This SuperSeries is composed of the SubSeries listed below.
SOX9 drives WNT pathway activation in prostate cancer.
Cell line
View SamplesSOX9 is critical for prostate development and is implicated in prostate cancer, we used transcriptome profiling in combination with SOX9 ChIP-seq to identify genes and pathways it regulates in normal or neoplastic epithelium.
SOX9 drives WNT pathway activation in prostate cancer.
Cell line
View SamplesIn this dataset, we report the gene expression of adjacent Gleason 3 and Gleason 4 foci microdissected from the same prostate cancer sample.
Gleason Score 7 Prostate Cancers Emerge through Branched Evolution of Clonal Gleason Pattern 3 and 4.
No sample metadata fields
View SamplesWe compared 22 primary Pca (hormone-dependent) versus 29 metastatic Pca (CRPC). The expression of genes related to cell cycle, proliferation, DNA synthesis, and androgen metablism are significantly increased in CRPC group. The expression of AR-stimulated genes were partially reactivated.
ERG induces androgen receptor-mediated regulation of SOX9 in prostate cancer.
No sample metadata fields
View SamplesIn clinical trials assessing neoadjuvant androgen deprivation therapy plus next-generation androgen receptor axis inhibitors, a subset of patients fail to demonstrate a complete pathologic response following treatment and radical prostatectomy. We performed transcriptome analyses on laser capture microdissected foci of residual tumor from these patients.
Neoadjuvant-Intensive Androgen Deprivation Therapy Selects for Prostate Tumor Foci with Diverse Subclonal Oncogenic Alterations.
Specimen part, Treatment
View SamplesWhole genome expression profiling in the presence and absence of annexin A2 [shRNA] identified fundamentally altered transcriptional programming that changes the radioresponsive transcriptome.
Annexin A2 modulates radiation-sensitive transcriptional programming and cell fate.
Treatment, Time
View SamplesUridylation of diverse RNA species represents an emerging theme in post-transcriptional gene regulation. In the microRNA pathway, such modifications regulate small RNA biogenesis and stability in plants, worms and mammals. Here, we report the first uridylyltransferase that acts on small RNAs in Drosophila, which we refer to as Tailor. Tailor is the source for the majority of 3´ end-modifications in microRNAs and predominantly targets precursor-hairpins. Uridylation modulates the characteristic two-nucleotide 3´ overhangs of microRNA hairpins, which regulates processing by Dicer-1 and destabilizes RNA hairpins. Furthermore, Tailor preferentially uridylates mirtron-hairpins, thereby impeding the production of non-canonical microRNAs. Mirtron-selectivity is explained by unique primary sequence specificity of Tailor, selecting RNA substrates ending with a 3´ guanosine, a feature not previously observed for TUTases. In contrast to mirtrons, conserved Drosophila pre-miRNAs are significantly depleted in 3´ guanosine, thereby escaping regulatory uridylation. Our data support the hypothesis that evolutionary adaptation to pre-miRNA uridylation shapes the nucleotide composition of pre-miRNA 3´ ends. Hence, hairpin-uridylation may serve as a barrier for the de novo creation of miRNAs in Drosophila. Overall design: mRNA sequencing of Drosophila S2 cells (3-times; control libraries) and three biological replicates of S2 cells stably depleted of CG1091/Tailor by CRISPR/Cas9
Uridylation of RNA Hairpins by Tailor Confines the Emergence of MicroRNAs in Drosophila.
Cell line, Subject
View SamplesRadiation lung injury is characterized by early inflammation and late fibrosis. The causes underlying the chronic, progressive nature of radiation injury are poorly understood. Here, we report that the gene expression of irradiated lung tissue correlates with that observed in the lungs in aged animals. We demonstrate that NOX4 expression and superoxide elaboration is increased in irradiated lungs and pneumocytes in a dose dependent fashion.
Role of type II pneumocyte senescence in radiation-induced lung fibrosis.
Sex, Age, Specimen part, Treatment, Time
View SamplesTo understand why cancer vaccine-induced T cells often fail to eradicate tumors, we studied immune responses in mice vaccinated with gp100 peptide emulsified in incomplete Freund's adjuvant (IFA), commonly used in clinical cancer vaccine trials. After gp100 peptide/IFA vaccination, tumor-specific CD8+ T cells (adoptively transferred from gp100-specific TCR-transgenic pmel-1 mice) accumulated not in tumors but at the persisting, antigen-rich vaccination site. Once there, primed T cells became dysfunctional and underwent antigen-driven, IFN- and FasL-mediated apoptosis, resulting in systemic hyporesponsiveness to subsequent vaccination. Provision of anti-CD40 antibody, TLR7 agonist and interleukin-2 (covax) reduced T cell apoptosis but did not prevent vaccination site sequestration. A non-persisting vaccine formulation shifted T cell localization towards tumors, inducing superior anti-tumor activity. Short-lived formulation also reduced systemic T cell dysfunction and promoted memory formation, as shown by gene expression profiling and other measures. Persisting peptide/IFA vaccine depots, currently used to vaccinate cancer patients, can induce specific T cell sequestration at vaccination sites followed by dysfunction and deletion; short-lived depot formulations may overcome these limitations and result in greater therapeutic efficacy of peptide-based cancer vaccines.
Persistent antigen at vaccination sites induces tumor-specific CD8⁺ T cell sequestration, dysfunction and deletion.
Specimen part, Time
View SamplesWe sequenced strand-specific mRNA from the heads of 3 groups of wild type zebrafish (Danio rerio) 5 days post fertilization. Overall design: Examination of the relative expression of genes in the developing zebrafish brain
BRF1 mutations alter RNA polymerase III-dependent transcription and cause neurodevelopmental anomalies.
No sample metadata fields
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