Gotowa bibliografia na temat „Reference-Free detected RNAs”
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Artykuły w czasopismach na temat "Reference-Free detected RNAs"
Lee, Bongyong, Alisha Babu, Aiguo Zhang i Michael Y. Sha. "Abstract 2191: Detection of actionable lung cancer fusion genes with known and novel partners from highly degraded FFPE material". Cancer Research 83, nr 7_Supplement (4.04.2023): 2191. http://dx.doi.org/10.1158/1538-7445.am2023-2191.
Pełny tekst źródłaTorossian, Nouritza, Dominika Foretek, Marc Gabriel, Linda Larbi Cherif, Charlotte Lecerf, Maud Kamal, Christophe Le Tourneau, Daniel Gautheret, Sergio Roman-Roman i Antonin Morillon. "Abstract 2774: Reference free transcriptomic characterization of chemoresistant triple negative breast cancers provides a promising reservoir of predictive biomarkers of early chemoresistance". Cancer Research 82, nr 12_Supplement (15.06.2022): 2774. http://dx.doi.org/10.1158/1538-7445.am2022-2774.
Pełny tekst źródłaSpielmann, Nadine, Diane Ilsley, Jian Gu, Kristi Lea, Joel Brockman, Sheila Heater, Robert Setterquist i David T. W. Wong. "The Human Salivary RNA Transcriptome Revealed by Massively Parallel Sequencing". Clinical Chemistry 58, nr 9 (1.09.2012): 1314–21. http://dx.doi.org/10.1373/clinchem.2011.176941.
Pełny tekst źródłaVan Eijs, Mick J. M., Nicolette C. Notermans, Tom Würdinger i Monique C. Minnema. "Platelet RNA Splicing Profiles Can Distinguish IgM MGUS Patients from Healthy Individuals". Blood 134, Supplement_1 (13.11.2019): 3771. http://dx.doi.org/10.1182/blood-2019-124325.
Pełny tekst źródłaCherng, Hua-Jay J., Xiaojing Yang, Ryan Yancey, Christian A. Gordillo, Ted B. Piorczynski, Hei T. Chan, Kenneth N. Ofori i in. "Methylated Whole Genome Cell-Free DNA Sequencing before Chimeric Antigen Receptor T-Cell Therapy for Large B-Cell Lymphoma Predicts Treatment Outcomes". Blood 142, Supplement 1 (28.11.2023): 4371. http://dx.doi.org/10.1182/blood-2023-178376.
Pełny tekst źródłaManning, Kyle, Dulaney Miller, Yang Yang, Jeff Cole, Shuran Xing, Christopher Benway, Christian Ray i in. "Abstract LB393: Exosome based multiomics combined with cfDNA methylation reveals complementary signatures in blood based liquid biopsy that carry promise for minimally invasive colorectal cancer screening". Cancer Research 84, nr 7_Supplement (5.04.2024): LB393. http://dx.doi.org/10.1158/1538-7445.am2024-lb393.
Pełny tekst źródłaEichelser, Corinna, Dieter Flesch-Janys, Jenny Chang-Claude, Klaus Pantel i Heidi Schwarzenbach. "Deregulated Serum Concentrations of Circulating Cell–Free MicroRNAs miR-17, miR-34a, miR-155, and miR-373 in Human Breast Cancer Development and Progression". Clinical Chemistry 59, nr 10 (1.10.2013): 1489–96. http://dx.doi.org/10.1373/clinchem.2013.205161.
Pełny tekst źródłaRozprawy doktorskie na temat "Reference-Free detected RNAs"
Torossian, Nouritza. "Study of long non-coding RNAs and reference-free detected RNAs as potential biomarkers and actors of Triple Negative Breast Cancers' chemoresistance". Electronic Thesis or Diss., Université Paris sciences et lettres, 2023. http://www.theses.fr/2023UPSLS057.
Pełny tekst źródłaTriple-negative breast cancers (TNBC) represent a heterogeneous subtype of breast cancers including 12% to 24% of all cases, having the poorest prognoses and often affecting young women. Treatment at localized stage is mainly based on chemotherapy, with no targeted therapy (except germline BRCA mutated patients). Nearly all patients receive the same Neo-Adjuvant Chemotherapy (NAC) with anthracyclines and taxanes, that badly impacts survival in the absence of pathological complete response (pCR). Therapeutic intensification, notably with addition of immunotherapy, is the current trend to increase pCR rate and improve survival. Standard gene expression signatures have failed to provide effective tools to predict TNBC chemoresistance, probably due to their incomplete nature, as they are mostly based on expression of protein coding genes and/or referenced transcripts and up to date there is no clinically useful transcriptomic signature predicting TNBC chemoresistance to NAC. Such a predictive signature would allow patient selection for therapeutic intensification. Therefore, it is important to explore the remaining 90% of the genome consisting of non-coding and non-referenced regions. One class of non-coding RNAs that is of great interest are long non-coding (lnc) RNAs, that are at least 200 nucleotides long, some of them being specifically expressed in cancer. Moreover, some lncRNAs have been shown to be implicated in different mechanisms of chemoresistance. LncRNAs are not fully well annotated in the human genome and new unreferenced transcripts, coding or not, and new isoforms of known genes are discovered daily.Therefore, the first goal of my PhD was to assess reference-free transcriptome as a potential reservoir of predictive biomarkers of TNBC chemoresistance. A cohort of 78 TNBCs before NAC was analyzed, comparing chemosensitive (chS) and chemoresistant (chR) cases based on international Residual Cancer Burden (RCB) score. A standard differential gene expression analysis (DE-seq) on annotated genes, and on new lncRNAs detected with a de novo RNA-profiler, and a reference-free analysis of differential fragments of transcripts without annotation bias were compared. Reference-free approach showed best separation of chS and chR patients in the training cohort. Further, based on comparison with an independent validation cohort, an optimized approach was proposed, where specific genomic regions with differential expression were selected. This technique gave a reproducible signature of chemoresistance between the two cohorts. In all, these results show the potential of a reference-free approach to generate a transcriptomic signature as predictive biomarker of early TNBC chemoresistance. Further investigation is needed to validate the signature using larger validation cohorts.The second objective of my PhD was to assess lncRNAs as potential actors/therapeutic targets in chR TNBCs. For that we selected lncRNAs upregulated in chR pre-NAC TNBCs (compared with chS pre-NAC TNBCs) and in chR post-NAC TNBCs (compared with chR pre-NAC TNBCs). Considering lncRNAs level and specificity of expression, genomic position, and pre-existing data of their potential function, three lncRNAs (AL450326.1, LINC02609 and MIR503HG) were retained for functional analysis. By knocking down levels of these lncRNAs in TNBC cell line model, an impact on Docetaxel cytotoxicity was assessed. All three lncRNAs knock downs showed an improved Docetaxel induced cytotoxicity. Knock down of AL450326.1 and LINC02609 resulted in a decreased spontaneous clonogenicity and increased Docetaxel induced cell death, giving a first indication of their mode of action. In all, we identified three lncRNAs playing a role in NAC chemoresistance. Further functional studies will allow to decipher the mechanisms by which the identified lncRNAs affect chemoresistance with the ultimate goal to identify new therapeutic approaches to circumvent NAC chemoresistance of TNBCs