remains poor. Therefore, development of chemotherapy resistance during RMS therapy represents an important problem and novel approaches to prevent or reverse drug resistance are essential. Activation of multidrug transporter genes, including MDR1, MRP1, LRP and TAP1 represents an important mechanism for drug resistance in RMS. However, the mechanism of expression of multidrug resistance genes in RMS is incompletely understood. Recent reports have suggested a ro...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Yoon, J. W., Lamm, M., Leong, K.-F., Iannaccone, S., Iannaccone, P., Walterhouse, D. Tags: Experimental and Molecular Therapeutics Source Type: research

Abstract 3966: PLK1 regulates PAX3-FOXO1 stability and its inhibition mediates regression of alveolar rhabdomyosarcoma xenograft tumors
Oncogenic addiction provides an opportunity to develop new treatment options, especially for childhood cancers. Pediatric tumors contain a lower number of oncogenic mutations compared to most adult cancers, suggesting stronger dependency on individual oncogenes, such as chimeric transcription factors that have the ability to control multiple oncogenic pathways. Taking advantage of this addiction, targeting of oncogenic transcription factors becomes a new powerful strategy for therapy of translocation positive pediatric tumors like alveolar rhabdomyosarcoma (aRMS), which is characterized by a very dismal prognosis. As trans...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Thalhammer, V., Herrero–Martin, D., Hecker, R., Laubscher, D., Lopez–Garcia, L., Wachtel, M., Bode, P., Schafer, B. Tags: Tumor Biology Source Type: research

Targeting of PAX3-FOXO1 by PLK1 Inhibition
In this report, we addressed this challenge by developing a two-armed screen for druggable upstream regulatory kinases in the PAX3/7-FOXO1 pathway. Screening libraries of kinome siRNA and small molecules, we defined PLK1 as an upstream-acting regulator. Mechanistically, PLK1 interacted with and phosphorylated PAX3-FOXO1 at the novel site S503, leading to protein stabilization. Notably, PLK1 inhibition led to elevated ubiquitination and rapid proteasomal degradation of the PAX3-FOXO1 chimeric oncoprotein. On this basis, we embarked on a preclinical validation of PLK1 as a target in a xenograft mouse model of aRMS, where the...
Source: Cancer Research - January 4, 2015 Category: Cancer & Oncology Authors: Thalhammer, V., Lopez–Garcia, L. A., Herrero–Martin, D., Hecker, R., Laubscher, D., Gierisch, M. E., Wachtel, M., Bode, P., Nanni, P., Blank, B., Koscielniak, E., Schafer, B. W. Tags: Molecular and Cellular Pathobiology Source Type: research

Chorein addiction in VPS13A overexpressing rhabdomyosarcoma cells.
In conclusion, chorein is expressed in various cancer cells. In cells with high chorein expression levels chorein silencing promotes apoptotic cell death, an effect paralleled by down-regulation of PI-3K activity and BCL-2/Bax expression ratio. PMID: 25871399 [PubMed - as supplied by publisher]
Source: Oncotarget - April 17, 2015 Category: Cancer & Oncology Tags: Oncotarget Source Type: research

Abstract 3792: SKP2 supports cell proliferation and is regulated by Notch signaling in myoblasts and embryonal rhabdomyosarcoma
Conclusion:Altogether, these preliminary experiments suggest that SKP2 could be regulated by Notch signaling in ERMS and that its inhibition hampers tumor cell proliferative capability.Note: This abstract was not presented at the meeting.Citation Format: Rossella Rota, Laura Adesso, Beatrice Conti, Roberta Ciarapica, Lavinia Raimondi, Maria De Salvo, Sonia Rodriguez, Nadia Carlesso, Lucio Miele, Franco Locatelli. SKP2 supports cell proliferation and is regulated by Notch signaling in myoblasts and embryonal rhabdomyosarcoma. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Rese...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Rota, R., Adesso, L., Conti, B., Ciarapica, R., De Raimondi, L., Salvo, M., Rodriguez, S., Carlesso, N., Miele, L., Locatelli, F. Tags: Molecular and Cellular Biology Source Type: research

Crizotinib-induced antitumour activity in human alveolar rhabdomyosarcoma cells is not solely dependent on ALK and MET inhibition
Conclusions: These results provide a further insight into the molecular mechanisms affected by crizotinib in ARMS cells inferring that it could be a useful therapeutic tool in ARMS cancer treatment.
Source: Journal of Experimental and Clinical Cancer Research - October 6, 2015 Category: Cancer & Oncology Authors: Francesca MegiorniHeather McDowellSimona CameroOlga MannarinoSimona CeccarelliMilena PaianoPaul LostyBarry PizerRajeev ShuklaAntonio PizzutiAnna ClericoCarlo Dominici Source Type: research