Relevant bibliographies by topics / MicroRNA profiling

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  1. Journal articles
  2. Dissertations / Theses
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  4. Book chapters
  5. Conference papers
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Academic literature on the topic 'MicroRNA profiling'

Author: Grafiati
Published: 10 September 2021
Last updated: 10 March 2023

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Journal articles on the topic "MicroRNA profiling"

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Jongen-Lavrencic, Mojca, Su Ming Sun, Menno K. Dijkstra, Peter J. M. Valk, and Bob Löwenberg. "MicroRNA expression profiling in relation to the genetic heterogeneity of acute myeloid leukemia." Blood 111, no. 10 (May 15, 2008): 5078–85. http://dx.doi.org/10.1182/blood-2008-01-133355.

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Abstract Acute myeloid leukemia (AML) is a highly diverse disease characterized by various cytogenetic and molecular abnormalities. MicroRNAs are small noncoding RNAs that show variable expression during myeloid differentiation. MicroRNA expression in marrow blasts in 215 cases of newly diagnosed and (cyto)genetically defined AML was assessed using quantitative reverse-transcription–polymerase chain reaction (RT-PCR) for 260 human microRNAs. In the same series, mRNA gene expression profiles were established, allowing a direct comparison between microRNA and mRNA expression. We show that microRNA expression profiling following unsupervised analysis reveals distinctive microRNA signatures that correlate with cytogenetic and molecular subtypes of AML (ie, AMLs with t(8;21), t(15;17), inv(16), NPM1, and CEBPA mutations). Significantly differentially expressed microRNAs for genetic subtypes of AML were identified. Specific microRNAs with established oncogenic and tumor suppressor functions, such as microRNA-155, microRNA-21, and let-7, appear to be associated with particular subtypes. Combinations of selected sets of microRNAs could predict cytogenetically normal AML with mutations in the genes of NPM1 and CEBPA and FLT3-ITD with similar accuracy as mRNA probe set combinations defined by gene expression profiling. MicroRNA expression apparently bears specific relationships to the heterogeneous pathobiology of AML. Distinctive microRNA signatures appear of potential value in the clinical diagnosis of AML.
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Kiseleva, Y. Y., K. G. Ptitsyn, S. P. Radko, V. G. Zgoda, and A. I. Archakov. "Digital droplet PCR - a prospective technological approach to quantitative profiling of microRNA." Biomeditsinskaya Khimiya 62, no. 4 (2016): 403–10. http://dx.doi.org/10.18097/pbmc20166204403.

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MicroRNA is a special type of regulatory molecules governing gene expression. Circulating microRNAs found in blood and other biological fluids are considered today as potential biomarkers of human pathology. Presently, quantitative alterations of particular microRNAs are revealed for a large number of oncological diseases and other disorders. The recently emerged method of digital droplet PCR (ddPCR) possesses a number of advantages making this method the most suitable for verification and validation of perspective microRNA markers of human pathologies. Among these advantages are the high accuracy and reproducibility of microRNA quantification as well as the capability to directly measure the absolute number of microRNA copies with the large dynamic range and a high throughput. The paper reviews microRNA biogenesis, the origin of circulating microRNAs, and methods used for their quantification. The special technical features of ddPCR, which make it an attractive method both for studying microRNAs as biomarkers of human pathologies and for basic research devoted to aspects of gene regulation by microRNA molecules, are also discussed.
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Wang, Xiaoxia, Chun Song, Xiao Zhou, Xiaorui Han, Jun Li, Zengwu Wang, Haibao Shang, Yuli Liu, and Huiqing Cao. "Mitochondria Associated MicroRNA Expression Profiling of Heart Failure." BioMed Research International 2017 (2017): 1–10. http://dx.doi.org/10.1155/2017/4042509.

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Heart failure (HF) is associated with mitochondrial dysfunction and energy metabolism impairment. MicroRNAs are implicated in the development of heart failure. However, the mitochondria enriched microRNA during heart failure remains elusive. Here, we generated a pressure overload-induced early and late stage heart failure model at 4 weeks and 8 weeks following transverse aortic constriction (TAC) in mice. We found that expression of mitochondrion protein COX4 was highly enriched in isolated mitochondria from cardiac tissues while GAPDH could hardly be detected. Furthermore, small RNA sequencing for mitochondria RNAs from failing hearts was performed. It was found that 69 microRNAs were upregulated and 2 were downregulated in early heart failure, while 16 microRNAs were upregulated and 6 were downregulated in late heart failure. 15 microRNA candidates were measured in both mitochondria and total cardiac tissues of heart failure by real-time PCR. MiR-696, miR-532, miR-690, and miR-345-3p were enriched in mitochondria from the failing heart at early stage. Bioinformatics analysis showed that mitochondria enriched microRNAs in HF were associated with energy metabolism and oxidative stress pathway. For the first time, we demonstrated microRNAs were enriched in mitochondria during heart failure, which established a link between microRNA and mitochondrion in heart failure.
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Liu, Xiqiang, Zugen Chen, Jinsheng Yu, James Xia, and Xiaofeng Zhou. "MicroRNA Profiling and Head and Neck Cancer." Comparative and Functional Genomics 2009 (2009): 1–11. http://dx.doi.org/10.1155/2009/837514.

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Head and neck/oral cancer (HNOC) is a devastating disease. Despite advances in diagnosis and treatment, mortality rates have not improved significantly over the past three decades. Improvement in patient survival requires a better understanding of the disease progression so that HNOC can be detected early in the disease process and targeted therapeutic interventions can be deployed. Accumulating evidence suggests that microRNAs play important roles in many human cancers. They are pivotal regulators of diverse cellular processes including proliferation, differentiation, apoptosis, survival, motility, and morphogenesis. MicroRNA expression patterns may become powerful biomarkers for diagnosis and prognosis of HNOC. In addition, microRNA therapy could be a novel strategy for HNOC prevention and therapeutics. Recent advances in microRNA expression profiling have led to a better understanding of the cancer pathogenesis. In this review, we will survey recent technological advances in microRNA profiling and their applications in defining microRNA markers/targets for cancer prediction, diagnostics, treatment, and prognostics. MicroRNA alterations that consistently identified in HNOC will be discussed, such as upregulation of miR-21, miR-31, miR-155, and downregulation of miR-26b, miR-107, miR-133b, miR-138, and miR-139.
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Chen, Zujian, Tianwei Yu, Robert J. Cabay, Yi Jin, Ishrat Mahjabeen, Xianghong Luan, Lei Huang, Yang Dai, and Xiaofeng Zhou. "miR-486-3p, miR-139-5p, and miR-21 as Biomarkers for the Detection of Oral Tongue Squamous Cell Carcinoma." Biomarkers in Cancer 9 (January 2017): 1179299X1700900. http://dx.doi.org/10.1177/1179299x1700900001.

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Oral tongue squamous cell carcinoma (TSCC) is a complex disease with extensive genetic and epigenetic defects, including microRNA deregulation. The aims of the present study were to test the feasibility of performing the microRNA profiling analysis on archived TSCC specimens and to assess the potential diagnostic utility of the identified microRNA biomarkers for the detection of TSCC. TaqMan array-based microRNA profiling analysis was performed on 10 archived TSCC samples and their matching normal tissues. A panel of 12 differentially expressed microRNAs was identified. Eight of these differentially expressed microRNAs were validated in an independent sample set. A random forest (RF) classification model was built with miR-486-3p, miR-139-5p, and miR-21, and it was able to detect TSCC with a sensitivity of 100% and a specificity of 86.7% (overall error rate = 6.7%). As such, this study demonstrated the utility of the archived clinical specimens for microRNA biomarker discovery. The feasibility of using microRNA biomarkers (miR-486-3p, miR-139-5p, and miR-21) for the detection of TSCC was confirmed.
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Segura-Wang, Maia, Bertrand Grenier, Suzana Ilic, Ursula Ruczizka, Maximiliane Dippel, Moritz Bünger, Matthias Hackl, and Veronika Nagl. "MicroRNA Expression Profiling in Porcine Liver, Jejunum and Serum upon Dietary DON Exposure Reveals Candidate Toxicity Biomarkers." International Journal of Molecular Sciences 22, no. 21 (November 7, 2021): 12043. http://dx.doi.org/10.3390/ijms222112043.

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Deoxynivalenol (DON), a frequent mycotoxin worldwide, impairs human and animal health. The response of microRNAs, small non-coding RNAs, to DON has been scarcely investigated, but holds remarkable potential for biomarker applications. Hence, we aimed to investigate DON-induced changes in the microRNA expression in porcine liver, jejunum and serum by combining targeted and untargeted analyses. Piglets received uncontaminated feed or feed containing 900 µg/kg and 2500 µg/kg DON for four weeks, followed by a wash-out period. In tissue, only slight changes in microRNA expression were detected, with ssc-miR-10b being downregulated in liver of DON-exposed piglets. In serum, several microRNAs were differentially expressed upon DON exposure, four of which were validated by qPCR (ssc-miR-16, ssc-miR-128, ssc-miR-451, ssc-miR-205). The serum microRNA response to DON increased over time and declined after removal of contaminated diets. Receiver operating curve analyses for individual microRNAs were significant, and a combination of the four microRNAs increased the predictive capacity for DON exposure. Predicted microRNA target genes showed enrichment of several pathways including PIK3-AKT, Wnt/β-catenin, and adherens junctions. This study gives, for the first time, a comprehensive view of the porcine microRNA response to DON, providing a basis for future research on microRNAs as biomarkers for mycotoxins.
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Adamia, Sophia, Samir B. Amin, Cheng Li, Christopher J. Patterson, Herve AvetLoiseau, Stephane Minvielle, Philippe Moreau, Kenneth C. Anderson, Nikhil C. Munshi, and Steven Treon. "High-Throughput Microrna Profiling in Patients with Waldenstrom’s Macroglobulinemia." Blood 112, no. 11 (November 16, 2008): 1704. http://dx.doi.org/10.1182/blood.v112.11.1704.1704.

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Abstract Waldenström’s macroglobulinemia (WM) is an incurable B cell malignancy characterized by the accumulation of IgM secreting clonally related bone marrow lymphoplasmacytic cells (LPC) including CD19+ B-cells and CD138+ plasma cells. Despite intense research efforts, the pathogenetic basis for this disease remains to be clarified. MicroRNAs are small noncoding RNAs that regulate the expression of protein-coding genes by inducing translational inhibition and through cleavage of targeted transcripts by partial or complete base pairing. We therefore evaluated the expression of 384 microRNAs in CD19+ and CD138+ sorted bone marrow lymphoplasmacytic from 13 untreated WM patients, and compared their expression profiling to analogous lymphoplasmacytic cells taken from the bone marrows of 13 healthy donors. Data obtained from microRNA arrays was analyzed using SDS, RQ manager, R and dChip softwares. Relative expression was calculated using the comparative Ct method through RQ manager and dChip softwares. Of the 384 microRNAs evaluated in CD19+ patient cells, miR-192, -125b, -21, -155 demonstrated significant upregulation, whereas miR-181c, -572, and -650 were significantly down regulated compared to healthy donor CD19+ bone marrow cells (p<0.05). Analysis of bone marrow derived CD138+ cells from WM patients demonstrated significant upregulation in miR-192, -193b, -17-3p, -585, -148b, whereas miR-29c, -155, -126, -148a, -125a, -181d, -30a-3p, let-7b, let-7c were downregulated in comparison to healthy donor CD138+ bone marrow cells (p<0.05). Importantly, characterization of the modulated microRNAs found in these studies demonstrated a critical role in growth and survival pathways through modulation of several genes including HOX, BCL-2 and c-myc. Taken together, these studies demonstrate significant differences in microRNA expression between comparable WM and healthy donor lymphoplasmacytic cell populations, and identify aberrancies in microRNAs with a pivotal role in the growth and survival of B-cells.
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Pimentel, Fernando, Patricia Bonilla, Yashwanth G. Ravishankar, Alec Contag, Nimish Gopal, Sarah LaCour, Trenton Lee, and Angelika Niemz. "Technology in MicroRNA Profiling." Journal of Laboratory Automation 20, no. 5 (October 2015): 574–88. http://dx.doi.org/10.1177/2211068214561788.

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Munker, Reinhold, and George A. Calin. "MicroRNA profiling in cancer." Clinical Science 121, no. 4 (April 20, 2011): 141–58. http://dx.doi.org/10.1042/cs20110005.

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The diagnosis of cancer has undergone major changes in the last 40 years. Once based purely on morphology, diagnosis has come to incorporate immunological, cytogenetic and molecular methods. Many cancers, especially leukaemias, are now defined by molecular markers. Gene expression profiling based on mRNA has led to further refinement of the classification and diagnosis of cancer. More recently, miRNAs (microRNAs), among other small non-coding RNA molecules, have been discovered and found to be major players in cell biology. miRNAs, having both oncogenic and tumour-suppressive functions, are dysregulated in many types of cancer. miRNAs also interfere with metastasis, apoptosis and invasiveness of cancer cells. In the present review, we discuss recent advances in miRNA profiling in human cancer. We discuss both frequent and rare tumour types and give an outlook on future developments.
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Iorio, Marilena V., and Carlo M. Croce. "MicroRNAs in Cancer: Small Molecules With a Huge Impact." Journal of Clinical Oncology 27, no. 34 (December 1, 2009): 5848–56. http://dx.doi.org/10.1200/jco.2009.24.0317.

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Every cellular process is likely to be regulated by microRNAs, and an aberrant microRNA expression signature is a hallmark of several diseases, including cancer. MicroRNA expression profiling has indeed provided evidence of the association of these tiny molecules with tumor development and progression. An increasing number of studies have then demonstrated that microRNAs can function as potential oncogenes or oncosuppressor genes, depending on the cellular context and on the target genes they regulate. Here we review our current knowledge about the involvement of microRNAs in cancer and their potential as diagnostic, prognostic, and therapeutic tools.
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Dissertations / Theses on the topic "MicroRNA profiling"

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Jurcevic, Sanja. "MicroRNA expression profiling in endometrial adenocarcinoma." Doctoral thesis, Örebro universitet, Institutionen för hälsovetenskap och medicin, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-41640.

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Laginestra, Maria Antonella <1975&gt. "MicroRNA profiling nei linfomi a cellule T periferiche." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2013. http://amsdottorato.unibo.it/5813/1/Tesi-Laginestra.pdf.

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I linfomi a cellule T periferiche rappresentano circa il 12% di tutte le neoplasie linfoidi.In questo studio, abbiamo effettuato un’analisi di miRNA profiling (TaqMan Array MicroRNA Cards A) su 60 campioni FFPE suddivisi in: PTCLs/NOS (N=25), AITLs (N=10), ALCLs (N=12) e cellule T normali (N=13). Abbiamo identificato 4 miRNA differenzialmente espressi tra PTCLs e cellule T normali. Inoltre, abbiamo identificato tre set di mirna che discriminano le tre entita di PTCLs nodali
AIMs: Here, we performed an extensive miRNA profiling of PTCLs in order to identify differentially expressed miRNA, either involved in their pathogenesis or potentially useful for their differential diagnosis. Methods: We studied by miRNA profiling (TaqMan Array MicroRNA Cards A) 60 samples including PTCLs/NOS (N=25), AITLs (N=10), ALCLs (N=12) and normal T cells (N=13); in addition, 40 independent PTCL cases were studied by qRT-PCR as validation. We assess a GEP and miRNA Profiling. Findings: we identified 256 miRNA differentiating the two groups. In conclusion, miRNA profiling allowed to identify miRNA possibly involved in PTCL pathogenesis and to develop a novel diagnostic tool for the differential diagnosis of the commonest subtypes.
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Laginestra, Maria Antonella <1975&gt. "MicroRNA profiling nei linfomi a cellule T periferiche." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2013. http://amsdottorato.unibo.it/5813/.

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I linfomi a cellule T periferiche rappresentano circa il 12% di tutte le neoplasie linfoidi.In questo studio, abbiamo effettuato un’analisi di miRNA profiling (TaqMan Array MicroRNA Cards A) su 60 campioni FFPE suddivisi in: PTCLs/NOS (N=25), AITLs (N=10), ALCLs (N=12) e cellule T normali (N=13). Abbiamo identificato 4 miRNA differenzialmente espressi tra PTCLs e cellule T normali. Inoltre, abbiamo identificato tre set di mirna che discriminano le tre entita di PTCLs nodali
AIMs: Here, we performed an extensive miRNA profiling of PTCLs in order to identify differentially expressed miRNA, either involved in their pathogenesis or potentially useful for their differential diagnosis. Methods: We studied by miRNA profiling (TaqMan Array MicroRNA Cards A) 60 samples including PTCLs/NOS (N=25), AITLs (N=10), ALCLs (N=12) and normal T cells (N=13); in addition, 40 independent PTCL cases were studied by qRT-PCR as validation. We assess a GEP and miRNA Profiling. Findings: we identified 256 miRNA differentiating the two groups. In conclusion, miRNA profiling allowed to identify miRNA possibly involved in PTCL pathogenesis and to develop a novel diagnostic tool for the differential diagnosis of the commonest subtypes.
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Bueno, Marinas Maria. "MicroRNA profiling in Arrhythmogenic Cardiomyopathy and prognostic markers." Doctoral thesis, Università degli studi di Padova, 2018. http://hdl.handle.net/11577/3427265.

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Background: Arrhythmogenic cardiomyopathy (AC) is a clinically and genetically heterogeneous myocardial disease, characterised by a progressive myocardial dystrophy with fibro-fatty replacement, and represents one of the major causes of sudden cardiac death in the young and athletes. Although half of AC patients harbour private desmosomal gene mutations, their low and age-dependent penetrance suggests the involvement of other regulatory molecules. MicroRNAs (miRNAs) are a group of endogenous short noncoding RNAs that regulate gene expression by sequence-specific recognition of their target transcripts. They have been associated with numerous pathophysiological conditions, including cardiovascular diseases; however, their role as key regulatory molecules in AC as well as their impact on the onset and progression of the disease is largely unknown. Purpose: miRNA profiling in genotype-positive AC-patients with different gene mutations in order to identify their potential as AC biomarkers. Methods: The study involved 59 subjects with a definite AC diagnosis, previously genotyped, and 14 healthy controls. 84-miRNA array was applied on 8 frozen right-ventricle (RV) myocardial tissue samples, from heart transplanted AC patients; 9 whole blood samples, from patients with definite AC diagnosis, and 6 healthy controls (HC). In the validation study, seven miRNAs were analysed on 42-AC and 8-HC blood samples. miRNA analysis was performed by qPCR, relative quantification ΔΔCt method and in silico target prediction. All data were expressed in fold-change values. Receiver operating characteristic (ROC) analysis was performed on validated miRNAs. Results: miRNA profiling on AC-tissue samples displayed a genotype-related profile, 19 miRNAs were differentially expressed in PKP2 carriers, 15 in DSP carriers and 14 in DSG2 carriers, when compared to healthy controls. A common signature between PKP2 and DSP carriers was identified with 14 miRNAs in common (PKP2/DSP profile). None of these miRNAs were shown within DSG2 profile. In silico target prediction identified Hippo Signaling Pathway as a common target for both profiles. Analysis of AC-tissue samples as a unique group confirmed 26 differentially expressed miRNAs (AC-tissue profile) with predicted targets in the AC pathway. AC-blood miRNA profiling demonstrated a 14-miRNA signature, with 10 miRNAs differentially expressed in common with AC-tissue profile. Hsa-miR-144-3p, -122-5p, -208a-3p and -494-3p as well as hsa-miR-21-5p, -155-5p and -320a were analysed on a larger cohort of 42-AC and 8-HC. Only hsa-mir-122-5p was significantly overexpressed (p-value<0,05). ROC analysis showed hsa-miR-122-5p to be a potential AC biomarker (area under the curve: 0.83). Conclusions: A genotype-related miRNA profile was observed in AC-tissue samples, as to reflect clinical variability. In addition, 10 miRNAs in common were identified between AC-tissue and AC-blood profiles, proving a specific miRNA signature for AC. These miRNA profiles targeted pathways involved in AC pathogenesis demonstrating their key roles in the onset and progression of the disease. Circulating level of hsa-miR-122-5p was significantly elevated in AC subjects, demonstrating its potential as a prognostic marker for heart failure in AC.
Introduzione. La Cardiomiopatia Aritmogena (AC) è una malattia clinicamente e geneticamente eterogenea del miocardio, caratterizzata da una progressiva distrofia miocardica con sostituzione fibro-adiposa, e rappresenta una delle principali cause di morte improvvisa nei giovani e negli atleti. Nonostante circa la metà dei pazienti affetti da AC presentino mutazioni nei geni desmosomiali, la bassa penetranza e dipendenza dall’età della patologia suggeriscono il coinvolgimento di altre molecole regolatrici. I microRNA (miRNA) sono un gruppo di molecole endogene, di RNA non codificante, che regolano l'espressione genica mediante lo specifico riconoscimento di sequenze target dei trascritti. Sono stati associati a numerose condizioni patofisiologiche, tra cui malattie cardiovascolari; tuttavia, il loro ruolo come molecole regolatrici nella AC e il loro impatto sull'insorgenza e sulla progressione della malattia è in gran parte sconosciuto. Scopo dello studio. Analizzare il profilo di espressione dei miRNA in pazienti affetti da AC genotipicamente positivi allo scopo di studiare il loro potenziale come biomarcatori prognostici. Materiali e metodi. Lo studio ha coinvolto 59 soggetti con una diagnosi clinica di AC, precedentemente genotipizzati, e 14 controlli sani (HC). Un array composto da 84-miRNA è stato testato su: 8 campioni di tessuto miocardico congelato del ventricolo destro, proveniente da pazienti trapiantati affetti da AC; 9 campioni di sangue intero congelato, da pazienti con diagnosi clinica di AC e 6 controlli sani. Nella fase di validazione sono stati analizzati sette miRNA su campioni di sangue provenienti da 42-AC e 8-HC. L'analisi è stata eseguita mediante qPCR seguita da quantificazione relativa con il metodo ΔΔCt e predizione in silico dei geni target. I risultati sono stati espressi in valori di “fold-change” e le curve ROC (Receiver Operating Characteristic) analizzate sui miRNA validati. Risultati. L’analisi dei miRNA su 8 campioni di tessuto di pazienti affetti da AC mostrava un profilo correlato al genotipo rispetto ai controlli sani, in particolare: 19 miRNA erano differenzialmente espressi nei portatori di una mutazione in PKP2, 15 nei portatori di una mutazioni in DSP e 14 nei portatori di una mutazione in DSG2. E’ stato identificato un profilo d’espressione in comune tra i portatori della mutazione in PKP2 e i portatori della mutazione in DSP, con 14 miRNA alterati (profilo PKP2/DSP). Nessuno di questi miRNA è stato trovato nel profilo DSG2. Lo studio in silico dei possibili geni target ha identificato la via di segnale “Hippo Signaling Pathway” come target comune per entrambi i profili (PKP2/DSP- DSG2). Considerando i campioni di tessuto AC come un unico gruppo indipendentemente dal gene mutato sono emersi 26 miRNA differenzialmente espressi (profilo AC-tessuto) che hanno come target geni coinvolti nel pathway AC. Lo studio dei miRNA nei 9 campioni di sangue dei pazienti affetti da AC ha dimostrato un profilo costituito 14-miRNA alterati, dei quali 10 alterati anche nel profilo AC-tessuto. Hsa-miR-144-3p, -122-5p, -208a-3p e -494-3p così come hsa-miR-21-5p, -155-5p e -320a sono stati infine validati su una coorte più ampia di 42-AC e 8-HC. Solo hsa-mir-122-5p è stato riscontrato come significativamente sovraespresso (valore p <0,05). L'analisi di curve ROC ha mostrato che hsa-miR-122-5p è un potenziale biomarcatore di AC (AUC: 0.83). Conclusione. Nei campioni AC di tessuto è stato osservato un profilo di miRNA correlato al genotipo, tale da rispecchiare la variabilità clinica della patologia. Inoltre, sono stati identificati 10 miRNA in comune tra i profili dei campioni AC di tessuto e sangue, evidenziando un profilo di espressione di miRNA specifico per AC. Entrambi i profili infatti (tessuto e sangue) hanno come target vie di segnale coinvolte nella patogenesi della AC, dimostrando un ruolo chiave nella insorgenza e la progressione della malattia. In particolare il livello di hsa-miR-122-5p in circolo era significativamente elevato nei soggetti affetti da AC, dimostrando il suo potenziale come marcatore prognostico della malattia.
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Kemp, Jacqueline Renee. "Genome-wide Angiotensin II regulated microRNA expression profiling: A smooth muscle-specific microRNA signature." Cleveland State University / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=csu1367845628.

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DE, SANCTIS Claudia. "MicroRNAs profiling in Dopaminergic neurons." Doctoral thesis, Università degli studi del Molise, 2018. http://hdl.handle.net/11695/83499.

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Lo sviluppo dei neuroni dopaminergici mesencefalici (mDA) è un fenomeno complesso e non ancora pienamente compreso. Molti studi hanno focalizzato la loro attenzione sul ruolo svolto da diversi fattori di trascrizione specifici e ben noti. L'obiettivo della mia tesi di dottorato è focalizzato su una classe relativamente nuova di regolatori post-trascrizionali denominati microRNA (miRNAs), in grado di regolare l'espressione genica legando le sequenze parzialmente complementari nelle regioni 3' non tradotte (UTR) degli mRNAs target. Per studiare il ruolo svolto dai miRNAs durante la differenziazione dei neuroni mDA, abbiamo scelto di analizzare il profilo di espressione dei miRNA usando piattaforme di Array. A tale scopo, abbiamo utilizzato un protocollo ottimizzato da cellule staminali di epiblasto di topo (epiSC) differenziate in neuroni mDA (Jeager et al.,2011). Dall'analisi bioinformatica dei dati dell'array, ottenuti dalle epiSC differenziate in neuroni mDA, abbiamo identificato alcuni candidati molto probabilmente implicati nella differenziazione e nella funzione dei neuroni DA. I miRNA candidati sono stati sottoposti a screening per la loro capacità di indurre il fenotipo DA. A questo scopo, ho generato vettori lentivirali inducibili per ciascun miRNAs e ho infettato colture primarie mesencefaliche di topo allo stadio E12.5. Tra tutti i miRNA candidati, miR-218 e miR-34b/c aumentano il numero di cellule TH + positive, suggerendo il loro possibile contributo nei neuroni mDA. Inoltre, miR-218 e miR-34b/c, risultano arricchiti sia nel mesencefalo dei topi (E13.5) che nelle cellule GFP + sortate al FACS, isolate da embrioni E13.5 Pitx3-GFP di topo, rispetto al controllo. I dati ottenuti dal saggio di Luciferasi e dal saggio di reporter a doppia fluorescenza suggeriscono che miR-34b/c legano e sopprimono la 3'UTR di Wnt1 e viene espresso durante la differenziazione dei neuroni mDA. Tramite analisi di ibridazione in situ e dati d’ immunoistochimica ho potuto verificare che miR-218 è espresso in particolare nel mesencefalo di topo allo stadio E14, dove co-localizza rostralmente con Isl-1 (marcatore di motoneuroni) e caudalmente con TH, Pitx3, Lmx1a (marcatori dopaminergico). Questi dati suggeriscono che miR-218 è espresso anche nei motoneuroni craniali, come descritto in altri recenti studi (Thiebes, K.P. et al., 2014; Amin, N.D et al., 2015). Per comprendere ulteriormente il ruolo di miR-218 nello sviluppo e nella funzione dei neuroni dopaminergici ho generato topi knock-out condizionali (cKO) per miR-218-2. Accoppiando miR-218-2 flox / flox con topi En1Cre /+ che esprimono Cre sotto il controllo del promotore di Engrailed 1 (En1, marker pro-dopaminergico), sarò in grado di comprendere il contributo di miR-218 nel sistema dopaminergico. I topi miR-218-2 flox / flox En1Cre /+ da osservazioni preliminari, hanno mostrato un fenotipo con danno motorio, ma per confermare questi dati sto attualmente effettuando test comportamentali e analisi in vivo. Attraverso il profilo di espressione di miRNAs, siamo in grado di comprendere il meccanismo e la funzione del sistema dopaminergico, poiché i miRNAs sono regolatori chiave nelle reti di espressione genica, possono influenzare molti processi biologici e in futuro potrebbero essere utilizzati come biomarkers per diagnosticare patologie legate al sistema nervoso.
Midbrain dopaminergic neurons (mDA) development is a complex and still not fully understood phenomenon. Many studies till now concentrated their attention on the roles played by several, specific and well-known transcription factors. The aim of my PhD thesis is focus on a relatively new class of post-transcriptional regulators named microRNAs (miRNAs) able to regulate gene expression by targeting partially complementary sequences in the 3’untranslated regions (UTRs) of the target mRNAs. To investigate the role played by miRNAs during mDA differentiation, we choose to analyze miRNAs expression profile by using miRNA Array platforms. To this purpose we used an optimized protocol from mouse Epiblast stem cells (epiSC) differentiated into DA neurons (Jeager et al. 2011). By bioinformatics analysis of the array data, obtained from epiSC differentiated into mDA neurons, we identified few candidates most likely implicated in the DA neurons differentiation and function. The candidate miRNAs were screened for their ability to induce DA phenotype. To this purpose, I generated inducible lentiviral vectors for each miRNA and I have infected mesencephalic primary cultures from mice at stage E12.5. Among all candidate miRNAs, miR-218 and miR-34b/c increase the number of TH+ positive cells, showing their possible contribution in the mDA neurons. Moreover, miR-218 and miR-34b/c, were enriched both in midbrain of mice (E13.5) and in FACS sorted GFP+ cells isolated from E13.5 Pitx3-GFP mice embryos when compared with control. Data obtained from Luciferase Assay and Dual Fluorescence Reporter Assay suggest that miR-34b/c target and suppress Wnt1 3’UTR and it is expressed during DA neurons differentiation. By performing In situ hybridization analysis and immunohistochemistry, I was able to detect miR-218 in particular in the mouse midbrain at stage E14, where co-localize rostrally with Isl-1 (motor neuron marker) and caudally with TH, Pitx3, Lmx1a (dopaminergic marker). This data suggests that miR-218 is expressed also in cranial motor neurons, as described in others recent studies (Thiebes, K.P. et al. 2014; Amin, N.D et al. 2015). To further understand the role of miR-218 in development and function of dopaminergic neurons I have generated the conditional knock-out (cKO) mice for miR-218-2. By mating miR-218-2 flox/flox with En1Cre/+ mice expressing the Cre under Engrailed 1 promoter (En1 is a pro-dopaminergic marker) I will be able to investigate the contribution of miR-218 in dopaminergic system. Preliminary observations on miR-218-2 flox/flox En1Cre/+ mice shown motor impairment phenotype, but to confirm this data I’m currently performing behavior tests and in vivo analysis. Through miRNA expression profiling we be able understand mechanism and function of dopaminergic system, because miRNAs are as key regulators in gene expression networks, can influence many biological processes and have also shown promise as biomarkers for neuro-disorders.
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Watson, Zara. "miRNA Expression Profiling in Papillary Thyroid Cancer." Thesis, University of Sydney, 2020. https://hdl.handle.net/2123/23285.

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Papillary thyroid cancer (PTC) is commonly diagnosed in Australia and has an increasing incidence; it is projected to be the 10th most commonly diagnosed cancer by the end of 20191. Fortunately it has a good outcome, with the mortality rate stable over the last 25 years at around 2%2. The challenge to the clinician is to determine the best diagnostic tools to aid in appropriate management of the disease. MicroRNA (miRNA) is an emerging tool in the diagnosis and management of cancers. We examined the expression of miRNAs in an Australian population with PTC, both those known to have altered expression and novel miRNAs. Tissues of 30 subjects were collected, 18 from whom we also had access to serum. The miRNAs were studied in thyroid tumour and normal tissue, lymph nodes and serum. MiRNAs mir-10b, miR-31, miR-100, miR-146b, miR-221, miR-222 and let-7d were studied, with miR-16, RNU48 and Cel-39 used as controls. Our study demonstrated significantly elevated expression of miRs -146b, -221 and -222 in tumour tissue vs normal tissue and a significantly decreased expression of miR-10b. We also showed that handling of serum samples has a significant impact on the results when analysing miRNAs, due to the effect of haemolysis. 1. Ferlay J SI, Ervik M, et al. GLOBOCAN 2012 v1.0, Cancer incidence and mortality worldwide: IARC cancerbase no. 11 In. Lyon, France: International Agency for Research on Cancer; 2013. 2. Siegel R, Ma J, Zou Z, Jemal A. Cancer statistics, 2014. CA Cancer J Clin. 2014;64(1):9-29.
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Morin, Ryan David. "Methods for microRNA profiling and discovery using massively parallel sequencing." Thesis, University of British Columbia, 2007. http://hdl.handle.net/2429/31683.

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MicroRNAs (miRNAs) are emerging as important, albeit poorly characterized, regulators of gene expression. Here, I review the current knowledge of miRNAs in humans, including their biogenesis, modes of action and various methods for studying them. To fully elucidate the various functions of miRNAs in humans, we require a more complete understanding of their numbers and expression changes amongst different cell types. This document includes a description of a new method for surveying the expression of miRNAs that employs the new Illumina sequencing technology. A set of methods is presented that enables identification of sequences belonging to known miRNAs as well as variability in their mature sequences. As well, a novel system for miRNA gene discovery using these data is described. Application of this approach to RNA from human embryonic stem cells (hESCs) obtained before and after differentiation into embryoid bodies (EBs) revealed the sequences and expression levels of 362 known plus 170 novel miRNA genes. Of these, 190 known and 31 novel microRNA sequences exhibited significant expression differences between these two developmental states. Owing to the increased number of sequence reads, these libraries currently represent the deepest miRNA sampling in any human cell type spanning nearly six orders of magnitude of expression. Predicted targets of the differentially expressed miRNAs were ranked to identify those that are likely under cooperative miRNA regulation in either hESCs or EBs. The predicted targets of those miRNAs enriched in either sample shared common features. Included amongst the high-ranked predicted gene targets are those implicated in differentiation, cell cycle control, programmed cell death and transcriptional regulation. Direct validation of these predicted targets or global discovery of miRNA targets should reveal the functions of these sequences in the differentiation of hESCs.
Science, Faculty of
Graduate
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Li, Su-Chen. "Small Intestinal Neuroendocrine Tumor Analyses : Somatostatin Analog Effects and MicroRNA Profiling." Doctoral thesis, Uppsala universitet, Endokrin Onkologi, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-233207.

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Small intestinal neuroendocrine tumors (SI-NETs) originate from serotonin-producing enterochromaffin (EC) cells in the intestinal mucosa. Somatostatin analogs (SSAs) are mainly used to control hormonal secretion and tumor growth. However, the molecular mechanisms leading to the control of SI-NETs are unknown. Although microRNAs (miRNAs) are post transcriptional regulators deeply studied in many cancers, are not well-defined in SI-NETs. We adopted a two-pronged strategy to investigate SSAs and miRNAs: first, to provide novel insights into how SSAs control NET cells, and second, to identify an exclusive SI-NET miRNA expression, and investigate the biological functions of miRNA targets. To accomplish the first aim, we treated CNDT2.5 cells with octreotide for 16 months. Affymetrix microarray was performed to study gene variation of CNDT2.5 cells in the presence or absence of octreotide. The study revealed that octreotide induces six genes, ANXA1, ARHGAP18, EMP1, GDF15, TGFBR2 and TNFSF15. To accomplish the second aim, SI-NET tissue specimens were used to run genome-wide Affymetrix miRNA arrays. The expression of five miRNAs (miR-96, -182, -183, -196a and -200a) was significantly upregulated in laser capture microdissected (LCM) tumor cells versus LCM normal EC cells, whereas the expression of four miRNAs (miR-31, -129-5p, -133a and -215) was significantly downregulated in LCM tumor cells. We also detected nine tissue miRNAs in serum samples, showing that the expression of five miRNAs is significantly increased in SSA treated patients versus untreated patients. Conversely, SSAs do not change miRNA expression of four low expressed miRNAs. Silencing miR-196a expression was used to investigate functional activities in NET cells. This experimental approach showed that four miR-196a target genes, HOXA9, HOXB7, LRP4 and RSPO2, are significantly upregulated in silenced miR-196a NET cells. In conclusion, ANXA1, ARHGAP18, EMP1, GDF15, TGFBR2 and TNFSF15 genes might regulate cell growth and differentiation in NET cells, and play a role in an innovative octreotide signaling pathway. The global SI-NET miRNA profiling revealed that nine selected miRNAs might be involved in tumorigenesis, and play a potential role as novel markers for follow-up. Indeed, silencing miR-196a demonstrated that HOXA9, HOXB7, LRP4 and RSPO2 genes are upregulated at both transcriptional and translational levels.
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Schulz, Nikola. "microRNA profiling and target identification in a mouse model for allergic asthma." Diss., lmu, 2012. http://nbn-resolving.de/urn:nbn:de:bvb:19-143012.

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Books on the topic "MicroRNA profiling"

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Rani, Sweta, ed. MicroRNA Profiling. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6524-3.

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Rani, Sweta, ed. MicroRNA Profiling. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-2823-2.

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Fan, Jian-Bing, ed. Next-Generation MicroRNA Expression Profiling Technology. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-427-8.

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Wang, Zhiguo. MicroRNA expression detection methods. Heidelberg: Springer, 2010.

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Next-generation MicroRNA expression profiling technology: Methods and protocols. New York: Humana Press, 2012.

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A, Lidbury Brett, and Mahalingam Suresh, eds. Gene profiling in drug design. Boca Raton: Taylor & Francis, 2008.

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Gusev, Yuriy, ed. Microrna Profiling in Cancer. World Scientific Publishing Co. Pte. Ltd., 2009. http://dx.doi.org/10.1142/9789814267540.

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MicroRNA Profiling: Methods and Protocols. Humana, 2018.

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Rani, Sweta. MicroRNA Profiling: Methods and Protocols. Springer, 2023.

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Rani, Sweta. Microrna Profiling: Methods and Protocols. Springer New York, 2016.

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Book chapters on the topic "MicroRNA profiling"

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Gao, Lu, and Feng Jiang. "MicroRNA (miRNA) Profiling." In Methods in Molecular Biology, 151–61. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3204-7_8.

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Rahimian, Neda, Javid Sadri Nahand, Michael R. Hamblin, and Hamed Mirzaei. "Exosomal MicroRNA Profiling." In Methods in Molecular Biology, 13–47. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2823-2_2.

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Garzon, Ramiro. "MicroRNA Profiling of Megakaryocytes." In DNA and RNA Profiling in Human Blood, 293–98. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-553-4_19.

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Daly, Melissa, and Lorraine O’Driscoll. "MicroRNA Profiling of Exosomes." In Methods in Molecular Biology, 37–46. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6524-3_5.

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Wang, Zhiguo, and Baofeng Yang. "miRNA Amplification Profiling (mRAP)." In MicroRNA Expression Detection Methods, 159–70. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-04928-6_9.

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Ioannidis, Jason, Judith Risse, and F. Xavier Donadeu. "Profiling of MicroRNAs in the Biofluids of Livestock Species." In MicroRNA Protocols, 65–77. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7601-0_5.

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Sharma, Amit, and Joseph C. Wu. "MicroRNA Expression Profiling of Human-Induced Pluripotent and Embryonic Stem Cells." In MicroRNA Protocols, 247–56. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-083-0_19.

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Grigorenko, Elena V., Elen Ortenberg, James Hurley, Andrew Bond, and Kevin Munnelly. "miRNA Profiling on High-Throughput OpenArray™ System." In MicroRNA and Cancer, 101–10. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-863-8_8.

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Zhao, Botao, Bing Huang, Wei Li, and Youxin Jin. "MicroRNA Expression Profiling During Neural Differentiation of Mouse Embryonic Carcinoma P19 Cells." In MicroRNA Protocols, 105–16. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-083-0_9.

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Hackenberg, Michael. "MicroRNA Expression Profiling and Discovery." In Bioinformatics for High Throughput Sequencing, 191–208. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4614-0782-9_11.

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Conference papers on the topic "MicroRNA profiling"

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Gilligan, Diana, Aakriti Pandita, Poornima Ramadas, Aarati Poudel, Nibal Saad, Ankit Anand, Alina Basnet, and Frank Middleton. "Abstract 5413: MicroRNA profiling in AML." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-5413.

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Tsai, Ming-Ju, Wei-An Chang, Chau-Chyun Sheu, Jen-Yu Hung, Yu-Chen Tsai, Ya-Ling Hsu, Po-Lin Kuo, and Inn-Wen Chong. "MicroRNA profiling of asthmatic bronchial epithelial cells." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa4923.

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Lerebours, F., G. Clairac, S. Tozlu-Kara, S. Vacher, R. Lidereau, and I. Bieche. "MicroRNA Expression Profiling of Inflammatory Breast Cancer." In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-6118.

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Roffel, M. P., I. M. Boudewijn, C. J. Vermeulen, A. J. Van Oosterhout, K. Affleck, K. R. Bracke, T. Maes, I. H. Heijink, C. Brandsma, and M. Van Den Berge. "MicroRNA profiling in bronchial biopsies of asthma patients." In ERS Lung Science Conference 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/23120541.lsc-2020.30.

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Roffel, M. P., I. M. Boudewijn, C. J. Vermeulen, A. van Oosterhout, K. Affleck, K. R. Bracke, T. Maes, I. H. Heijink, C. A. A. Brandsma, and M. van den Berge. "MicroRNA Profiling in Bronchial Biopsies of Asthma Patients." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1059.

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Roffel, Mirjam P., Ilse M. Boudewijn, Jos Van Nijnatten, Corneel J. Vermeulen, Antoon J. M. Van Oosterhout, Karen Affleck, Ken R. Bracke, et al. "MicroRNA profiling in bronchial biopsies of asthma patients." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.619.

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Stupak, E. V., Yu A. Veryaskina, S. E. Titov, L. G. Achmerova, V. V. Stupak, M. K. Ivanov, I. F. Zhimulev, and N. N. Kolesnikov. "MicroRNA profiling in the malignant progression of gliomas." In PHYSICS OF CANCER: INTERDISCIPLINARY PROBLEMS AND CLINICAL APPLICATIONS (PC’16): Proceedings of the International Conference on Physics of Cancer: Interdisciplinary Problems and Clinical Applications 2016. Author(s), 2016. http://dx.doi.org/10.1063/1.4960284.

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Zhang, Wei, Tong Zhou, Viswanathan Natarajan, Imre Noth, Roberto F. Machado, and Joe G. Garcia. "Profiling Of Microrna Expression In Idiopathic Pulmonary Fibrosis." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a6004.

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Lu, Ya-Ching, and Ann-Joy Cheng. "Abstract 3032: MicroRNA profiling in head and neck cancer." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-3032.

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Fassan, Matteo, Stefano Volinia, Jeff Palatini, Marco Pizzi, Raffaele Baffa, Roberto Clemente, Christian Rizzetto, et al. "Abstract 3050: MicroRNA expression profiling of human Barrett's carcinogenesis." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-3050.

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Reports on the topic "MicroRNA profiling"

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Sun, Lina, Yanan Han, Hua Wang, Huanyu Liu, Shan Liu, Hongbin Yang, Xiaoxia Ren, and Ying Fang. MicroRNAs as Potential Biomarkers for the Diagnosis of Inflammatory Bowel Disease: A Systematic Review and Meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, February 2022. http://dx.doi.org/10.37766/inplasy2022.2.0027.

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Review question / Objective: The purpose of this systematic review was to systematically review the clinical studies regarding miRNAs as diagnostic biomarkers for inflammatory bowel disease and assess the overall diagnostic accuracy of miRNAs. Condition being studied: The symptoms of inflammatory bowel disease (IBD) are highly variable. The diagnosis of IBD must be made through medical history, physical, laboratory, radiologic, endoscopic, and histological examinations. However, these diagnostic techniques are not specific and sometimes even equivocal. Therefore, reliable biomarkers are urgently needed in the diagnosis of IBD. Several clinical and preclinical researches have shown that dysregulated microRNAs (miRNAs) play a crucial role in IBD development. miRNAs, as single-stranded noncoding RNAs that contain 22-24 nucleotides, can post-transcriptionally regulate gene expression by blocking mRNA translation or degrading target mRNAs. miRNAs are widely involved in physiological and pathological cellular processes, such as differentiation, proliferation and apoptosis. Besides, they are stable, noninvasive, and resistant to degradation by ribonucleases, making them valuable targets in the diagnosis, monitoring, prognosis, and treatment of diseases. To date, inconsistent results have been found about miRNA expression profiling in the patients with IBD. Moreover, the diagnostic accuracy of miRNAs for IBD has not been reported in any meta-analysis.
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Lers, Amnon, and Pamela J. Green. Analysis of Small RNAs Associated with Plant Senescence. United States Department of Agriculture, March 2013. http://dx.doi.org/10.32747/2013.7593393.bard.

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Senescence is an agriculturally significant process due to its negative impact to crop yield and postharvest quality. The genetic regulatory systems controlling senescence induction and progress respond to both developmental and environmental stress signals and involve numerous gene expression changes. Knowledge about the key molecular factors which control senescence is very limited. MicroRNAs (miRNAs) are a class of small RNAs which typically function by guiding cleavage of target messenger RNAs. They have been shown to play major roles in a variety of plant processes including development, responses to environmental stresses, and senescence. The long-term goal of this work is to elucidate roles of small RNAs associated with plant senescence. The hypothesis underlying this research is that miRNA-mediated regulation makes important contributions to the senescence process in plants. Specific, original research objectives included: 1) Profiling of small RNAs from senescing plants; 2) Data Analysis and public access via a user-friendly web interface; 3) Validation of senescence-associated miRNAs and target RNAs; 4) Development of transgenic plants for functional analysis of miRNAs in Arabidopsis. Major revisions made in the research compared to the original work plan included 1) Exclusion of the planned work with tomato as recommended by the BARD review panel; 2) Performing miRNA study also in senescing Arabidopsis siliques, in addition to senescing leaves. To identify senescenceregulation of miRNAs in Arabidopsis thaliana, eight small RNA libraries were constructed and sequenced at four different stages of development and senescence from both leaves and siliques, resulting in more than 200 million genome-matched sequences. Parallel Analysis of RNA Ends (PARE) libraries, which enable the large-scale examination of miRNA-guided cleavage products, were also constructed and sequenced, resulting in over 750 million genome-matched sequences. These massive datasets lead to the identification of new miRNAs, as well as new regulation of known miRNAs and their target genes during senescence, many of which have established roles in nutrient responsiveness and cell structural integrity. In keeping with remobilization of nutrients thought to occur during senescence, many miRNAs and targets had opposite expression pattern changes between leaf and silique tissues during the progression of senescence. Taken together, these findings highlight the integral role that miRNAs may play in the remobilization of resources and alteration of cellular structure that is known to occur in senescence. Experiments were initiated for functional analysis of specific senescence-associated miRNAs and respective target genes. Transgenic Arabidopsis plants were generated in which miR408, found in this study to be significantly induced in leaf senescence, was over-expressed either constitutively or under a senescence-specific promoter. These plants are currently being characterized for any altered phenotypes. In addition T-DNA knock out mutants for various target genes identified in this research are being analyzed. This work provides insights about specific miRNAs that contribute to leaf and silique senescence. The knowledge generated may suggest new strategies to monitor and alter the progression of senescence in crops for agricultural improvement.
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Whitham, Steven A., Amit Gal-On, and Tzahi Arazi. Functional analysis of virus and host components that mediate potyvirus-induced diseases. United States Department of Agriculture, March 2008. http://dx.doi.org/10.32747/2008.7591732.bard.

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The mechanisms underlying the development of symptoms in response to virus infection remain to be discovered in plants. Insight into symptoms induced by potyviruses comes from evidence implicating the potyviral HC-Pro protein in symptom development. In particular, recent studies link the development of symptoms in infected plants to HC-Pro's ability to interfere with small RNA metabolism and function in plant hosts. Moreover, mutation of the highly conserved FRNK amino acid motif to FINK in the HC-Pro of Zucchini yellow mosaic virus (ZYMV) converts a severe strain into an asymptomatic strain, but does not affect virus accumulation in cucurbit hosts. The ability of this FINK mutation to uncouple symptoms from virus accumulation creates a unique opportunity to study symptom etiology, which is usually confounded by simultaneous attenuation of both symptoms and virus accumulation. Our goal was to determine how mutations in the conserved FRNK motif affect host responses to potyvirus infection in cucurbits and Arabidopsis thaliana. Our first objective was to define those amino acids in the FRNK motif that are required for symptoms by mutating the FRNK motif in ZYMV and Turnip mosaic virus (TuMV). Symptom expression and accumulation of resulting mutant viruses in cucurbits and Arabidopsis was determined. Our second objective was to identify plant genes associated with virus disease symptoms by profiling gene expression in cucurbits and Arabidopsis in response to mutant and wild type ZYMV and TuMV, respectively. Genes from the two host species that are differentially expressed led us to focus on a subset of genes that are expected to be involved in symptom expression. Our third objective was to determine the functions of small RNA species in response to mutant and wild type HC-Pro protein expression by monitoring the accumulation of small RNAs and their targets in Arabidopsis and cucurbit plants infected with wild type and mutant TuMV and ZYMV, respectively. We have found that the maintenance of the charge of the amino acids in the FRNK motif of HC-Pro is required for symptom expression. Reduced charge (FRNA, FRNL) lessen virus symptoms, and maintain the suppression of RNA silencing. The FRNK motif is involved in binding of small RNA species including microRNAs (miRNA) and short interfering RNAs (siRNA). This binding activity mediated by the FRNK motif has a role in protecting the viral genome from degradation by the host RNA silencing system. However, it also provides a mechanism by which the FRNK motif participates in inducing the symptoms of viral infection. Small RNA species, such as miRNA and siRNA, can regulate the functions of plant genes that affect plant growth and development. Thus, this binding activity suggests a mechanism by which ZYMVHC-Pro can interfere with plant development resulting in disease symptoms. Because the host genes regulated by small RNAs are known, we have identified candidate host genes that are expected to play a role in symptoms when their regulation is disrupted during viral infections. As a result of this work, we have a better understanding of the FRNK amino acid motif of HC-Pro and its contribution to the functions of HC-Pro, and we have identified plant genes that potentially contribute to symptoms of virus infected plants when their expression becomes misregulated during potyviral infections. The results set the stage to establish the roles of specific host genes in viral pathogenicity. The potential benefits include the development of novel strategies for controlling diseases caused by viruses, methods to ensure stable expression of transgenes in genetically improved crops, and improved potyvirus vectors for expression of proteins or peptides in plants.
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