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Auswahl der wissenschaftlichen Literatur zum Thema „RNA signature“

Autor: Grafiati

Veröffentlicht am 12. April 2025

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Zeitschriftenartikel zum Thema "RNA signature"

Liu, Jie, Wenmin Deng, Zhiwen Xiao, Xiaofeng Huang, Minmin Lin und Zhen Long. „Identification of RNA Modification-Associated Alternative Splicing Signature as an Independent Factor in Head and Neck Squamous Cell Carcinoma“. Journal of Immunology Research 2022 (13.09.2022): 1–19. http://dx.doi.org/10.1155/2022/8976179.

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Objective. Head and neck squamous cell carcinoma (HNSCC) is a highly heterotopic malignant tumor. Alternative splicing (AS) and RNA modification have been reported to be involved in tumorigenesis. Therefore, we constructed RNA modification-associated AS (RMA-AS) signature model to predict the prognosis of HNSCC. Methods. AS events and RNA-modified gene expression information were downloaded from TCGA-HNSCC database. Univariate Cox regression analysis was employed for analyzing prognosis-related AS events. RMA-AS events were obtained by constructing a coexpression network between RNA modification-associated genes and AS events using WGCNA package. The prognostic signatures were analyzed by LASSO, univariate Cox, and multivariate Cox regression. Kaplan-Meier survival analysis, proportional hazard model, and ROC curve were performed to verify the prognostic value. “ESTIMATE” R package, ssGSEA algorithm, and CIBERSORT method were used to detect immune microenvironment in HNSCC. Cytoscape was utilized to build a regulatory network of splicing factor-regulated RMA-AS. Results. There were 16,574 prognostic AS events and 4 differentially expressed RNA modification-associated genes in HNSCC. Based on RMA-AS events, we obtained a risk model consisting of 14 AS events, named RMA-AS_Score. The samples were divided into RMA-AS_Score high- and RMA-AS_Score low-risk groups, according to the risk score. The RMA-AS_Score high group was related to poor prognosis. Moreover, the RMA-AS_Score signature was an independent prognostic predictor and was related to tumor grade. Meanwhile, the AUC value of RMA-AS_Score was 0.652, which is better than other clinical characteristics. Besides, a nomogram prediction model of quantitative prognosis has also been developed, which has robust effectiveness in predicting prognosis. In addition, the prognostic signature was observably related to immune microenvironment and immune checkpoint. Finally, 14 splicing factors were identified and constructed into a network of splicing factor-regulated RMA-AS. Conclusion. We identified the RMA-AS signature of HNSCC. This signature could be treated as an independent prognostic predictor.

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Stupnikov, Alexey, Paul G. O’Reilly, Caitriona E. McInerney, Aideen C. Roddy, Philip D. Dunne, Alan Gilmore, Hayley P. Ellis et al. „Impact of Variable RNA-Sequencing Depth on Gene Expression Signatures and Target Compound Robustness: Case Study Examining Brain Tumor (Glioma) Disease Progression“. JCO Precision Oncology, Nr. 2 (November 2018): 1–17. http://dx.doi.org/10.1200/po.18.00014.

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Purpose Gene expression profiling can uncover biologic mechanisms underlying disease and is important in drug development. RNA sequencing (RNA-seq) is routinely used to assess gene expression, but costs remain high. Sample multiplexing reduces RNA-seq costs; however, multiplexed samples have lower cDNA sequencing depth, which can hinder accurate differential gene expression detection. The impact of sequencing depth alteration on RNA-seq–based downstream analyses such as gene expression connectivity mapping is not known, where this method is used to identify potential therapeutic compounds for repurposing. Methods In this study, published RNA-seq profiles from patients with brain tumor (glioma) were assembled into two disease progression gene signature contrasts for astrocytoma. Available treatments for glioma have limited effectiveness, rendering this a disease of poor clinical outcome. Gene signatures were subsampled to simulate sequencing alterations and analyzed in connectivity mapping to investigate target compound robustness. Results Data loss to gene signatures led to the loss, gain, and consistent identification of significant connections. The most accurate gene signature contrast with consistent patient gene expression profiles was more resilient to data loss and identified robust target compounds. Target compounds lost included candidate compounds of potential clinical utility in glioma (eg, suramin, dasatinib). Lost connections may have been linked to low-abundance genes in the gene signature that closely characterized the disease phenotype. Consistently identified connections may have been related to highly expressed abundant genes that were ever-present in gene signatures, despite data reductions. Potential noise surrounding findings included false-positive connections that were gained as a result of gene signature modification with data loss. Conclusion Findings highlight the necessity for gene signature accuracy for connectivity mapping, which should improve the clinical utility of future target compound discoveries.

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Albitar, Maher, Sally Agersborg, Ahmad Charifa, Hong Zhang, Andrew Ip, Katherine Linder, Andrew L. Pecora, Jamie Koprivnikar, Andre Goy und James McCloskey. „Establishing Distinct Cytokine Signatures Differentiating between Acute Myeloid Leukemia, Myelodysplastic Syndrome, and Chip Using Bone Marrow RNA or Cell-Free RNA (cfRNA)“. Blood 144, Supplement 1 (05.11.2024): 4295. https://doi.org/10.1182/blood-2024-203870.

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Cytokines are essential for various immune functions and the overall inflammatory response to myeloid neoplasms in bone marrow. They play a major role in bone marrow microenvironment in normal and abnormal hematopoiesis. Cytokines exert their functions by interacting with their receptors, and full evaluation of the cytokines' roles requires evaluating their receptors as well. Using next generation sequencing (NGS) and machine learning, we measured the expression of 36 cytokines/chemokines and cytokine receptors in the bone marrow (BM) of patients with acute myeloid leukemia (AML), myelodysplastic syndrome (MDS), and clonal hematopoiesis of indeterminate potential (CHIP), and established cytokine signatures that differentiate between these diseases. We also explored if peripheral blood cell-free RNA (cfRNA) reflects BM environment. Methods: RNA was extracted from the bone marrow (BM) samples of patients with AML (N=515), MDS (N=825), and CHIP (N=915). cfRNA was extracted from the peripheral blood of patients with AML (N=30), MDS (N=184), and CHIP (N=502). BM RNA and cfRNA were sequenced using a 1500-gene targeted RNA next generation sequencing (NGS) panel. More than 80 million reads and a percentage of spliced reads above 20% were required for acceptable evaluation. The expression levels of 36 cytokines/chemokines were used in this analysis. Using Bayesian statistics, each of the 36 biomarkers was ranked based on its sensitivity and specificity of distinguishing between two diagnostic classes with 10-fold cross validation by leave-one-out. Random forest algorithms were developed using two-thirds of the BM samples and top-ranked biomarkers to build signatures that distinguished between two diagnostic classes. One-third of the bone marrow samples were used for testing these algorithms. Each model was then used to test if cfRNA samples showed the same results obtained from BM samples. Results: In distinguishing between AML and MDS, we first used Bayesian statistics with 10-fold cross validation to rank the studied 36 cytokines/chemokines and receptors. After ranking, random forest showed that a cytokine signature of 20 top-ranked biomarkers can reliably distinguish between BM with MDS from BM with AML (AUC: 0.874, CI: 0.843-.906). The biomarkers in the signature are: TNFRSF10D, TNFAIP3, TNFRSF4, IL3RA, IL8, TGFBR3, CXXC4, IL1RAP, IL7R, IFNG, TNFRSF10B, IL2, TNF, TGFBR2, CXCR4, TNFRSF14, CTLA4, IL12RB2, TGFBI, IL21R. Using the same algorithm and the same biomarkers but as measured using peripheral blood cfRNA, AML was distinguishable from MDS (AUC: 0.706, CI: 0.617-0.795). Using a similar approach, we were able to distinguish between BM with MDS and BM with CHIP using random forest and a cytokine signature of 20 biomarkers (AUC: 0.761, CI: 0.722-0.800). The biomarkers in this signature are TGFBR2, TNFRSF14, CXCR4, IL1RAP, TNFRSF10D, TNFAIP3, IL8, IL12RB2, IL1B, CTLA4, IL7R, IL21R, TNFRSF9, TNF, IL3, TNFRSF17, TGFBR3, TNFRSF4, TNFRSF10B, and IL13RA2, in order. Using the same signature and biomarkers but as measured using peripheral blood cfRNA from patients with MDS or CHIP, we were able to distinguish between the two diseases with AUC of 0.712 (CI: 0.668-0.756). While both signatures share multiple biomarkers (IL8, CTLA4, CXCR4...), the signature distinguishing AML from MDS is uniquely using IL3, IL1B and TNFRSF17 while the signature for distinguishing MDS from CHIP is uniquely using CXX4, IL2, and TGFB1. Conclusions: There are unique cytokines/chemokines and receptor signatures for each of the AML, MDS, and CHIP. This indicates that these biomarkers are crucial for defining each of these diseases. Furthermore, our data shows that cfRNA is reliable in reflecting bone marrow findings and can be used as an alternative to bone marrow samples for measuring and monitoring these signatures.

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Al Mahi, Naim, Erik Y. Zhang, Susan Sherman, Jane J. Yu und Mario Medvedovic. „Connectivity Map Analysis of a Single-Cell RNA-Sequencing -Derived Transcriptional Signature of mTOR Signaling“. International Journal of Molecular Sciences 22, Nr. 9 (22.04.2021): 4371. http://dx.doi.org/10.3390/ijms22094371.

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In the connectivity map (CMap) approach to drug repositioning and development, transcriptional signature of disease is constructed by differential gene expression analysis between the diseased tissue or cells and the control. The negative correlation between the transcriptional disease signature and the transcriptional signature of the drug, or a bioactive compound, is assumed to indicate its ability to “reverse” the disease process. A major limitation of traditional CMaP analysis is the use of signatures derived from bulk disease tissues. Since the key driver pathways are most likely dysregulated in only a subset of cells, the “averaged” transcriptional signatures resulting from bulk analysis lack the resolution to effectively identify effective therapeutic agents. The use of single-cell RNA-seq (scRNA-seq) transcriptomic assay facilitates construction of disease signatures that are specific to individual cell types, but methods for using scRNA-seq data in the context of CMaP analysis are lacking. Lymphangioleiomyomatosis (LAM) mutations in TSC1 or TSC2 genes result in the activation of the mTOR complex 1 (mTORC1). The mTORC1 inhibitor Sirolimus is the only FDA-approved drug to treat LAM. Novel therapies for LAM are urgently needed as the disease recurs with discontinuation of the treatment and some patients are insensitive to the drug. We developed methods for constructing disease transcriptional signatures and CMaP analysis using scRNA-seq profiling and applied them in the analysis of scRNA-seq data of lung tissue from naïve and sirolimus-treated LAM patients. New methods successfully implicated mTORC1 inhibitors, including Sirolimus, as capable of reverting the LAM transcriptional signatures. The CMaP analysis mimicking standard bulk-tissue approach failed to detect any connection between the LAM signature and mTORC1 signaling. This indicates that the precise signature derived from scRNA-seq data using our methods is the crucial difference between the success and the failure to identify effective therapeutic treatments in CMaP analysis.

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Lu, Zhihao, Huan Chen, Shuang Li, Xi Jiao, Lihong Wu, Jianing Yu, Lin Shen und Henghui Zhang. „A RNA signature predicts outcomes in immune checkpoint blockade treated gastrointestinal cancer patients.“ Journal of Clinical Oncology 37, Nr. 15_suppl (20.05.2019): e14071-e14071. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.e14071.

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e14071 Background: Cancer therapy has been greatly revolutionized in recent years by the conceptual developments in the field of cancer immunology. Growing evidence support the utility of immune checkpoint inhibition (ICB) in gastrointestinal (GI) cancer. However, a central question lies in understanding how therapeutic responsiveness is predicted. Methods: To address this, we evaluated tumor FFPE specimens from 97 patients who received ICB treatment. All patients were randomly assigned into discovery (60%) and validation (40%) cohorts. Tumor RNA before ICB treatment was analyzed on a multiplex RNA immune oncology (RNA IO) profiling sequencing panel. Results: We show that four immune-related gene expression signatures were upregulated in responders versus non-responders in the discovery cohort. Three of the four signatures showed significant correlation with clinic response and disease control rates. However, two previously reported RNA signatures, PD-L1 expression and MMR status revealed less predictive values in GI cancers. More importantly, we identified that higher levels of a 19-gene signature were remarkably associated with favorable overall survival (OS) and progression-free survival (PFS) when compared to patients with lower levels of signature in both the discovery and validation cohorts. Of note, a joint biomarker of tumor mutation burden (TMB) and the 19-gene signature may better stratify responders from non-responders in GI cancer patients. Conclusions: Our data provide evidence that a responsive feature, defined by a multi-gene expression pattern across different GI cancer types, can be obtained via a RNA quantitative strategy and may be explored as a future pan-cancer biomarker.

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Li, Chenyang, Thinh T. Nguyen, Jian-Rong Li, Xingzhi Song, Ignacio I. Wistuba, Andy Futureal, Jianhua Zhang et al. „Abstract 97: Multiregional profiling revealed intra-tumor transcriptomic heterogeneity associated with the prognosis in non-small cell lung cancer“. Cancer Research 83, Nr. 7_Supplement (04.04.2023): 97. http://dx.doi.org/10.1158/1538-7445.am2023-97.

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Abstract Introduction: Intratumor heterogeneity (ITH) describes the distinct tumor cell populations and microenvironments within the same tumor, which may profoundly impact cancer evolution and clinical outcomes. Non-small cell lung cancer (NSCLC) is not only a genetically diverse disease but also has high transcriptomic heterogeneity (RNA-ITH). The RNA-ITH limits the reproducibility of expression-based prognostic models, which is poorly understood. Methods: To address the issue, we investigated the effect of RNA-ITH on prognosis at both gene and signature levels using multiregional RNA-seq data from 45 NSCLC patients (145 regions) in the TRACERx study. We also performed multiregional RNA-seq of 25 NSCLC tumors (64 regions) for independent validation. Results: At the gene level, we found that the maximal expression of hazardous genes (Hazard Ration (HR) > 1) and the minimal expression of protective (HR < 1) genes across different regions within a tumor are more prognostic than their average expression. As for prognostic signatures, we first designed five different functions to transform the multiregional expression of signature genes into patient-level values. To calculate individual risk scores, we applied them to assist two existing prognostic gene signatures, ORACLE (Outcome Risk Associated Clonal Lung Expression) and WTGS (whole-transcriptomic gene signature). As a result, the best performance was achieved using the combination of maximal hazardous signature expressions and minimal protective signature expressions. We next developed a new signature called PACEG (Prognosis-Associated Clonally Expressed Genes) and proposed a multiregional assay for higher prognostic accuracy in NSCLC. We demonstrated significant improvement in PACEG performance by leveraging RNA-ITH captured by multiregional expression of signature genes. Finally, we utilized the same strategy to study the impact of tumor immune microenvironment ITH on patient prognosis. Consistently, the minimal/maximal infiltration of protective/hazardous immune cells across tumor regions was the best measurement associated with prognosis in NSCLC. These results were independently validated by our local datasets. Conclusions: The prognosis of NSCLC patients is often driven by the most aggressive tumor subclones. Our study proposed a novel strategy to incorporate RNA-ITH with expression-based prognostic models. Multiple distinct tumor regions should be considered to overcome the ITH issue for better prognostic evaluation, e.g., using the minimal/maximal expression of protective/hazardous signature genes across all regions to calculate the risk score in individuals. We also developed the PACEG panel composed of 26 genes that could be potentially applied in clinical specimens to identify high-risk NSCLC patients who may benefit from intensified adjuvant therapy. Citation Format: Chenyang Li, Thinh T. Nguyen, Jian-Rong Li, Xingzhi Song, Ignacio I. Wistuba, Andy Futureal, Jianhua Zhang, Shawna M. Hubert, Jia Wu, Jianjun Zhang, Chao Cheng. Multiregional profiling revealed intra-tumor transcriptomic heterogeneity associated with the prognosis in non-small cell lung cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 97.

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Wen, Huaming, Ryan A. Gallo, Xiaosheng Huang, Jiamin Cai, Shaoyi Mei, Ammad Ahmad Farooqi, Jun Zhao und Wensi Tao. „Incorporating Differential Gene Expression Analysis with Predictive Biomarkers to Identify Novel Therapeutic Drugs for Fuchs Endothelial Corneal Dystrophy“. Journal of Ophthalmology 2021 (28.06.2021): 1–8. http://dx.doi.org/10.1155/2021/5580595.

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Purpose. Based on the differential gene expression analysis for predictive biomarkers with RNA-Sequencing data from Fuchs endothelial corneal dystrophy (FECD) patients, we are aiming to evaluate the efficacy of Library of Integrated Network-based Cellular Signatures (LINCS) perturbagen prediction software to identify novel pharmacotherapeutic targets that can revert the pathogenic gene expression signatures and reverse disease phenotype in FECD. Methods. A publicly available RNA-seq dataset was used to compare corneal endothelial specimens from controls and patients with FECD. Based on the differential gene expression analysis for predictive biomarkers, we evaluated the efficacy of LINCS perturbagen prediction software to identify novel therapeutic targets that can revert the pathogenic gene expression signatures and reverse disease phenotypes in FECD. Results. The RNA-seq dataset of the corneal endothelial cells from FECD patients revealed the differential gene expression signatures of FECD. Many of the differential expressed genes are related to canonical pathways of the FECD pathogenesis, such as extracellular matrix reorganization and immunological response. The expression levels of genes VSIG2, IL18, and ITGB8 were significantly increased in FECD compared with control. Meanwhile, the expression levels of CNGA3, SMOX, and CERS1 were significantly lower in the FECD than in control. We employed LINCS L1000 Characteristic Direction Signature Search Engine (L1000-CDS2) to investigate pathway-based molecular treatment. L1000-CDS2 predicted that small molecule drugs such as histone deacetylase (HDAC) inhibitors might be a potential candidate to reverse the pathological gene expression signature in FECD. Conclusions. Based on differential gene expression signatures, several candidate drugs have been identified to reverse the disease phenotypes in FECD. Gene expression signature with LINCS small molecule prediction software can discover novel preclinical drug candidates for FECD.

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Wang, Kang, Yajing Zhu, Ioannis Zerdes, Emmanouil Sifakis, Georgios Manikis, Dimitrios Salgkamis, Nikolaos Tsiknakis et al. „Abstract PO2-07-06: Multimodal learning predictor of HER2-positive breast cancer therapy response in the randomized PREDIX HER2 trial“. Cancer Research 84, Nr. 9_Supplement (02.05.2024): PO2–07–06—PO2–07–06. http://dx.doi.org/10.1158/1538-7445.sabcs23-po2-07-06.

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Abstract Background: The PREDIX HER2 trial, compared six courses of docetaxel, trastuzumab, and pertuzumab (DTP) vs. trastuzumab emtansine (T-DM1) as neoadjuvant treatment for HER2-positive breast cancer (BC). Similar rates of pathologic complete response (pCR) were seen. Methods: Clinicopathological, shallow whole-genome sequencing (CUTseq, n=176), whole exome sequencing (WES, n=192), and RNA-sequencing (RNA-seq, n=187) data were generated using fresh-frozen baseline core biopsies. Potential tumor intrinsic resistance factors and microenvironment components were quantified by multi-omics analysis, including BC-specific somatic mutations and copy number alterations (CNA), COSMIC mutational signatures, CNA-based chromosomal instability signatures (CIN), subclone percentage, PAM50 subtype, GGI/PIK3CA score, HER2DX score, immune profiles (Danaher signature score, TIDE score and immune repertoires). We assessed the association of biomarkers with pCR in each treatment arm using logistic regression adjusting for hormone receptor (HR) status, and evaluated their predictive value by adding the interaction term (biomarker x treatment arm). In addition, a machine learning (ML) analysis was conducted from different classifiers, comprising unimodal ML-based models from clinical, RNA and DNA information, respectively. Model performance was assessed using the mean and standard deviation (mean ± std) of the area under receiver operator characteristic curve (AUC), positive predictive value (PPV) and negative predictive value (NPV) using a nested stratified cross-validation (CV) schema of 200 outer shuffle splits and 100 inner 5-fold CV to mitigate potential risk of overfitting. Results: In DTP arm, patients with higher ERBB2 copy ratio (ORadj=1.98, p=0.004) or mRNA (ORadj=3.08, p< 0.001) or HER2-enriched subtype (PAM50) (ORadj=1.78, p=0.02) had higher pCR rates, while ESR1 gene expression (ORadj=0.59, p=0.07) predicted treatment resistance despite adjustment for HR status. Conversely, response to T-DM1 was less likely to depend on ERBB2 profiles and only PAM50 HER2 enriched subtype (ORadj=1.53, p=0.1) showed higher pCR rate (52% vs. 25%) than other subtypes. Both ESR1 (ORadj=0.4, p=0.008) and PGR (ORadj=0.5, p=0.03) gene expression were independent predictors of T-DM1 resistance. Pre-treatment immune exclusion metrics could predict resistance to DTP (endothelial cell, ORadj=0.67, p=0.07) and T-DM1 (neutrophils, ORadj=0.54, p=0.02; mast cells, ORadj=0.57, p=0.02; cancer-associated fibroblasts, ORadj=0.67, p=0.09)), respectively. Predefined metrics such as PIK3CA signature score (ORadj =1.67, p=0.04) and Taxane response score (ORadj =1.64, p=0.03) were positively related to pCR in DTP arm. Genome instability, involving CIN CX2 signature (impaired homologous recombination) (ORadj=1.71, p=0.05), COSMIC signature6 (ORadj =1.53, p=0.07) and signature13 (ORadj =1.57, p=0.05), predicted benefit from DTP. The biomarker-treatment interaction tests were significant for HER2DX (pinteraction=0.004) and COSMIC signature15 (defective DNA mismatch repair) (pinteraction=0.007): lower HERDX score (ORadj =0.73, p=0.14) or higher COSMIC signature15 score (ORadj =1.51, p=0.1) could identify patients benefiting from T-DM1, while being resistant to DTP (HERDX: ORadj =1.46, p=0.13; signature15: ORadj =0.70, p=0.1). In the ML models, clinical information yielded an AUC=0.62±0.07, PPV=0.64±0.12 and NPV=0.64±0.06; for DNA data, AUC was equal to 0.70±0.08, PPV=0.72±0.09 and NPV=0.71±0.07; an adaptive boosting ensemble learning on RNA reported slightly increased pCR prediction performance (AUC=0.72±0.06, PPV=0.64±0.06, NPV=0.80±0.09). Conclusion: This study demonstrates that antibody–drug conjugates and standard treatment harbor strikingly distinctive biomarkers across tumor ecosystem. Further external validation and integrated ML model comprising all unimodal models are ongoing. Citation Format: Kang Wang, Yajing Zhu, Ioannis Zerdes, Emmanouil Sifakis, Georgios Manikis, Dimitrios Salgkamis, Nikolaos Tsiknakis, Luuk Harbers, Nicola Crosetto, Jonas Bergh, Alexios Matikas, Thomas Hatschek, Theodoros Foukakis. Multimodal learning predictor of HER2-positive breast cancer therapy response in the randomized PREDIX HER2 trial [abstract]. In: Proceedings of the 2023 San Antonio Breast Cancer Symposium; 2023 Dec 5-9; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2024;84(9 Suppl):Abstract nr PO2-07-06.

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Erbe, Rossin, Michelle M. Stein, Tim A. Rand und Justin Guinney. „Abstract 2281: A tumor-intrinsic signature involving immunosuppression via MIF-CD74 signaling is associated with overall survival in ICT-treated lung adenocarcinoma“. Cancer Research 84, Nr. 6_Supplement (22.03.2024): 2281. http://dx.doi.org/10.1158/1538-7445.am2024-2281.

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Abstract Introduction: Immune checkpoint therapies (ICT) have changed cancer care, yielding robust and durable responses in a subset of patients. Identifying patients who are likely to respond to ICT remains an ongoing challenge. In addition, only a portion of patients with clinical biomarkers respond to therapy. Signatures of RNA expression have been developed to predict response, the majority of which focus on T-cell and cytotoxicity markers, yet have been unable to substantially improve outcome predictions. Here, we present a RNA signature that instead describes tumor-intrinsic immune resistance and a potential mechanism of immunosuppression via tumor signaling on macrophages, derived from single-cell RNA-sequencing (scRNA-seq). Methods: We performed dimensionality reduction using a Variational Autoencoder (VAE) on 30 scRNA-seq samples from 15 lung adenocarcinoma (LUAD) patients, comprising a total of 183,873 cells from the Cell Ranger pipeline. The VAE model was trained on each sample for 250 iterations, yielding 20 signatures from each patient, for a total of 300 signatures. The relationship of each signature with real-world overall survival (rwOS) across 1,983 bulk RNA-sequenced LUAD patients treated with an FDA approved ICT was assessed via a Cox proportional hazards model with risk set adjustment, using TMB and line of therapy as covariates. The NATMI python package was used to identify putative active ligand-receptor interactions between tumor cells and the immune environment. Results: Among the VAE encodings, we identified an immune resistance signature significantly associated with decreased rwOS across the patient cohort (HR = 4.2 [2.8-6.3], adjusted p = 4.3e-10). This signature was derived from a small cluster of neoplastic cells (4.4% of cells) in a patient sample that was otherwise dominated by immune cells, including a substantial fraction of cytotoxic CD8 T cells (24.5%). The strongest predicted ligand-receptor interactions were found between the neoplastic cells and macrophages, via the MIF-CD74 interaction, an interaction we found upregulated in multiple single-cell tumor samples. Further, MIF RNA expression alone was significantly associated with rwOS across the 1,983 patient LUAD cohort (HR = 1.5 [1.1-2.1], p = 0.004). Discussion: MIF-CD74 is a known immunosuppressive interaction and MIF signaling from tumor cells on macrophages has been previously shown to have immunosuppressive effects in a mouse model of melanoma that were largely reversible via MIF-CD74 blockade. Taken together, these results identify a signature of tumor intrinsic immune suppression that can indicate patients likely to experience reduced benefit from ICT. In addition, this signature provides evidence to support blockade of the MIF-CD74 axis as a means to enhance anti-tumor immune responses in LUAD. Citation Format: Rossin Erbe, Michelle M. Stein, Tim A. Rand, Justin Guinney. A tumor-intrinsic signature involving immunosuppression via MIF-CD74 signaling is associated with overall survival in ICT-treated lung adenocarcinoma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 2281.

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Qiu, Lipeng, Tao Wang, Qi Ge, Han Xu, Yihang Wu, Qi Tang und Keping Chen. „Circular RNA Signature in Hepatocellular Carcinoma“. Journal of Cancer 10, Nr. 15 (2019): 3361–72. http://dx.doi.org/10.7150/jca.31243.

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Dissertationen zum Thema "RNA signature"

Mullani, Nowsheen. „An RNA Signature Links Oxidative Stress To Cellular Senescence“. Electronic Thesis or Diss., Sorbonne université, 2019. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2019SORUS560.pdf.

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Le stress oxydatif est l’une des voies menant à la sénescence cellulaire. Bien que les dommages causés par les espèces réactives de l'oxygène aux protéines et à l'ADN soient bien décrits, notre compréhension de la manière dont la transcription peut participer à l'apparition de la sénescence est encore limitée. Au niveau de la transcription, le stress oxydatif entraîne l’accumulation d’ARN promoteurs (ARNAu) et d’ARN amplificateur (ARNs), conséquence de la libération défectueuse du RNAPII de la chromatine, un phénomène connu sous le nom de RNAPII crawling. Nous avons observé que l'exploration de RNAPII était également détectée en aval d'une petite série de gènes connus pour être régulés par HP1Υ au niveau de leur terminaison. L'exploration de ce phénomène a donné un résultat inattendu, en ce sens qu'il a révélé un effet inhibiteur du peroxyde d'hydrogène sur le complexe exosome d'ARN impliqué dans la dégradation des ARN polyadénylés. Le RNAPII rampant a pour résultat la transcription de séquences d’ALU situées au voisinage des promoteurs et amplificateurs et en aval de gènes sans intron et de petites séries de gènes contenant un intron. Comme les séquences ALU contiennent des séquences A codées par le génome, elles doivent normalement être dégradées par l’exosome de l’ARN. Cependant, comme le stress oxydatif inhibe également cette activité d'ARNase, les ARNm contenant des séquences d'ALU transcrites par hasard se stabilisent et sont détectés dans le cytoplasme et même dans les fractions de polysomes. Ce phénomène peut participer à l'apparition de la réponse à l'interféron associée au stress oxydatif
Oxidative Stress is one of the routes leading to cellular senescence. While the damages that reactive oxygen species inflict on proteins and DNA are well described, our insight on how transcription may participate in the onset of senescence is still limited. At a transcriptional level, oxidative stress results in accumulation of promoter RNAs (uaRNAs) and enhancer RNAs (eRNAs) as a consequence of defective release of the RNAPII from the chromatin a phenomenon known as RNAPII crawling. We observed that RNAPII crawling was also detected downstream of a small series of genes known to be regulated by HP1Υ at the level of their termination. Exploring this phenomenon yielded an unexpected result in the sense that it revealed an inhibiting effect of hydrogen peroxide on the RNA exosome complex involved in degradation of polyadenylated RNAs. The crawling RNAPII results in the transcription of ALU sequences located in the neighborhood of promoters and enhancers and downstream of intron-less genes and of small series of intron-containing genes. As ALU sequences contain genome encoded A tracts, they should normally be degraded by the RNA exosome. Yet, as oxidative stress also inhibits this RNAse activity, mRNAs containing serendipitously transcribed ALU sequences get stabilized and are detected in the cytoplasm and even polysome fractions. This phenomenon may participate in the onset of the interferon response associated with oxidative stress

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Harling, Leanne. „Investigating the micro-RNA and metabolic signature of human postoperative atrial fibrillation“. Thesis, Imperial College London, 2014. http://hdl.handle.net/10044/1/29130.

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Atrial fibrillation (AF) is the commonest disorder of cardiac rhythm. Following coronary artery surgery approximately 1 in 3 patients will develop de novo post-operative AF (POAF) leading not only to prolonged hospital stay but also to increased morbidity and mortality. The pathophysiology of this arrhythmia is highly complex, and combines factors such as ion channel dysfunction, inflammation, oxidative stress, fibrosis and autonomic dysfunction that through electrical and structural remodelling promote both triggering and maintenance of this arrhythmia. For many years POAF has been regarded as a reactive phenomenon, occurring in response to post surgical inflammatory stressors and electrolyte imbalance. However, it is also possible that in a proportion of patients, prior cardiomyocyte remodelling predisposes to atrial arrhythmogenesis when exposed to surgical stress. Understanding the genomic and metabolic mechanisms that underlie this substrate may not only provide novel diagnostic biomarkers to identify at risk patients, but also isolate previously unrecognised therapeutic targets for prevention and treatment. In this work, a clinical observational study was utilised to obtain microRNA, gene expression and metabolic profiles of patients developing POAF after coronary artery bypass graft (CABG) surgery. Based on these results, a network of genomic and subsequent downstream pathway interactions was established to characterise the atrial substrate of post-operative AF. Furthermore, analysis of pre-operative blood was performed in order to identify novel microRNA that may provide a platform for biomarker development. Finally, the metabolic signature of the atrial myocardium and its relationship with the surrounding epicardial adipose were investigated to complete a comprehensive overview of the central mechanisms thought to underlie POAF pathogenesis. This work demonstrates that prior to surgery and the onset of arrhythmia, several distinct genomic and post-translational characteristics are evident in the both the myocardium and circulating blood of patients going on to develop POAF. Analysis of right atrial biopsies highlights a characteristic microRNA profile associated with POAF, and identifies target genes regulating intracellular signalling pathways, leukocyte recruitment, and ion channel remodelling. Furthermore, selected gene expression analysis demonstrates a de-differentiated phenotype similar to that seen in chronic AF, whilst at the same time establishing that disordered cardiomyocyte calcium handling is apparent at the time of surgery. Finally, analysis of the pre-operative circulating blood serum highlights microRNA selectively upregulated in POAF and establishes the potential for future biomarker development. In summary, the results presented here support the presence of a pre-existing atrial substrate in POAF, suggesting the potential exists for high-risk patients to be identified prior to surgery and the onset of arrhythmia. Furthermore, for the first time a number of similarities have been made apparent between post-operative and chronic AF, implying a common mechanistic spectrum of structural and electrical remodelling. As a consequence, the results presented in this thesis have not only improved our understanding of the complex interplay of factors leading to the pathogenesis of AF, but also provide a platform for both the development of a unique clinical biomarker and the identification of novel therapeutic targets.

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Hossain, Mahmud. „Characterization of non-protein coding ribonucleic acids by their signature digestion products and mass spectrometry“. University of Cincinnati / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1204947468.

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Hauenschild, Ralf [Verfasser]. „RNA-Seq and CoverageAnalyzer reveal sequence dependent reverse transcription signature of N-1-methyladenosine / Ralf Hauenschild“. Mainz : Universitätsbibliothek Mainz, 2017. http://d-nb.info/1129476375/34.

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Yepmo, Mélissa. „Signature unique de l’ARN circulaire dans les muscles squelettiques humains de différentes sensibilités à l’insuline“. Electronic Thesis or Diss., Strasbourg, 2023. http://www.theses.fr/2023STRAJ109.

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Les ARN circulaires désignent une classe d'ARN non codants qui se caractérisent par une structure en boucle fermée de manière covalente. Sur le plan fonctionnel, ils peuvent agir sur la physiologie cellulaire en inhibant les microARN et en régulant l'expression des gènes et des protéines. La fonction émergente de ces ARNc n'est pas entièrement comprise, mais des études initiales ont récemment montré que les ARNc sont impliqués dans la régulation de la sécrétion d'insuline. A travers ces travaux, nous avons cherché à identifier les ARNc dans le muscle squelettique au niveau des fibres glycolytiques et oxydatives de patients sains ou atteints de diabète de type 2. Nos résultats ont démontré une signature unique en ARN circulaire non seulement en fonction du statut (sain ou DT2) mais aussi en fonction du type de fibres musculaires (triceps ou soleus). Notre étude a pu mettre en évidence pour la première fois un nouveau moyen de régulation de l’expression des gènes et des protéines, indépendamment de ce qui est déjà connu au niveau du muscle squelettique. Ces résultats permettent l’identification de nouveaux acteurs impliqués dans le développement du diabète de type 2 avec l’identification potentielle de nouvelles cibles thérapeutiques
Circular RNAs are a class of non-coding RNAs characterized by a covalently closed loop structure. Functionally, they can act on cell physiology by inhibiting microRNAs and regulating gene and protein expression. The emerging function of circRNAs is not fully understood, but initial studies have recently shown that they are involved in the regulation of insulin secretion. In this work we tried to identify circRNAs in skeletal muscle at the level of glycolytic and oxidative fibers in healthy and type 2 diabetic patients. Our results showed a unique circular RNA signature not only as a function of status (healthy or T2DM) but also as a function of muscle fibre type (triceps or soleus). For the first time, our study has been able to identify a new way of regulating gene and protein expression independently of what is already known in skeletal muscle. These results allowed us to identify new key molecules involved in the development of type 2 diabetes, with the potential to identify new therapeutic targets

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Panasenkava, Veranika. „Utilisation de cellules souches pluripotentes induites combinée à une approche transcriptomique pour améliorer le diagnostic moléculaire des troubles du neurodéveloppement chez l’homme“. Electronic Thesis or Diss., Université de Rennes (2023-....), 2024. http://www.theses.fr/2024URENB060.

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L'holoprosencéphalie (HPE) est une maladie rare qui affecte le développement de la ligne médiane du cerveau antérieur dès les premiers stades embryonnaires, rendant son diagnostic moléculaire complexe. Elle résulte principalement d’altérations génétiques entraînant une réduction de l'activité de la voie de signalisation Sonic Hedgehog (SHH). Cependant, un diagnostic moléculaire précis n’est possible que pour 30% des patients, ce qui souligne l’importance de développer des nouvelles approches diagnostiques. Le principal obstacle réside dans l'impossibilité d'accéder au tissu primaire affectée par la pathologie, soit le neuroectoderme antérieur. Pour surmonter cet obstacle, j’ai mis au point un modèle in vitro du développement du neuroectoderme antérieur en utilisant des cellules souches pluripotentes induites. Ce modèle m’a permis de produire des données transcriptomiques permettant d’évaluer les impacts moléculaires de la déficience en SHH et de définir des signatures transcriptomiques décrivant les variations de l'activité de la voie SHH pouvant être corrélées à la sévérité des phénotypes d’HPE. Ce travail a également révélé de nouveaux gènes co-exprimés et régulés par SHH, qui pourraient constituer de nouveaux marqueurs génétiques de l'HPE. Ces avancées ouvrent la voie à la création d’outils de diagnostic innovants, visant à améliorer la précision du diagnostic pour les patients atteints d'HPE
Abstract : Holoprosencephaly (HPE) is a rare disorder that affects the development of the midline of the forebrain during the earliest stages of embryogenesis, making molecular diagnosis challenging. It primarily results from genetic alterations that lead to a reduction in the activity of the Sonic Hedgehog (SHH) signaling pathway. However, a precise molecular diagnosis is only possible for 30% of patients, highlighting the importance of developing new diagnostic approaches. The main challenge is the inaccessibility of the primary tissue, specifically the anterior affected by HPE, namely the anterior neuroectoderm. To overcome this challenge, I established an in vitro model of anterior neuroectoderm using induced pluripotent stem cells. This model allowed me to generate transcriptomic data to assess the molecular impacts of SHH deficiency and define transcriptomic signatures that describe variations in SHH pathway activity, which may correlate with the severity of HPE phenotypes. This work also revealed new co-expressed and SHH-regulated genes, which could serve as new genetic markers for HPE. These advances pave the way for innovative diagnostic tools aimed at improving diagnostic accuracy for patients with HPE

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Gendron, Judith. „Les longs ARN non codants, une nouvelle classe de régulateurs génomique tissu-spécifique : signature moléculaire spécifique des neurones dopaminergiques et sérotoninergiques“. Thesis, Paris 6, 2017. http://www.theses.fr/2017PA066518.

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Seul 1,2% du génome code des protéines :98,8% est non-codant,cependant 93% du génome est transcrit, principalement en longs ARN non-codants (lncRNA). Or ces lncRNA constituent une nouvelle classe de régulateurs génomique agissant à tous les niveaux d’expression des gènes et ils sont fortement spécifiques du tissu,modulés au cours du temps et en conditions physiopathologiques.Ainsi,nous proposons que chaque cellule spécifiée exprime son répertoire de lncRNA spécifique avec une carte des zones de chromatines ouvertes renseignant son identité cellulaire.Dans cette perspective,nous avons isolé par FACS 2types cellulaires impliqués dans des pathologies: i) des neurones dopaminergiques humains(nDA) différenciés à partir d’hiPS et ii) des neurones DA et sérotoninergiques (n5-HT)murins.Sur ces 2types neuraux isolés,nous avons identifié 1363 lncRNA exprimés dans les nDA (dont 989nouveaux) constituant le répertoire des neurones DA et 1257 lncRNA dans les n5-HT (719nouveaux) constituant le répertoire des n5-HT.Or leur comparaison a montré que seuls 194 lncRNA sont communs aux 2types cellulaires:la majorité des lncRNA est exprimée soit dans les nDA soit dans les n5-HT,attestant leur spécificité cellulaire.De plus,39%des zones de chromatines ouvertes/potentiellement régulatrices des nDA ne sont pas non plus retrouvées dans les n5-HT.Ainsi, nous avons généré un catalogue d’éléments non codants constituant des signatures moléculaires spécifiques des nDA et n5-HT,ouvrant de nouvelles pistes physiopathologiques:Dans cette optique,les signatures non codantes DA ont été comparées avec les SNP associés à la maladie de Parkinson et des études de fonction sur des lncRNA candidats ont été réalisées
Only 1.2% of the genome codes for proteins; 98.8% is thus non-coding, despite 93% of the human genome being actively transcribed, mostly in long non-coding RNA (lncRNA).These lncRNA constitute a new class of genomic regulator capable of acting at all levels of gene expression and their expression is highly tissue-specific,modulated during the time and under normal/pathological conditions.Thus, we propose that each specified cell expresses a specific repertoire of lncRNA correlated to open/active chromatin regions specifying its cellular identity.In this context, we isolated by FACS 2neural types involved in many pathologies: i) human dopaminergic neurons (nDA) differentiated from hiPS and ii) DA and serotoninergic (n5-HT) neurons. From these 2neural types, we identified 1,363 lncRNA in nDA (among which 989 new, whether 73%) constituting the repertoire of nDA, and 1,257 lncRNA (among which 719 new) constituting the repertoire of n5-HT. Moreover,their comparison has shown that only 194 lncRNA are common to both neural types:thus the majority of lncRNA is expressed either in nDA or in n5-HT, indicating a high degree of cell-specificity.In addition, 39% of open chromatin regions, potentially regulatory, were also not detected in the n5-HT.Thus, we have generated DA and 5-HT specific catalogues of non-coding elements of the genome, which constitute DA and 5-HT specific molecular signatures, that could participate in deepening our knowledge regarding nDA or n5-HT development and dysfunctions. With this in mind,these DA specific elements have been compared with the SNP described as Parkinson Disease risk variants and candidate lncRNA were selected to perform studies of function

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Castleberry, Colette M. „Quantitative Identification of Non-coding RNAs by Isotope Labeling and LC-MS/MS“. University of Cincinnati / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1258474676.

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Jebbawi, Fadi. „Etude des lymphocytes T régulateurs naturels CD8+CD25+: signature micro-ARN et effets des micro-ARNs sur l'expression de FOXP3, CTLA-4 et GARP“. Doctoral thesis, Universite Libre de Bruxelles, 2014. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209338.

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Mon travail de thèse a consisté à caractériser une sous-population de lymphocytes T régulateurs naturels de phénotype CD8+CD25+.

Nous avons purifié les CD8+CD25+ nTregs et vérifié par cytométrie de flux leur expression en FOXP3 et CTLA-4. Puis nous avons pu montrer que ces cellules possèdent des propriétés suppressives dans un test d’inhibition de la prolifération de lymphocytes T activés allogéniquement. Les lymphocytes CD8+CD25+ nTregs expriment les gènes FOXP3, CTLA-4, GARP et CCL-4 et les cytokines IL-10 et TGF-β. Par contre, les gènes CD28, ICOS, FOXO1 et Helios sont sous-exprimés dans les nTregs CD8+CD25+ par rapport aux lymphocytes T CD8+CD25-.

Nous avons établi une signature micro-ARN qui comprend 10 micro-ARNs différentiellement exprimés :7 micro-ARNs sous-exprimés "miR-9, -24, -31, -155, -210, -335 et -449 " et 3 micro-ARNs surexprimés " miR-214, -205 et -509". De plus, nous avons pu explorer la relevance biologique de cette signature micro-ARN en montrant dans un premier temps que les miRs "-31, -24, -210, -335" ciblent spécifiquement la région 3'UTR de FOXP3, de même les miR-9 et miR-155 ciblent la région 3'UTR de CTLA-4, et les miR-24, et -335 ciblent la région 3'UTR de GARP. Ceci a été fait par des expériences de co-transfections suivies d'une mesure de l'activité rapportrice luciférase. De plus, nous avons pu démontrer par des expériences de transduction lentivirale ex vivo, de cellules T primaires, que des micro-ARNs de la signature régulent l’expression de FOXP3, CTLA-4 et GARP dans les Tregs naturels CD8+CD25+ humains.

Cette étude montre l'importance des micro-ARNs dans la régulation post-transcriptionnelle des gènes impliqués dans la fonction régulatrice des lymphocytes T régulateurs.

Doctorat en Sciences
info:eu-repo/semantics/nonPublished

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Sousa, Rodrigo Guarischi Mattos Amaral de. „O transcritoma da retinopatia induzida por oxigênio e uma assinatura gênica prognóstica baseada em angiogênese para predição de recidiva de cancer de mama“. Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/95/95131/tde-28092017-112917/.

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Angiogênese é o processo de formação de novos vasos sanguíneos a partir dos vasos existentes. É um processo vital, mas muitas doenças também dependem deste mecanismo para obter nutrientes e progredir. Estas \"doenças dependentes de angiogênese\" incluem cânceres, retinopatias e degeneração macular. Alguns inibidores da angiogênese foram desenvolvidos na última década, com o objetivo de auxiliar no manejo dessas doenças e melhorar a qualidade de vida dos pacientes. A maioria destes compostos funciona inibindo a ligação de VEGFA/VEGFR2, que também é um elemento importante para a sobrevivência de células endoteliais quiescentes; e isso pode explicar parcialmente eventos adversos observados em alguns ensaios clínicos. Nossa hipótese é que a melhoria das terapias anti-angiogênicas depende de uma compreensão melhor e mais ampla desse processo, especialmente quando relacionada à progressão das doenças. Utilizando RNA-Seq e um modelo animal bem aceito de angiogênese, o modelo murino de Retinopatia Induzida por Oxigênio, exploramos o transcritoma e identificamos 153 genes diferencialmente expressos durante a angiogênese. Uma extensiva validação de vários genes realizada por qRT-PCR e hibridização in-situ confirmou a superexpressão de Esm1 em células endoteliais de tecidos com angiogênese ativa. A análise de enriquecimento desta lista de genes confirmou a ligação da angiogênese com genes frequentemente mutados em tumores, consistente com a conhecida ligação entre câncer e angiogênese, e forneceu sugestões de fármacos já aprovados que podem ser reutilizados para controlar a angiogênese em circunstâncias patológicas. Finalmente, com base neste panorama amplo da angiogênese, fomos capazes de criar um biomarcador molecular com poder prognóstico para a predição da recidiva de câncer de mama, com aplicações clínicas promissoras. Em resumo, este trabalho revelou com sucesso genes relacionados à angiogênese e forneceu novas alternativas terapêuticas, incluindo potenciais fármacos para reposicionamento. Esse conjunto de genes diferencialmente expressos é também um recurso valioso para investigações futuras.
Angiogenesis is the process of formation of new blood vessels based on existing vessels. It is a vital process but many diseases also rely on this mechanism to get nourishment and progress. These so called angiogenesis-dependent diseases include cancers, retinopathies and macular degeneration. Some angiogenesis inhibitors were developed in the past decade, aiming to help the management of such diseases and improve patients quality of life. Most of these compounds work by inhibiting VEGFA/VEGFR2 binding, which is also a key element to the survival of quiescent endothelial cells; this may partly explain unanticipated adverse events observed in some clinical trials. We hypothesize that the improvement of anti-angiogenesis therapies hinges on a better and broader understanding of the process, especially when related to diseases\' progression. Using RNA-seq and a well accepted animal model of angiogenesis, the murine model of Oxygen Induced Retinopathy, we have explored the transcriptome landscape and identified 153 genes differentially expressed in angiogenesis. An extensive validation of several genes carried out by qRT-PCR and in-situ hybridization confirmed Esm1 overexpression in endothelial cells of tissues with active angiogenesis, providing confidence on the results obtained. Enrichment analysis of this gene list endorsed a narrow link of angiogenesis and frequently mutated genes in tumours, consistent with the known connection between cancer and angiogenesis, and provided suggestions of already approved drugs that may be repurposed to control angiogenesis under pathological circumstances. Finally, based on this comprehensive landscape of angiogenesis, we were able to create a prognostic molecular biomarker for prediction of breast cancer relapse, with promising clinical applications. In summary, this work successfully unveiled angiogenesis-related genes, providing novel therapeutic alternatives, including potential drugs for repositioning. The set of differentially expressed genes is also a valuable resource for further investigations.

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Mehr Quellen

Bücher zum Thema "RNA signature"

Steele, E. J. Lamarck's signature: How retrogenes are changing Darwin's natural selection paradigm. Reading, Mass: Perseus Books, 1998.

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A, Lindley Robyn, und Blanden Robert V, Hrsg. Lamarck's signature: How retrogenes are changing Darwin's natural selection paradigm. St Leonards, NSW: Allen & Unwin, 1999.

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Schneier, Bruce. Cryptographie appliquée: Protocoles, algorithmes et codes sources en C. 2. Aufl. Paris: Vuibert, 2001.

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Martin, Keith M. Digital Signature Schemes. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198788003.003.0007.

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In this chapter, we discuss digital signature schemes. We start by considering the general requirements of a digital signature scheme. We show first that a digital signature scheme could be established using symmetric techniques. We then consider the more conventional use of public-key cryptography to create digital signature schemes. We compare two different approaches to building a digital signature scheme and illustrate how to manifest these using RSA. We then discuss practical issues concerning digital signature schemes, including different aspects of their security. We close by providing a detailed comparison between digital signatures and handwritten signatures which serves to both illustrate the strengths and vulnerabilities of digital signature schemes.

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Buchteile zum Thema "RNA signature"

Vogg, Matthias Christian, und Brigitte Galliot. „Combining RNAi-Mediated β-Catenin Inhibition and Reaggregation to Study Hydra Whole-Body Regeneration“. In Methods in Molecular Biology, 635–47. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2172-1_34.

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AbstractIn addition to its ability to regenerate any amputated body part, the Hydra freshwater polyp shows the amazing ability to regenerate as a full polyp after a complete dissociation of its tissues. The developmental processes at work in reaggregates undergoing whole-body regeneration can be investigated at the molecular level by RNA interference (RNAi). Here we provide a protocol that combines β-catenin RNAi with reaggregation. This protocol serves as a basis to generate “RNAi-reaggregates,” followed by the extraction of high-quality RNA for the precise quantification of gene expression by real-time PCR. This protocol is efficient, providing both a molecular signature, with the significant downregulation of β-catenin and Wnt3, as well as a robust phenotype, the lack of axis formation, which is observed in all reaggregates.

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Schrauder, Michael G., und Reiner Strick. „From the Genetic Make-Up to the Molecular Signature of Non-Coding RNA in Breast Cancer“. In Nucleic Acids as Molecular Diagnostics, 129–54. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2014. http://dx.doi.org/10.1002/9783527672165.ch06.

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Bombaci, Mauro, Ivan Ferrari, Saveria Mazzara und Riccardo L. Rossi. „Refinement of Single-Cell RNA-seq Gene Expression Signatures with Combiroc“. In RNA Technologies, 61–74. Cham: Springer Nature Switzerland, 2024. http://dx.doi.org/10.1007/978-3-031-62178-9_3.

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Katzenbeisser, Stefan. „RSA Signatures“. In Recent Advances in RSA Cryptography, 111–36. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1431-2_8.

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Micali, Silvio, und Ronald L. Rivest. „Transitive Signature Schemes“. In Topics in Cryptology — CT-RSA 2002, 236–43. Berlin, Heidelberg: Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/3-540-45760-7_16.

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Johnson, Robert, David Molnar, Dawn Song und David Wagner. „Homomorphic Signature Schemes“. In Topics in Cryptology — CT-RSA 2002, 244–62. Berlin, Heidelberg: Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/3-540-45760-7_17.

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Komano, Yuichi, Kazuo Ohta, Atsushi Shimbo und Shinichi Kawamura. „Toward the Fair Anonymous Signatures: Deniable Ring Signatures“. In Topics in Cryptology – CT-RSA 2006, 174–91. Berlin, Heidelberg: Springer Berlin Heidelberg, 2006. http://dx.doi.org/10.1007/11605805_12.

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Bleichenbacher, Daniel. „Compressing Rabin Signatures“. In Topics in Cryptology – CT-RSA 2004, 126–28. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-540-24660-2_10.

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Aguilar-Melchor, Carlos, Martin R. Albrecht, Thomas Bailleux, Nina Bindel, James Howe, Andreas Hülsing, David Joseph und Marc Manzano. „Batch Signatures, Revisited“. In Topics in Cryptology – CT-RSA 2024, 163–86. Cham: Springer Nature Switzerland, 2024. http://dx.doi.org/10.1007/978-3-031-58868-6_7.

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Pointcheval, David, und Olivier Sanders. „Short Randomizable Signatures“. In Topics in Cryptology - CT-RSA 2016, 111–26. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-29485-8_7.

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Konferenzberichte zum Thema "RNA signature"

Gasparini, Pierluigi, Lorenza Landi, Stefania Carasi, Carmelo Tibaldi, Luciano Cascione, Greta Alì, Armida D'Incecco et al. „Abstract 3061: Micro-RNA signature differences in lung cancer patients withALKtranslocation,EGFRmutations andKRASmutations.“ In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-3061.

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Guerrero, Sergi, Rudolf Fehrmann und Marcel ATM van Vugt. „Abstract 1406: Towards an RNA expression-based signature for oncogene-induced replication stress“. 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.am2017-1406.

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Jang, Jin Sung. „Abstract 4354: Molecular signature of multiple myeloma progression through single-cell RNA-seq“. 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.am2018-4354.

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Perik-Zavodskaia, O. Yu, R. Yu Perik-Zavodskii, Yu A. Shevchenko, M. S. Fisher, M. O. Volynets, S. Alrhmoun, K. V. Nazarov et al. „SINGLE СELL RNA SEQUENCING REVEALS TRANSCRIPTOMIC INSIGHTS OF NY-ESO-1 SPECIFIC TCR T-CELLS IN SK-MEL-37 MELANOMA MODEL“. In OpenBio-2023. ИПЦ НГУ, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-28.

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TCR T-cell therapy is one of the most promising approaches for the treatment of solid tumors. In this work, we assessed the immune transcriptome of NY-ESO-1-specific TCR T-cells by single cell RNA sequencing before and after injection of such cells into SkMel-37 melanoma xenograft mice and found a pronounced cytotoxic molecular signature and an in vivo cytotoxic effect.

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Sachs, Zohar, Rebecca S. LaRue, Klara Noble, Susan K. Rathe, Aaron L. Sarver, Ngoc A. Ha und David A. Largaespada. „Abstract B34: Single cell RNA sequencing identifies the NRASG12V-mediated AML self-renewal signature.“ In Abstracts: AACR Special Conference on Hematologic Malignancies: Translating Discoveries to Novel Therapies; September 20-23, 2014; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1557-3265.hemmal14-b34.

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Sahu, Divya, und Ajay Goel. „Abstract 650: Transcriptomic profiling identifies an enhancer RNA signature for recurrence prediction in colorectal cancer“. 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.am2021-650.

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Marques, Michelle, David Simpson, Ron Chen, Dedeepya Vaka, Marcus Breese, Allayne Brunner, Rob West und Alejandro Sweet-Cordero. „Abstract A31: The long noncoding RNA lnc277 mediates a repressive gene signature in Ewing's 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-a31.

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reddy, Karthik reddy kami, Balasubramanyam Karanam, Cristian Coarfa, Yair Lotan, Roni J. Bollag, Martha K. Terris und Nagireddy Putluri. „Abstract 4501: RNA seq analysis reveals altered immune specific gene signature in African American bladder cancer“. In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-4501.

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Pruneri, Giancarlo, Vincenzo Bagnardi, Davide Disalvatore, Giuseppe Curigliano, Nicole Rotmensz, Carmen Criscitiello, Darl D. Flake II et al. „Abstract P4-11-15: Risk stratification within luminal B breast cancer using a second generation prognostic RNA signature“. In Thirty-Seventh Annual CTRC-AACR San Antonio Breast Cancer Symposium; December 9-13, 2014; San Antonio, TX. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.sabcs14-p4-11-15.

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Varadan, Vinay, Kristy Miskimen, Sitharthan Kamalakaran, Angel Janevski, Nilanjana Banerjee, Nicole Williams, Maysa Abu-Khalaf, William Sikov, Nevenka Dimitrova und Lyndsay Harris. „Abstract 4566: RNA-seq identifies a TGF-β signature that predicts response to preoperative bevacizumab in breast cancer.“ In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-4566.

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Berichte der Organisationen zum Thema "RNA signature"

Liao, Dezhong. RNA Chimeras as a Gene Signature of Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, Juni 2014. http://dx.doi.org/10.21236/ada612049.

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Liao, D. J. RNA Chimeras as a Gene Signature of Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, Mai 2013. http://dx.doi.org/10.21236/ada582144.

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Bar-Joseph, Moshe, William O. Dawson und Munir Mawassi. Role of Defective RNAs in Citrus Tristeza Virus Diseases. United States Department of Agriculture, September 2000. http://dx.doi.org/10.32747/2000.7575279.bard.

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This program focused on citrus tristeza virus (CTV), the largest and one of the most complex RNA-plant-viruses. The economic importance of this virus to the US and Israeli citrus industries, its uniqueness among RNA viruses and the possibility to tame the virus and eventually turn it into a useful tool for the protection and genetic improvement of citrus trees justify these continued efforts. Although the overall goal of this project was to study the role(s) of CTV associated defective (d)-RNAs in CTV-induced diseases, considerable research efforts had to be devoted to the engineering of the helper virus which provides the machinery to allow dRNA replication. Considerable progress was made through three main lines of complementary studies. For the first time, the generation of an engineered CTV genetic system that is capable of infecting citrus plants with in vitro modified virus was achieved. Considering that this RNA virus consists of a 20 kb genome, much larger than any other previously developed similar genetic system, completing this goal was an extremely difficult task that was accomplished by the effective collaboration and complementarity of both partners. Other full-length genomic CTV isolates were sequenced and populations examined, resulting in a new level of understanding of population complexities and dynamics in the US and Israel. In addition, this project has now considerably advanced our understanding and ability to manipulate dRNAs, a new class of genetic elements of closteroviruses, which were first found in the Israeli VT isolate and later shown to be omnipresent in CTV populations. We have characterized additional natural dRNAs and have shown that production of subgenomic mRNAs can be involved in the generation of dRNAs. We have molecularly cloned natural dRNAs and directly inoculated citrus plants with 35S-cDNA constructs and have shown that specific dRNAs are correlated with specific disease symptoms. Systems to examine dRNA replication in protoplasts were developed and the requirements for dRNA replication were defined. Several artificial dRNAs that replicate efficiently with a helper virus were created from infectious full-genomic cDNAs. Elements that allow the specific replication of dRNAs by heterologous helper viruses also were defined. The T36-derived dRNAs were replicated efficiently by a range of different wild CTV isolates and hybrid dRNAs with heterologous termini are efficiently replicated with T36 as helper. In addition we found: 1) All CTV genes except of the p6 gene product from the conserved signature block of the Closteroviridae are obligate for assembly, infectivity, and serial protoplast passage; 2) The p20 protein is a major component of the amorphous inclusion bodies of infected cells; and 3) Novel 5'-Co-terminal RNAs in CTV infected cells were characterized. These results have considerably advanced our basic understanding of the molecular biology of CTV and CTV-dRNAs and form the platform for the future manipulation of this complicated virus. As a result of these developments, the way is now open to turn constructs of this viral plant pathogen into new tools for protecting citrus against severe CTV terms and development of virus-based expression vectors for other citrus improvement needs. In conclusion, this research program has accomplished two main interconnected missions, the collection of basic information on the molecular and biological characteristics of the virus and its associated dRNAs toward development of management strategies against severe diseases caused by the virus and building of novel research tools to improve citrus varieties. Reaching these goals will allow us to advance this project to a new phase of turning the virus from a pathogen to an ally.

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Denis, F., F. Jacobs und C. A. Wood. RSA Blind Signatures. RFC Editor, Oktober 2023. http://dx.doi.org/10.17487/rfc9474.

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Crowley, David E., Dror Minz und Yitzhak Hadar. Shaping Plant Beneficial Rhizosphere Communities. United States Department of Agriculture, Juli 2013. http://dx.doi.org/10.32747/2013.7594387.bard.

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PGPR bacteria include taxonomically diverse bacterial species that function for improving plant mineral nutrition, stress tolerance, and disease suppression. A number of PGPR are being developed and commercialized as soil and seed inoculants, but to date, their interactions with resident bacterial populations are still poorly understood, and-almost nothing is known about the effects of soil management practices on their population size and activities. To this end, the original objectives of this research project were: 1) To examine microbial community interactions with plant-growth-promoting rhizobacteria (PGPR) and their plant hosts. 2) To explore the factors that affect PGPR population size and activity on plant root surfaces. In our original proposal, we initially prqposed the use oflow-resolution methods mainly involving the use of PCR-DGGE and PLFA profiles of community structure. However, early in the project we recognized that the methods for studying soil microbial communities were undergoing an exponential leap forward to much more high resolution methods using high-throughput sequencing. The application of these methods for studies on rhizosphere ecology thus became a central theme in these research project. Other related research by the US team focused on identifying PGPR bacterial strains and examining their effective population si~es that are required to enhance plant growth and on developing a simulation model that examines the process of root colonization. As summarized in the following report, we characterized the rhizosphere microbiome of four host plant species to determine the impact of the host (host signature effect) on resident versus active communities. Results of our studies showed a distinct plant host specific signature among wheat, maize, tomato and cucumber, based on the following three parameters: (I) each plant promoted the activity of a unique suite of soil bacterial populations; (2) significant variations were observed in the number and the degree of dominance of active populations; and (3)the level of contribution of active (rRNA-based) populations to the resident (DNA-based) community profiles. In the rhizoplane of all four plants a significant reduction of diversity was observed, relative to the bulk soil. Moreover, an increase in DNA-RNA correspondence indicated higher representation of active bacterial populations in the residing rhizoplane community. This research demonstrates that the host plant determines the bacterial community composition in its immediate vicinity, especially with respect to the active populations. Based on the studies from the US team, we suggest that the effective population size PGPR should be maintained at approximately 105 cells per gram of rhizosphere soil in the zone of elongation to obtain plant growth promotion effects, but emphasize that it is critical to also consider differences in the activity based on DNA-RNA correspondence. The results ofthis research provide fundamental new insight into the composition ofthe bacterial communities associated with plant roots, and the factors that affect their abundance and activity on root surfaces. Virtually all PGPR are multifunctional and may be expected to have diverse levels of activity with respect to production of plant growth hormones (regulation of root growth and architecture), suppression of stress ethylene (increased tolerance to drought and salinity), production of siderophores and antibiotics (disease suppression), and solubilization of phosphorus. The application of transcriptome methods pioneered in our research will ultimately lead to better understanding of how management practices such as use of compost and soil inoculants can be used to improve plant yields, stress tolerance, and disease resistance. As we look to the future, the use of metagenomic techniques combined with quantitative methods including microarrays, and quantitative peR methods that target specific genes should allow us to better classify, monitor, and manage the plant rhizosphere to improve crop yields in agricultural ecosystems. In addition, expression of several genes in rhizospheres of both cucumber and whet roots were identified, including mostly housekeeping genes. Denitrification, chemotaxis and motility genes were preferentially expressed in wheat while in cucumber roots bacterial genes involved in catalase, a large set of polysaccharide degradation and assimilatory sulfate reduction genes were preferentially expressed.

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Blaze, M., J. Ioannidis und A. Keromytis. DSA and RSA Key and Signature Encoding for the KeyNote Trust Management System. RFC Editor, März 2000. http://dx.doi.org/10.17487/rfc2792.

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Allende López, Marcos, Diego López, Sergio Cerón, Antonio Leal, Adrián Pareja, Marcelo Da Silva, Alejandro Pardo et al. Quantum-Resistance in Blockchain Networks. Inter-American Development Bank, Juni 2021. http://dx.doi.org/10.18235/0003313.

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This paper describes the work carried out by the Inter-American Development Bank, the IDB Lab, LACChain, Cambridge Quantum Computing (CQC), and Tecnológico de Monterrey to identify and eliminate quantum threats in blockchain networks. The advent of quantum computing threatens internet protocols and blockchain networks because they utilize non-quantum resistant cryptographic algorithms. When quantum computers become robust enough to run Shor's algorithm on a large scale, the most used asymmetric algorithms, utilized for digital signatures and message encryption, such as RSA, (EC)DSA, and (EC)DH, will be no longer secure. Quantum computers will be able to break them within a short period of time. Similarly, Grover's algorithm concedes a quadratic advantage for mining blocks in certain consensus protocols such as proof of work. Today, there are hundreds of billions of dollars denominated in cryptocurrencies that rely on blockchain ledgers as well as the thousands of blockchain-based applications storing value in blockchain networks. Cryptocurrencies and blockchain-based applications require solutions that guarantee quantum resistance in order to preserve the integrity of data and assets in their public and immutable ledgers. We have designed and developed a layer-two solution to secure the exchange of information between blockchain nodes over the internet and introduced a second signature in transactions using post-quantum keys. Our versatile solution can be applied to any blockchain network. In our implementation, quantum entropy was provided via the IronBridge Platform from CQC and we used LACChain Besu as the blockchain network.

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PHILLIPS, DANIEL, WENBIN GUO und RUNXUAN ZHANG. Analysis of Multiple Years of RNA-Seq Data Using the 3D-RNA-Seq Application Reveals Seasonal Signatures of Differential Gene and Transcript-Level Expression, Alternative-Splicing, and Transcript... Journal of Young Investigators, August 2021. http://dx.doi.org/10.22186/jyi.40.8.9-22.

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Weis, B. The Use of RSA/SHA-1 Signatures within Encapsulating Security Payload (ESP) and Authentication Header (AH). RFC Editor, Januar 2006. http://dx.doi.org/10.17487/rfc4359.

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Sury, O. Use of the SHA-256 Algorithm with RSA, Digital Signature Algorithm (DSA), and Elliptic Curve DSA (ECDSA) in SSHFP Resource Records. RFC Editor, April 2012. http://dx.doi.org/10.17487/rfc6594.

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