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Cancer: Neuroblastoma

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Total 288 results found since Jan 2013.

Stabilizing effect of tyrosine trimers on pDNA and siRNA polyplexes.
Abstract Nine sequence-defined, polycationic oligomers were synthesized containing motifs of three consecutive tyrosines (Y3) as stabilizing components for pDNA and siRNA polyplex assembly. For pDNA, a combination of terminal oligotyrosines and cysteines was necessary and sufficient for stable polyplex formation. Stable siRNA binding required a combination of terminal cysteines and oligotyrosines, as well as a central hydrophobic modification (oligotyrosines or fatty acids). The phenolic group within the aromatic amino acids of Y3 containing oligomers further increased the endosomal buffer capacity. As a result, t...
Source: Biomaterials - January 4, 2013 Category: Materials Science Authors: Troiber C, Edinger D, Kos P, Schreiner L, Kläger R, Herrmann A, Wagner E Tags: Biomaterials Source Type: research

Abstract 5423: Novel targeted therapy for neuroblastoma: Silencing the MXD3 gene using siRNA
Neuroblastoma is a cancer of the sympathetic nervous system and the most common extracranial solid tumor in children. Almost half of neuroblastoma patients have a high-risk phenotype at diagnosis: metastatic disease. Prognosis of these patients is very poor with only 30% survival despite the most intensive therapies currently available. In addition, patients who respond successfully to treatment suffer from side effects from chemo and radiation therapies, leading to life-long irreversible complications. Therefore, there is a desperate need for a neuroblastoma-targeted therapy that is more effective and has fewer side effec...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Duong, C., Chen, C., Yoshida, S., Barisone, G., Nolta, J., Diaz, E., Nitin, N., Satake, N. Tags: Clinical Research (Excluding Clinical Trials) Source Type: research

Novel targeted therapy for neuroblastoma: Silencing the MXD3 gene using siRNA.
CONCLUSIONS: These results indicate that MXD3 is a potential new target and MXD3 siRNA nanocomplexes are a novel therapeutic approach for neuroblastoma.Pediatric Research accepted article preview online, 18 April 2017. doi:10.1038/pr.2017.74. PMID: 28419087 [PubMed - as supplied by publisher]
Source: Pediatric Research - April 18, 2017 Category: Pediatrics Authors: Duong C, Yoshida S, Chen C, Barisone G, Diaz E, Li Y, Beckett L, Chung J, Antony R, Nolta J, Nitin N, Satake N Tags: Pediatr Res Source Type: research

Downregulation of survivin by siRNA inhibits invasion and promotes apoptosis in neuroblastoma SH-SY5Y cells.
Abstract Neuroblastoma is a solid tumor that occurs mainly in children. Malignant neuroblastomas have a poor prognosis because conventional chemotherapeutic agents are not very effective. Survivin, a member of the inhibitor of the apoptosis protein family, plays a significant role in cell division, inhibition of apoptosis, and promotion of cell proliferation and invasion. Previous studies found that survivin is highly expressed in some malignant neuroblastomas and is correlated with poor prognosis. The aim of this study was to investigate whether survivin could serve as a potential therapeutic target of human neur...
Source: Braz J Med Biol Res - May 23, 2014 Category: Research Authors: Zhang L, Liang H, Cao W, Xu R, Ju XL Tags: Braz J Med Biol Res Source Type: research

Target delivery of MYCN siRNA by folate-nanoliposomes delivery system in a metastatic neuroblastoma model
In this study, we established a bone marrow and bone metastasis xenograft mouse model by injecting the LA-N-5 cell into the bone marrow cavity. Fluorescence microscopy, TUNEL Assay, Quantitative RT-PCR and western blot were conducted to analysis the distribution of folate-nanoliposomes entrapped MYCN (V-myc myelocytomatosis viral related oncogene) siRNA in mice and the relevant suppression effect. Results: The folate-nanoliposomes entrapped MYCN siRNA can be specifically distributed in tumor tissues. Further study shows that folate-nanoliposomes entrapped MYCN siRNA lead to MYCN mRNA expression significantly down-regulated (>50%, and p
Source: Cancer Cell International - June 27, 2013 Category: Cancer & Oncology Authors: Qiqi ZhuChen FengWeiwei LiaoYan ZhangSuoqin Tang Source Type: research

Abstract B31: Combined siRNA and small molecule screening identifies Aurora B kinase as an effective target in MYCN-driven neuroblastoma
Despite advances in multimodal treatment, neuroblastoma (NB) is often fatal for children with high-risk disease and many survivors need to cope with long-term side effects from high-dose chemotherapy and radiation. To identify new therapeutic targets, we performed a siRNA screen of the druggable genome combined with a small molecule screen of 465 compounds targeting 39 different mechanisms of actions in four NB cell lines. We identified 58 genes as targets, including AURKB, in at least one cell line. In the drug screen, aurora kinase inhibitors (nine molecules) and in particular the AURKB-selective compound, barasertib, we...
Source: Cancer Research - April 3, 2016 Category: Cancer & Oncology Authors: Bogen, D., Wei, J. S., Azorsa, D. O., Ormanoglu, P., Buehler, E., Guha, R., Keller, J. M., Griner, L. A. M., Ferrer, M., Song, Y. K., Liao, H., Mendoza, A., Gryder, B. E., Sindri, S., He, J., Wen, X., , Zhang, S., Shern, J. F., Yohe, M. E., Taschner-Mandl Tags: Targeted Therapeutics and Resistance Source Type: research

Abstract 499: RUNX2 protects human neuroblastoma cells against apoptosis
In conclusion, our study suggests that hypoxia up regulates RUNX2 in NB1691 cells in a HIF2α- dependent manner and RUNX2 protects neuroblastoma cells against apoptosis. Citation Format: Manu Gnanamony, Indra Mohanam, Sanjeeva Mohanam. RUNX2 protects human neuroblastoma cells against apoptosis. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 499. doi:10.1158/1538-7445.AM2014-499
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Gnanamony, M., Mohanam, I., Mohanam, S. Tags: Molecular and Cellular Biology Source Type: research

Development of ATP13A2-deficient In vitro Model for PARK9 Parkinson’s Disease
Conclusion: ATP13A2-deficient PD model was successfully developed.
Source: Current Signal Transduction Therapy - November 3, 2021 Category: Molecular Biology 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 1453: MicroRNA replacement and RNAi-mediated silencing of ALK as combined targeted therapies for neuroblastoma
The effective treatment of advanced Neuroblastoma (NB) is still a challenge in pediatric oncology, because the clinical use of most therapeutics is limited by insufficient drug delivery to the tumor and high systemic toxicity. The discovery of the RNAi has great promise for anti-cancer therapeutics but, as in high-grade solid tumors a single ‘oncogene addiction’ is rare, multi-'gene' target combinations are required and a targeted delivery system is mandatory to successfully translate RNAi-based therapeutics into the clinics. It is now ascertained the master role of ALK and related genes such as PHOX2B, able to promote...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Perri, P., Paolo, D. D., Priddy, L., Fiore, A. D., Brignole, C., Pastorino, F., Brown, D., Ponzoni, M. Tags: Molecular and Cellular Biology Source Type: research

Detailed Dissection of UBE3A-Mediated DDI1 Ubiquitination
Discussion Poly-ubiquitinated proteins targeted for degradation might be recognized directly by proteasomal receptors or by proteasomal shuttling proteins. The first shuttling proteins – Ddi1, Rad23 and Dsk2 – were identified and characterized in Saccharomyces cerevisiae (Lambertson et al., 1999; Kaplun et al., 2005). Proteasomal shuttles contain an N-terminal ubiquitin-like (UBL) domain that interacts with the 26S proteasome (Finley, 2009), and a C-terminal ubiquitin-binding domain domain (UBD) that binds to ubiquitin or poly-ubiquitin chains (Bertolaet et al., 2001). When ubiquitinated, substrates are capt...
Source: Frontiers in Physiology - May 2, 2019 Category: Physiology Source Type: research

Amlodipine prevents apoptotic cell death by correction of elevated intracellular calcium in a primary neuronal model of Batten disease (CLN3 disease).
Abstract CLN3 disease (Spielmeyer-Vogt-Sjogren-Batten disease) is a severe pediatric neurodegenerative disorder for which there is currently no effective treatment. The disease is characterized by progressive neuronal death, which may be triggered by abnormal intracellular calcium levels leading to neuronal apoptosis. Previously, we demonstrated reversal of the calcium effect in a neuroblastoma cell line using amlodipine and other calcium channel antagonists. In the present studies, we developed a CLN3 siRNA-inhibited primary rat neuron model to further study etoposide-induced calcium changes and apoptosis in CLN3...
Source: Biochemical and Biophysical Research communications - June 12, 2013 Category: Biochemistry Authors: Warnock A, Tan L, Li C, Haack KA, Narayan SB, Bennett MJ Tags: Biochem Biophys Res Commun Source Type: research

New therapeutic strategies in neuroblastoma: combined targeting of a novel tyrosine kinase inhibitor and liposomal siRNAs against ALK.
Authors: Di Paolo D, Yang D, Pastorino F, Emionite L, Cilli M, Daga A, Destefanis E, Di Fiore A, Piaggio F, Brignole C, Xu X, Liang C, Gibbons J, Ponzoni M, Perri P Abstract Many different aberrations in the Anaplastic Lymphoma Kinase (ALK) were found to be oncogenic drivers in several cancers including neuroblastoma (NB), therefore ALK is now considered a critical player in NB oncogenesis and a promising therapeutic target. The ALK-inhibitor crizotinib has a limited activity against the various ALK mutations identified in NB patients. We tested: the activity of the novel ALK-inhibitor X-396 administered alone or i...
Source: Oncotarget - August 26, 2015 Category: Cancer & Oncology Tags: Oncotarget Source Type: research

GSE74626 Differential gene expression in neuroblastoma cells after transfection with control siRNA, MYCN siRNA or TFAP4 siRNA.
Contributors : Chengyuan Xue ; Tao LiuSeries Type : Expression profiling by arrayOrganism : Homo sapiensWe analyed the gene expression profiles after knocking down MYCN or TFAP4. Results showed that transcription factor MYCN and TFAP4 commonly regulats a subset of genes that may contribute to neuroblastoma cells proliferation and migration.
Source: GEO: Gene Expression Omnibus - November 2, 2016 Category: Genetics & Stem Cells Tags: Expression profiling by array Homo sapiens Source Type: research

Knockdown of LRP/LR induces apoptosis in pancreatic cancer and neuroblastoma cells through activation of caspases.
Abstract The 37kDa/67kDa laminin receptor (LRP/LR) serves various physiological and pathological roles such as enhancing tumour-related processes including metastasis, angiogenesis, cellular viability and telomerase activation in cancerous cell lines. The present study investigates the effect of siRNA mediated downregulation of LRP/LR on pancreatic cancer (AsPC-1) and neuroblastoma (IMR-32) cells. MTT and BrdU assays revealed that siRNA mediated downregulation of LRP resulted in a significant reduction in cell viability and cell proliferation. In addition, knock-down of LRP resulted in phosphatidylserine externali...
Source: Experimental Cell Research - September 9, 2017 Category: Cytology Authors: Chetty CJ, Ferreira E, Jovanovic K, Weiss SFT Tags: Exp Cell Res Source Type: research