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We began analyzing https://translational-medicine.biomedcentral.com/articles/10.1186/s12967-019-1837-z, but it redirected us to https://translational-medicine.biomedcentral.com/articles/10.1186/s12967-019-1837-z. The analysis below is for the second page.

Title[redir]:
m6A RNA modification and its writer/reader VIRMA/YTHDF3 in testicular germ cell tumors: a role in seminoma phenotype maintenance | Journal of Translational Medicine | Full Text
Description:
Background Covalent RNA modifications, such as N-6-methyladenosine (m6A), have been associated with various biological processes, but their role in cancer remains largely unexplored. m6A dynamics depends on specific enzymes whose deregulation may also impact in tumorigenesis. Herein, we assessed the differential abundance of m6A, its writer VIRMA and its reader YTHDF3, in testicular germ cell tumors (TGCTs), looking for clinicopathological correlates. Methods In silico analysis of TCGA data disclosed altered expression of VIRMA (52%) and YTHDF3 (48%), prompting subsequent validation. Formalin-fixed paraffin-embedded tissues from 122 TGCTs (2005–2016) were selected. RNA extraction, cDNA synthesis and real-time qPCR (Taqman assays) for VIRMA and YTHDF3 were performed, as well as immunohistochemistry for VIRMA, YTHDF3 and m6A, for staining intensity assessment. Associations between categorical variables were assessed using Chi square and Fisher’s exact test. Distribution of continuous variables between groups was compared using the nonparametric Mann–Whitney and Kruskal–Wallis tests. Biomarker performance was assessed through receiver operating characteristics (ROC) curve construction and a cut-off was established by Youden’s index method. Statistical significance was set at p < 0.05. Results In our cohort, VIRMA and YTHDF3 mRNA expression levels differed among TGCT subtypes, with Seminomas (SEs) depicting higher levels than Non-Seminomatous tumors (NSTs) (p < 0.01 for both). A positive correlation was found between VIRMA and YTHDF3 expression levels. VIRMA discriminated SEs from NSTs with AUC = 0.85 (Sensitivity 77.3%, Specificity 81.1%, PPV 71.6%, NPV 85.3%, Accuracy 79.7%). Immunohistochemistry paralleled transcript findings, as patients with strong m6A immunostaining intensity depicted significantly higher VIRMA mRNA expression levels and stronger VIRMA immunoexpression intensity (p < 0.001 and p < 0.01, respectively). Conclusion Abundance of m6A and expression of VIRMA/YTHDF3 were different among TGCT subtypes, with higher levels in SEs, suggesting a contribution to SE phenotype maintenance. VIRMA and YTHDF3 might cooperate in m6A establishment in TGCTs, and their transcript levels accurately discriminate between SEs and NSTs, constituting novel candidate biomarkers for patient management.

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Keywords {🔍}

virma, ythdf, article, google, scholar, cancer, cell, expression, tumors, levels, tumor, germ, immunoexpression, mrna, rna, cas, transcript, testicular, ses, samples, immunostaining, tgcts, patients, additional, modification, analysis, metastatic, intensity, tgct, seminoma, higher, porto, genes, file, strong, clinical, group, fig, cohort, nsts, data, nmethyladenosine, subtypes, figure, writer, staining, compared, results, nonseminomatous, depicted,

Topics {✒️}

springer nature beta-glucoronidase—gusb—assay id hs99999908 formalin-fixed paraffin-embedded tissues common cytogenetic background state privacy rights clinical files n6-methyladenosine-encoded epitranscriptomics formalin-fixed paraffin-embedded ten micrometer sections authors scientific editing conclusion abundance information rna n6-methyladenosine methyltransferase rna n6-methyladenosine methyltransferase rights anti-virma rabbit polyclonal anti-m6a rabbit monoclonal anti-ythdf3 rabbit polyclonal histological sections ffpe rna/dna purification conclusion ythdf2-dependent posttranscriptional silencing post-translational rna modifications germ cell tumors discussion discussion 213–204 germ-cell cancer germ cell cancer 5 μm sections real-time qpcr germ cell development te postpubertal-type teratoma pure postpubertal-type teratoma germ-cell neoplasia germ cell neoplasia nonparametric mann–whitney test original author privacy choices/manage cookies content retrospective nature risk group assignment testicular cancer survivors classical serum markers testicular cancer incidence bmc testicular cancer biomarkers gene expression control beta-glucoronidase igcccg nat cell biol postpubertal-type teratoma

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RNA modifications: what have we learned and where are we headed?
Testicular germ cell tumors go epigenetics: will miR-371a-3p replace classical serum biomarkers?
Will testicular germ cell tumors remain untargetable?

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      headline:m6A RNA modification and its writer/reader VIRMA/YTHDF3 in testicular germ cell tumors: a role in seminoma phenotype maintenance
      description:Covalent RNA modifications, such as N-6-methyladenosine (m6A), have been associated with various biological processes, but their role in cancer remains largely unexplored. m6A dynamics depends on specific enzymes whose deregulation may also impact in tumorigenesis. Herein, we assessed the differential abundance of m6A, its writer VIRMA and its reader YTHDF3, in testicular germ cell tumors (TGCTs), looking for clinicopathological correlates. In silico analysis of TCGA data disclosed altered expression of VIRMA (52%) and YTHDF3 (48%), prompting subsequent validation. Formalin-fixed paraffin-embedded tissues from 122 TGCTs (2005–2016) were selected. RNA extraction, cDNA synthesis and real-time qPCR (Taqman assays) for VIRMA and YTHDF3 were performed, as well as immunohistochemistry for VIRMA, YTHDF3 and m6A, for staining intensity assessment. Associations between categorical variables were assessed using Chi square and Fisher’s exact test. Distribution of continuous variables between groups was compared using the nonparametric Mann–Whitney and Kruskal–Wallis tests. Biomarker performance was assessed through receiver operating characteristics (ROC) curve construction and a cut-off was established by Youden’s index method. Statistical significance was set at p < 0.05. In our cohort, VIRMA and YTHDF3 mRNA expression levels differed among TGCT subtypes, with Seminomas (SEs) depicting higher levels than Non-Seminomatous tumors (NSTs) (p < 0.01 for both). A positive correlation was found between VIRMA and YTHDF3 expression levels. VIRMA discriminated SEs from NSTs with AUC = 0.85 (Sensitivity 77.3%, Specificity 81.1%, PPV 71.6%, NPV 85.3%, Accuracy 79.7%). Immunohistochemistry paralleled transcript findings, as patients with strong m6A immunostaining intensity depicted significantly higher VIRMA mRNA expression levels and stronger VIRMA immunoexpression intensity (p < 0.001 and p < 0.01, respectively). Abundance of m6A and expression of VIRMA/YTHDF3 were different among TGCT subtypes, with higher levels in SEs, suggesting a contribution to SE phenotype maintenance. VIRMA and YTHDF3 might cooperate in m6A establishment in TGCTs, and their transcript levels accurately discriminate between SEs and NSTs, constituting novel candidate biomarkers for patient management.
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      dateModified:2019-03-12T00:00:00Z
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         M6A
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         YTHDF3
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         general
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      name:Department of Pathology and Molecular Immunology, Institute of Biomedical Sciences Abel Salazar, University of Porto (ICBAS-UP), Porto, Portugal
      name:Cancer Biology and Epigenetics Group (CBEG), IPO Porto Research Center (CI-IPOP), Portuguese Oncology Institute of Porto (IPO Porto) & Porto Comprehensive Cancer Center (P.CCC), Porto, Portugal
      name:Department of Pathology, Portuguese Oncology Institute of Porto (IPOP), Porto, Portugal
      name:Department of Pathology, Portuguese Oncology Institute of Porto (IPOP), Porto, Portugal
      name:Department of Pathology, Portuguese Oncology Institute of Porto (IPOP), Porto, Portugal
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      name:Department of Urology, Portuguese Oncology Institute of Porto (IPOP), Porto, Portugal
      name:Center for Genomic Science of IIT@SEMM, Fondazione Istituto Italiano di Tecnologia (IIT), Milan, Italy
      name:Cancer Biology and Epigenetics Group (CBEG), IPO Porto Research Center (CI-IPOP), Portuguese Oncology Institute of Porto (IPO Porto) & Porto Comprehensive Cancer Center (P.CCC), Porto, Portugal
      name:Department of Pathology, Portuguese Oncology Institute of Porto (IPOP), Porto, Portugal
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      name:Department of Pathology and Molecular Immunology, Institute of Biomedical Sciences Abel Salazar, University of Porto (ICBAS-UP), Porto, Portugal

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