Thematische Bibliographien / RNA therapeutic

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Auswahl der wissenschaftlichen Literatur zum Thema „RNA therapeutic“

Autor: Grafiati

Veröffentlicht am 1. April 2023

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Zeitschriftenartikel zum Thema "RNA therapeutic"

Mahy, BWJ. „Therapeutic RNA?“ Reviews in Medical Virology 15, Nr. 6 (2005): 349–50. http://dx.doi.org/10.1002/rmv.485.

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Liu, Xiang, Yu Zhang, Shurong Zhou, Lauren Dain, Lei Mei und Guizhi Zhu. „Circular RNA: An emerging frontier in RNA therapeutic targets, RNA therapeutics, and mRNA vaccines“. Journal of Controlled Release 348 (August 2022): 84–94. http://dx.doi.org/10.1016/j.jconrel.2022.05.043.

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EVERTS, SARAH. „RNA DISTRACTION IS THERAPEUTIC“. Chemical & Engineering News 87, Nr. 29 (20.07.2009): 15. http://dx.doi.org/10.1021/cen-v087n029.p015a.

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Poller, Wolfgang, Juliane Tank, Carsten Skurk und Martina Gast. „Cardiovascular RNA Interference Therapy“. Circulation Research 113, Nr. 5 (16.08.2013): 588–602. http://dx.doi.org/10.1161/circresaha.113.301056.

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Understanding of the roles of noncoding RNAs (ncRNAs) within complex organisms has fundamentally changed. It is increasingly possible to use ncRNAs as diagnostic and therapeutic tools in medicine. Regarding disease pathogenesis, it has become evident that confinement to the analysis of protein-coding regions of the human genome is insufficient because ncRNA variants have been associated with important human diseases. Thus, inclusion of noncoding genomic elements in pathogenetic studies and their consideration as therapeutic targets is warranted. We consider aspects of the evolutionary and discovery history of ncRNAs, as far as they are relevant for the identification and selection of ncRNAs with likely therapeutic potential. Novel therapeutic strategies are based on ncRNAs, and we discuss here RNA interference as a highly versatile tool for gene silencing. RNA interference-mediating RNAs are small, but only parts of a far larger spectrum encompassing ncRNAs up to many kilobasepairs in size. We discuss therapeutic options in cardiovascular medicine offered by ncRNAs and key issues to be solved before clinical translation. Convergence of multiple technical advances is highlighted as a prerequisite for the translational progress achieved in recent years. Regarding safety, we review properties of RNA therapeutics, which may immunologically distinguish them from their endogenous counterparts, all of which underwent sophisticated evolutionary adaptation to specific biological contexts. Although our understanding of the noncoding human genome is only fragmentary to date, it is already feasible to develop RNA interference against a rapidly broadening spectrum of therapeutic targets and to translate this to the clinical setting under certain restrictions.

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&NA;. „Therapeutic potential of RNA??interference“. Inpharma Weekly &NA;, Nr. 1411 (November 2003): 2. http://dx.doi.org/10.2165/00128413-200314110-00001.

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Stevenson, Mario. „Therapeutic Potential of RNA Interference“. New England Journal of Medicine 351, Nr. 17 (21.10.2004): 1772–77. http://dx.doi.org/10.1056/nejmra045004.

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Han, Xuexiang, Michael J. Mitchell und Guangjun Nie. „Nanomaterials for Therapeutic RNA Delivery“. Matter 3, Nr. 6 (Dezember 2020): 1948–75. http://dx.doi.org/10.1016/j.matt.2020.09.020.

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Sioud, Mouldy, und Marianne Leirdal. „Therapeutic RNA and DNA enzymes“. Biochemical Pharmacology 60, Nr. 8 (Oktober 2000): 1023–26. http://dx.doi.org/10.1016/s0006-2952(00)00395-6.

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Novina, C. D. „Therapeutic potential of RNA interference“. Biomedicine & Pharmacotherapy 58, Nr. 4 (Mai 2004): 270. http://dx.doi.org/10.1016/j.biopha.2002.12.001.

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van Ommen, Gert-Jan B., und Annemieke Aartsma-Rus. „Advances in therapeutic RNA-targeting“. New Biotechnology 30, Nr. 3 (März 2013): 299–301. http://dx.doi.org/10.1016/j.nbt.2013.01.005.

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Dissertationen zum Thema "RNA therapeutic"

Kavitha, Siva. „RNA-based therapeutic approaches for FTDP-17“. Doctoral thesis, Università degli studi di Trento, 2015. https://hdl.handle.net/11572/367651.

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Neurodegenerative diseases are linked to altered splicing mechanisms (Mills et al., 2012). Fronto temporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) is one such disease that stems from the differential splicing caused due to mutations in Microtubule associated protein tau (MAPT) gene (Esther et al., 2002). This PhD thesis focuses on developing RNA-based therapeutic approaches to address FTDP-17. CHAPTER 1 introduces a broad range of topics such as splicing mechanism, neurodegenerative diseases associated with splice defects, therapeutic tools to modulate such splice defects in the context of neurogenetic diseases and possible applications of available tools for FTDP-17. CHAPTER 2 explores an exon skipping strategy to modulate splice defects in the context of FTD-17 using small nuclear RNAs (snRNAs). CHAPTER 3 is based on a short interfering RNA (siRNA) approach to modulate post-transcriptional gene silencing of specific isoform associated to FTDP-17. CHAPTER 4 employs long non coding RNA (lncRNA) to mediate post transcriptional repression of tau protein associated to FTDP-17 and deciphers its auxiliary role in splicing of exon 10 CHAPTER 5 elaborates on the future perspectives of all the above mentioned approaches to find a cure for FTDP-17.

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Kavitha, Siva. „RNA-based therapeutic approaches for FTDP-17“. Doctoral thesis, University of Trento, 2015. http://eprints-phd.biblio.unitn.it/1552/1/PhD_thesis_Siva_K_June_2015.pdf.

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White, Melanie Denise. „RNA interference as a therapeutic approach in prion disease“. Thesis, University College London (University of London), 2008. http://discovery.ucl.ac.uk/1445182/.

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Prion diseases are fatal, transmissible neurodegenerative disorders characterised by accumulation throughout the brain of PrPSc, an abnormally folded isoform of the normal cellular prion protein, PrP. PrPSc is associated with infectivity but is not directly neurotoxic and targeting it is of limited efficacy in prion therapeutics. However, PrP-null mice are resistant to prion infection and neurotoxicity. Transgene-c mediated depletion of neuronal PrP in mice with established prion infection reverses early spongiosis, neuronal loss and cognitive deficits, and prevents clinical disease progression. Thus, reducing PrPC expression in the brain through extrinsic means is likely to be an effective therapy for prion diseases. RNA interference can be exploited to mediate gene silencing and can be stably achieved in non-dividing cells such as neurons by incorporation of the small interfering RNAs into replication-deficient lentiviruses. The work described in this thesis strongly validates the use of lentiviral-mediated RNA interference as a therapeutic approach in prion disease. Reducing PrPc expression with siRNA duplexes enabled clearance of PrPSc and infectivity from prion-infected cells in vitro. Lentiviruses constructed to express the interfering sequences demonstrated effective reduction of PrPc expression in vitro. Stable expression of the interfering RNA molecules in vivo through lentiviral transduction of the hippocampus reduced local pathology and significantly prolonged survival in a mouse model of prion disease. This represents an important and novel advance in the treatment of established prion disease with relevance for all prion strains.

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Wu, Connie Ph D. Massachusetts Institute of Technology. „Engineering periodic short hairpin RNA delivery systems for enhanced therapeutic efficacy“. Thesis, Massachusetts Institute of Technology, 2019. https://hdl.handle.net/1721.1/121821.

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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Chemical Engineering, 2019
Cataloged from PDF version of thesis.
Includes bibliographical references.
RNA interference (RNAi) presents a highly promising approach for cancer therapeutics via specific silencing of disease-implicated genes, but its clinical translation remains severely limited by barriers in delivering short interfering RNA (siRNA). Numerous delivery vehicles have been developed to protect siRNA from degradation, promote target cell uptake, and facilitate endosomal escape into the cytoplasm, where RNAi occurs. However, in vivo instability, low silencing efficiency, undesired toxicity, and immunogenicity remain challenges for current siRNA delivery systems, particularly as the low valency and high rigidity of siRNA make it difficult to condense into stable nanoparticles. Here we engineer the siRNA cargo to make it more amenable to stable encapsulation by using a polymeric form of siRNA, or periodic short hairpin RNA (p-shRNA), as well as design a biodegradable polycationic carrier for efficient in vivo delivery of p-shRNA.
Consisting of tens of linked siRNA repeats, p-shRNA is synthesized by the repeated action of T7 RNA polymerase around a circular DNA template. We first leverage molecular engineering design an open-ended p-shRNA structure that is efficiently processed inside cells into siRNAs, greatly enhancing its silencing potency. Furthermore, the much higher valency and flexibility of p-shRNA compared to siRNA enable more stable complexation with delivery materials. To exploit these advantages of p-shRNA, we optimize biodegradable polycations with hydrophobic regions that promote stable condensation and efficient intracellular release. Our approach unveils key design rules governing p-shRNA delivery, and we develop stabilized p-shRNA complexes that show in vivo therapeutic efficacy in a syngeneic melanoma mouse model. Finally, we extend our p-shRNA platform to act as a dual therapeutic agent, harnessing innate immune activation together with gene silencing.
By modulating the surface of the p-shRNA complexes with an anionic polypeptide, we dramatically enhance innate immune recognition of p-shRNA by pattern recognition receptors while maintaining high silencing efficiency. These dually acting complexes can target ovarian tumors in vivo and prolong survival in a syngeneic ovarian cancer mouse model. Our findings establish a potent, multifunctional RNAi platform that can potentially move RNAi therapeutics closer to clinical translation by addressing the delivery and in vivo efficacy challenges faced by current siRNA systems.
National Science Foundation Graduate Research Fellowshipgrant #1122374
Koch Institute Ludwig Center for Molecular Oncology Graduate Fellowship
Congressionally Directed Medical Research Program Ovarian Cancer Research Program Teal Innovator Award from the Department of Defense (13-1-0151)
by Connie Wu.
Ph. D.
Ph.D. Massachusetts Institute of Technology, Department of Chemical Engineering

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BALESTRA, Dario. „Modified U1snRNAs as innovative therapeutic strategy for inherited coagulation factor deficiencies“. Doctoral thesis, Università degli studi di Ferrara, 2012. http://hdl.handle.net/11392/2388781.

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The theoretical framework in which this study is framed concerns the internationalization of production dynamics of firms abroad. The international literature in this field argues that there is not a conventional definition nor a universally tested theory that can explain all forms of foreign-owned production (see, among others, Dunning, 1988b and 1993a, Ietto-Gillies, 2005 and 2007). In this complex context, a large amount of Italian literature has been published around the theoretical framework of internationalization of production of Italian companies abroad (Tattara, Corò and Volpe, 2006, Mariotti and Mutinelli, 2005, et.al.). Nevertheless, a limited number of quantitative studies are available about the topic of Italian firms “migration” in Romania - as a particular expression of productive internationalization of our companies in this Country (Majocchi, 2002, Unimpresa Romania, 2005 and Antenna Veneto Romania, 2005). Thus, in order to investigate it by an industrial policy perspective a multilevel modelling approach has been applied. In particular, a two level model has been used to determine the effects of Romanian regions (romanian judets) in which Italian manufacturing firms internationalized the production in 2009 on their industrial performance. Based on a business register-based survey a business register of the Italian business community in Romania has been created. The data on Italian manufacturing firms located in Romania in 2009 have been selected from this register. The dataset used for the analysis includes 796 cases of firms internationalized in Romania. Therefore, a two level model has been carried out in order to determine the effects of intra-industry characteristics of these firms (i.e. Firm size and Firm Industrial specialization) on their industrial performance in 2009 both at individual and area level. The model results have shown that: as the firms dimension increase they have to be extremely sensible in the choice of the romanian region in which they want to (de)localize the production. Furthermore, the choice of the romanian region of productive delocalization has to be chosen by firms according to their sectors of activity.

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Al-Mazedi, Maryam. „A therapeutic approach to chronic myeloid leukaemia using short hairpin RNA molecules“. Thesis, King's College London (University of London), 2012. https://kclpure.kcl.ac.uk/portal/en/theses/a-therapeutic-approach-to-chronic-myeloid-leukaemia-using-short-hairpin-rna-molecules(185139fb-ed9b-46d7-a5a8-04532c44640b).html.

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Chronic myeloid leukaemia (CML) was one of the first cancers to be linked to a chromosomal abnormality, the Philadelphia chromosome. This chromosome results in a translocation between chromosomes 9 and 22, where the ABL gene on chromosome 9, a tyrosine kinase, is translocated to the BCR gene region on chromosome 22 giving rise to an abnormal BCR/ABL fusion gene. The resultant fusion gene has an abnormally upregulated tyrosine kinase activity that results in an increase in the proliferation of immature white blood cells, thus leading to the development of CML. There are several breakpoints that can occur in the BCR gene two of which give rise to 95% of CML cases. These fusion points are called the β3α2 and β2α2 depending on where the chromosomal breakages occur in the BCR gene. The aim of the project was to establish a new method of treatment for CML through the use of RNAi to abolish the increase in tyrosine kinase activity of the abnormal fusion gene product. The K562 and KCL22 cell lines incorporating the β3α2 and β2α2 fusion points respectively were used in this project. The fusion points were cloned and sequenced. The human U6 and H1 promoters, were selected for the production of the antisense molecules and were obtained by PCR of K562 cDNA. Short hairpin RNA molecules were designed to the sequences of the β3α2 and the β2α2 fusion points. These designed shRNA molecules were synthesized as oligonucleotides and were incorporated into a reverse PCR primer. Cassettes containing shRNA molecules and a respective promoter were produced by means of PCR and the products cloned into pB12mcs-‐eGFP vector, which was used as a GFP reporter system. Constructs were then transfected into the appropriate cell lines, and expression studies including qPCR and Western blot analysis were conducted, to examine the effects of the designed shRNA constructs to their target sites on both mRNA and protein levels. In addition, these experiments also indicate the efficiency of the construct and also their specificity to their targets. qPCR and Western blot analysis, show that both the shRNA molecules designed against the β3α2 and the β2α2 fusion points, efficiently induced RNAi based gene silencing to their target sites. In addition, the designed constructs show high specificity to only its target sites and not to other unrelated or related genes. These results point towards the use of molecular modulation of gene expression as a promising strategy for potential CML therapy.

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Jubair, Luqman Khaleel. „Next-Generation Cancer Therapies: The Therapeutic Potential of RNA-Directed Gene-Editing“. Thesis, Griffith University, 2018. http://hdl.handle.net/10072/382679.

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The discovery of the bacterial Clustered, Regularly Interspaced Short Palindromic Repeats (CRISPR) and associated Cas9 protein, and its ability to edit genes in mammalian cells is poised to revolutionise our ability to treat genetic diseases, particularly in the cancer setting where the driver genes are known. Indeed, CRISPR/Cas9 was shown to effectively edit any gene of interest with high efficiency and at low cost. However, a major challenge to treating cancer is the heterogeneity of the genetic alterations and the ongoing accumulation of new mutations that enable cancers to survive and drug resistance to emerge. With the increasing knowledge of cancer biology, thanks to the advances in DNA sequencing technologies, the low cost, and the ability to edit genes with CRISPR/Cas9 with high efficiency, it is now possible to develop more targeted anticancer therapeutics with promising outcomes. Despite the exceptional CRISPR/Cas9 gene-editing features, the early studies found several limitations to its potential use as a human gene therapy, such as the targeting specificity of CRISPR/Cas9, the in vivo delivery of the treatment with minimal systemic toxicity, the in vivo efficacy under immunocompetent conditions, the immunogenicity of CRISPR/Cas9 and the delivery vehicle when delivered systemically, and whether the introduced edits would induce an immune response. Particularly for cancer treatment, challenges can be broadly categorized into: the in vivo efficacy of CRISPR/Cas9 therapeutics, the in vivo delivery of the treatment to target tissue with high transfection efficiency, and the heterogeneity of genetic mutations in cancer, and thus targeting a known gene may not be enough to cure cancer. To enable the utilisation of CRISPR/Cas9 as an anticancer therapy, the above-mentioned challenges need to be addressed. We utilised the well-established Human Papillomavirus (HPV)-driven cervical cancer models due to their addiction on the expression of HPV oncogenes, namely E6 and E7, for their survival and progression, and thus enabled us to assess the efficacy and the delivery of CRISPR/Cas9 therapies, independent of cancer heterogeneity. To improve the on-target specificity, we assessed the feasibility of using the highly specific variant of Cas9, the catalytically inactive Cas9 fused to the dimerization-dependent cutting domain, FokI, or FokI-dCas9, and compared its editing efficiency on target genes and the effect on downstream protein expression compared to the wild type (WT) Cas9. Our results proved that the FokI-dCas9 is ineffective as a cancer therapeutic, particularly when the target genes are short. We further explored the repair mechanism of the CRISPR/Cas9-mediated double-stranded breaks (DSB) and found that the high-fidelity homology-directed repair (HDR) was modest, accounting for ≈ 8%, compared to the random non-homology end joining (NHEJ) repair, which accounted for ≈ 80% of the edited cells, with a significant inhibition of cancer cell proliferation. We also showed that the cell death was apoptotic, mediated by the reactivation of the tumour suppressor p53 protein when E6 gene was targeted, or the restoration of retinoblastoma protein (Rb) when E7 gene was targeted. To test the feasibility of the intravenous delivery of CRISPR/Cas9, we optimised a protocol to package the treatment in PEGylated liposomes by using the Hydration-of-Freeze-Dried-Matrix (HFDM) method and showed that these liposomes effectively protected the payload against serum nucleases. Furthermore, the intravenously administered CRISPR/Cas9 against HPV 16E7 and HPV 18E7 oncogenes, coated in PEGylated liposomes, effectively cleared established cervical cancer xenografts in immunocompromised mouse models. Next, we aimed to explore if the in vivo efficacy would be affected by the immunogenicity of the treatment under immunocompetent conditions. We showed for the first time that CRISPR/Cas9 therapies eliminated HPV16E7-driven tumour xenografts entirely in syngeneic mice, with no significant inflammation or hepatic toxicity. In addition, an ideal therapeutic outcome would be the induction of an immunogenic cell death (ICD), such that recurrent tumours would be eliminated by the host immune system. Therefore, we explored the immunogenicity of cell death and showed for the first time that CRISPR/Cas9-mediated cell death was not immunogenic. Overall, this research demonstrates that CRISPR/Cas9 therapeutics are very effective for the treatment of oncogene-addicted cancers. We showed that the PEGylated liposomes can be an ideal delivery vehicle for CRISPR/Cas9 therapies despite the large payloads, with no significant immune response or toxicity, and provided new insights into harnessing CRISPR/Cas9 technology as an anticancer therapeutic.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Griffith Health
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Elmén, Joacim. „Nucleic acid based therapeutic approaches /“. Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-047-8/.

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Hong, Lingzi. „Act1-Mediated RNA Metabolism in IL-17-Driven Inflammatory Diseases“. Case Western Reserve University School of Graduate Studies / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=case162673878106271.

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Chitiprolu, Maneka. „Novel Regulatory Mechanisms of Autophagy in Human Disease: Implications for the Development of Therapeutic Strategies“. Thesis, Université d'Ottawa / University of Ottawa, 2018. http://hdl.handle.net/10393/38441.

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The dysfunction of autophagy pathways has been linked to the development and progression of numerous human diseases, in particular neurological disorders and cancer. Investigating these pathological autophagy mechanisms is essential to gain insights into the underlying disease mechanisms, identify novel biomarkers, and develop targeted therapies. In this thesis, I present three manuscripts that investigate the regulatory mechanisms of autophagy machinery in human diseases. In the first manuscript (Chitiprolu et al., 2018), we investigated the mechanism of p62-mediated selective autophagic clearance of RNA stress granules implicated in Amyotrophic Lateral Sclerosis (ALS). Repeat expansions in C9ORF72, the major cause of ALS, reduce C9ORF72 levels but how this impacts stress granules is uncertain. By employing mass spectrometry, high resolution imaging and biochemical assays, we demonstrated that the autophagy receptor p62 associates with C9ORF72 to eliminate stress granules by autophagy. This requires p62 to associate with proteins that are symmetrically methylated on arginines. Patients with C9ORF72 repeat expansions accumulate symmetric arginine dimethylated proteins which co-localize with p62. This suggests that C9ORF72 initiates a cascade of ALS-linked proteins (C9ORF72, p62, SMN, FUS) to recognize stress granules for degradation by autophagy and hallmarks of a defect in this process are observable in ALS patients. The second manuscript (Guo, Chitiprolu et al., 2014) describes the mechanism by which autophagy degrades retrotransposon RNA from both long and short interspersed elements, thereby preventing new retrotransposon insertions into the genome. By employing quantitative imaging tools, we demonstrated that retrotransposon RNA localizes to RNA granules that are selectively degraded by the autophagy receptors NDP52 and p62. Mice lacking a copy of Atg6/Beclin1, a gene critical for autophagy, also accumulate both retrotransposon RNA and genomic insertions. This suggests a mechanism for the increased tumorigenesis upon autophagy inhibition and therefore a role for autophagy in tempering evolutionary change. Finally, the third manuscript (Guo, Chitiprolu et al., 2017) examines the intersection of autophagy machinery with exosome release and function in cancer metastasis. By employing dynamic light scattering, Nanosight particle tracking, electron microscopy, super-resolution imaging and Western blotting, we robustly quantified exosome identity and purity in multiple cell lines. We demonstrated that exosome production is strongly reduced in cells lacking Atg5 and Atg16L1, but this is independent of Atg7 and canonical autophagy. The effect of Atg5 on exosome production promotes the migration and in vivo metastasis of orthotopic breast cancer cells. These findings delineate autophagy-independent pathways by which autophagy-related genes can contribute to metastasis. Taken together, data presented in the three manuscripts highlight the molecular mechanisms of autophagy core machinery proteins and selective receptors such as Atg5, p62 and NDP52, in the pathogenesis of cancer and neurodegeneration. In these diseases characterized by mutations in autophagy pathways, the mechanisms we uncover provide insights into their causes and serve as potential therapeutic targets.

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Bücher zum Thema "RNA therapeutic"

A, Mulligan James. MicroRNA: Expression, detection, and therapeutic strategies. New York: Nova Science, 2011.

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Sioud, Mouldy. RNA interference: Challenges and therapeutic opportunities. New York: Humana Press, 2015.

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Hiroshi, Takaku, und Yamamoto Naoki 1945-, Hrsg. RNAi therapeutics, 2006. Trivandrum, Kerala, India: Transworld Research Network, 2006.

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Arbuthnot, Patrick, und Marc S. Weinberg. Applied RNAi: From fundamental research to therapeutic applications. Norfolk, UK: Caister Academic Press, 2014.

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RNA therapeutics: Function, design, and delivery. New York: Humana Press, 2010.

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Yasko, Amy. Heal your body naturally: The power of RNA. [United States]: Matrix Development Pub., 2004.

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1947-, Scanlon Kevin J., Hrsg. Therapeutic applications of ribozymes. Totowa, N.J: Humana Press, 1998.

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Therapeutic applications of ribozymes and riboswitches: Methods and protocols. New York: Humana Press, 2014.

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Thomas, Tuschl, Rossi John J und New York Academy of Sciences, Hrsg. Oligonucleotide therapeutics. Boston, Mass: Blackwell on behalf of the New York Academy of Sciences, 2006.

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1922-, Weiss Benjamin, Hrsg. Antisense oligodeoxynucleotides and antisense RNA: Novel pharmacological and therapeutic agents. Roca Raton, Fla: CRC Press, 1997.

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Buchteile zum Thema "RNA therapeutic"

Kang, Moo Rim, Gongcheng Li, Tiejun Pan, Jin-Chun Xing und Long-Cheng Li. „Development of Therapeutic dsP21-322 for Cancer Treatment“. In RNA Activation, 217–29. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-4310-9_16.

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Sioud, Mouldy. „RNA Interference: Mechanisms, Technical Challenges, and Therapeutic Opportunities“. In RNA Interference, 1–15. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1538-5_1.

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Iversen, Per Ole, und Mouldy Sioud. „Engineering Therapeutic Cancer Vaccines That Activate Antitumor Immunity“. In RNA Interference, 263–68. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1538-5_15.

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Pierce, Jacob B., Haoyang Zhou, Viorel Simion und Mark W. Feinberg. „Long Noncoding RNAs as Therapeutic Targets“. In Long Noncoding RNA, 161–75. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-92034-0_9.

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Seth, Shaguna, Michael V. Templin, Gregory Severson und Oleksandr Baturevych. „A Potential Therapeutic for Pandemic Influenza Using RNA Interference“. In RNA Interference, 397–422. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-588-0_26.

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Guha, Shalini, Priyanka Barman, Aruniti Manawa und Sukesh R. Bhaumik. „Nuclear Export of mRNAs with Disease Pathogenesis and Therapeutic Implications“. In RNA Technologies, 371–95. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-08415-7_17.

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Cheng, Yi, Dong Zhang, Travis Hurst, Xiaoqin Zou, Paloma H. Giangrande und Shi-Jie Chen. „RNA Structural Modeling for Therapeutic Applications“. In RNA Nanotechnology and Therapeutics, 447–61. 2. Aufl. Boca Raton: CRC Press, 2022. http://dx.doi.org/10.1201/9781003001560-47.

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Yoo, Ji Young, Balveen Kaur, Tae Jin Lee und Peixuan Guo. „MicroRNAs in Human Cancers and Therapeutic Applications“. In RNA Nanotechnology and Therapeutics, 529–42. 2. Aufl. Boca Raton: CRC Press, 2022. http://dx.doi.org/10.1201/9781003001560-54.

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Szymański, Maciej, und Jan Barciszewski. „Noncoding RNAs as Therapeutic Targets“. In RNA Technologies and Their Applications, 393–418. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-12168-5_18.

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Akaneya, Yukio. „A New Approach for Therapeutic Use by RNA Interference in the Brain“. In RNA Interference, 313–24. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-588-0_20.

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Konferenzberichte zum Thema "RNA therapeutic"

Ke, Yonggang, DongMoon Shin und Georgia Chen. „Abstract 3635: RNA-based nanostructures for therapeutic siRNA delivery“. In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-3635.

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Endo-Takahashi, Yoko, Yoichi Negishi, Ryo Suzuki, Kazuo Maruyama, Yukihiko Aramaki, Yoichiro Matsumoto, Lawrence A. Crum und Gail Reinette ter Haar. „Novel siRNA-loaded Bubble Liposomes with Ultrasound Exposure for RNA Interference“. In 10TH INTERNATIONAL SYMPOSIUM ON THERAPEUTIC ULTRASOUND (ISTU 2010). AIP, 2011. http://dx.doi.org/10.1063/1.3607930.

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Loeb, David M., Breelyn A. Wilky, Catherine Kim, Elizabeth Montgomery und Venu Raman. „Abstract A77: RNA helicase DDX3 – A novel therapeutic target in sarcoma“. In Abstracts: AACR Special Conference: Pediatric Cancer at the Crossroads: Translating Discovery into Improved Outcomes; November 3-6, 2013; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.pedcan-a77.

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Hao, Liangliang, Justin Lo und Sangeeta Bhatia. „Abstract 5088: Tumor penetrating RNA delivery for therapeutic benefit of pancreatic cancer“. In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-5088.

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Pachera, E., A. Wunderlin, S. Assassi, G. Salazar, M. Frank-Bertoncelj, R. Dobrota, M. Brock et al. „OP0086 Long noncoding RNA H19X as a new therapeutic target for fibrosis“. In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.4877.

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Woo, C., N. Clark, A. Sarode, N. Kaushal, K. Tran, T. Efthymiou, J. Abysalh et al. „A Messenger RNA (mRNA)-Based Therapeutic Designed to Treat Primary Ciliary Dyskinesia“. In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a1138.

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Goueli, Said A., und Kevin Hsiao. „Abstract 1162: Monitoring COVID-19 RNA methyltransferases activities for developing therapeutic drugs“. In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-1162.

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Ghazaly, Essam A., John Le Quesne, Dahai Jiang, Selanere L. Mangala, James Chettle, Cristian Rodriguez-Aguayo, Gabriel Lopez-Berestein et al. „Abstract B30: The RNA-binding protein LARP1 is a cancer therapeutic target“. In Abstracts: AACR Special Conference on Translational Control of Cancer: A New Frontier in Cancer Biology and Therapy; October 27-30, 2016; San Francisco, CA. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.transcontrol16-b30.

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Mitra, Sheetal A., Anirban P. Mitra, Jonathan D. Buckley, William A. May, Philipp Kapranov, Robert J. Arceci und Timothy J. Triche. „Abstract A43: Therapeutic importance of a long noncoding RNA in Ewing sarcoma“. In Abstracts: AACR Special Conference: Pediatric Cancer at the Crossroads: Translating Discovery into Improved Outcomes; November 3-6, 2013; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.pedcan-a43.

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Berichte der Organisationen zum Thema "RNA therapeutic"

Chu, Jimmy, Kathryn Black, Luis Santos und Steven Wall. The challenges of using RNA as a therapeutic or a gene-editing tool. Biophorum, November 2021. http://dx.doi.org/10.46220/2021cgt006.

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ARIZONA STATE UNIV TEMPE CANCER RESEARCH INST. Discovery and Development of Therapeutic Drugs Against Lethal Human RNA Viruses: A Multidisciplinary Assault. Fort Belvoir, VA: Defense Technical Information Center, März 1992. http://dx.doi.org/10.21236/ada251561.

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Pettit, George R. Discovery and Development of Therapeutic Drugs against Lethal Human RNA Viruses: a Multidisciplinary Assault. Fort Belvoir, VA: Defense Technical Information Center, Juli 1991. http://dx.doi.org/10.21236/ada239742.

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Pettit, George R. Discovery and Development of Therapeutic Drugs against Lethal Human RNA- Viruses: A Multidisciplinary Assault. Fort Belvoir, VA: Defense Technical Information Center, Februar 1990. http://dx.doi.org/10.21236/ada219393.

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Chen, Shuo. Anti-Androgen Receptor RNA Enzyme as a Novel Therapeutic Agent for Prostate Cancer In Vivo. Fort Belvoir, VA: Defense Technical Information Center, August 2006. http://dx.doi.org/10.21236/ada462865.

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Chakraborty, Srijani. The Dawn of RNA Therapeutics. Spring Library, Dezember 2020. http://dx.doi.org/10.47496/sl.blog.19.

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Giordano, Tony. Development of RNAi Libraries for Target Validation and Therapeutics. Fort Belvoir, VA: Defense Technical Information Center, März 2006. http://dx.doi.org/10.21236/ada452228.

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Mao, Hai-Quan. Nanoparticle Delivery of RNAi Therapeutics for Ocular Vesicant Injury. Fort Belvoir, VA: Defense Technical Information Center, April 2014. http://dx.doi.org/10.21236/ada613316.

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Moore, Melissa. Phase II - Procurement of State of the Art Research Equipment to Support Faculty Members with the RNA Therapeutics Institute, a component of the Advanced Therapeutics Cluster at the University of Massachusetts Medical School. Office of Scientific and Technical Information (OSTI), Oktober 2011. http://dx.doi.org/10.2172/1037882.

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Chen, Xiaole, Peng Wang, Yunquan Luo, Yi-Yu Lu, Wenjun Zhou, Mengdie Yang, Jian Chen, Zhi-Qiang Meng und Shi-Bing Su. Therapeutic Efficacy Evaluation and Underlying Mechanisms Prediction of Jianpi Liqi Decoction for Hepatocellular Carcinoma. Science Repository, September 2021. http://dx.doi.org/10.31487/j.jso.2021.02.04.sup.

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Annotation:

Objective: The aim of this study was to assess the therapeutic effects of Jianpi Liqi decoction (JPLQD) in hepatocellular carcinoma (HCC) and explore its underlying mechanisms. Methods: The characteristics and outcomes of HCC patients with intermediate stage B who underwent sequential conventional transcatheter arterial chemoembolization (cTACE) and radiofrequency ablation (RFA) only or in conjunction with JPLQD were analysed retrospectively. The plasma proteins were screened using label-free quantitative proteomics analysis. The effective mechanisms of JPLQD were predicted through network pharmacology approach and partially verified by ELISA. Results: Clinical research demonstrated that the Karnofsky Performance Status (KPS), traditional Chinese medicine (TCM) syndrome scores, neutropenia and bilirubin, median progression-free survival (PFS), and median overall survival (OS) in HCC patients treated with JPLQD were superior to those in patients not treated with JPLQD (all P<0.05). The analysis of network pharmacology, combined with proteomics, suggested that 52 compounds targeted 80 potential targets, which were involved in the regulation of multiple signaling pathways, especially affecting the apoptosis-related pathways including TNF, p53, PI3K-AKT, and MAPK. Plasma IGFBP3 and CA2 were significantly up-regulated in HCC patients with sequential cTACE and RFA therapy treated with JPLQD than those in patients not treated with JPLQD (P<0.001). The AUC of the IGFBP3 and CA2 panel, estimated using ROC analysis for JPLQD efficacy evaluation, was 0.867. Conclusion: These data suggested that JPLQD improves the quality of life, prolongs the overall survival, protects liver function in HCC patients, and exhibits an anticancer activity against HCC. IGFBP3 and CA2 panels may be potential therapeutic targets and indicators in the efficacy evaluation for JPLQD treatment, and the effective mechanisms involved in the regulation of multiple signaling pathways, possibly affected the regulation of apoptosis.

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