In this dataset, we included expression data obtained from 30 resected human PDAC tumors, to examine what genes are differentially expressed in different cohorts that might lead to various outcomes
Identification of unique neoantigen qualities in long-term survivors of pancreatic cancer.
Specimen part
View SamplesThe Adar1 deaminase inactive mutant mouse tissue samples were obtain from the Walkley lab as described in http://www.ncbi.nlm.nih.gov/pubmed/26275108. We performed mmPCR-seq on the samples and measured the editing levels of. Overall design: Fetal mRNA profiles of E12.5 wild type (WT) and ADAR E861A mutant mice were generated by deep sequencing using Illumina HiSeq 2000.
Dynamic landscape and regulation of RNA editing in mammals.
Specimen part, Cell line, Subject
View SamplesThe aim was to investigate the effect of postoperative intra-abdominal infection on the gene expression patterns of peripheral blood leukocytes (PBL) after surgery for colorectal cancer
Peripheral blood leucocytes show differential expression of tumour progression-related genes in colorectal cancer patients who have a postoperative intra-abdominal infection: a prospective matched cohort study.
Specimen part, Disease, Disease stage
View SamplesIn the current study, we used exon arrays and clinical samples from a previous trial (SAKK 19/05) to investigate the expression variations at the exon-level of 3 genes potentially playing a key role in modulating treatment response (EGFR, KRAS, VEGFA).
EGFR exon-level biomarkers of the response to bevacizumab/erlotinib in non-small cell lung cancer.
Sex, Specimen part, Disease, Disease stage, Treatment
View SamplesRANK-positive and RANK-negative luminal progenitor cells were isolated by FACS from histologically normal human breast tissue from wild-type human donors. RNA-seq gene expression profiling was used to find differentially expressed genes between the RANK-positive and RANK-negative cell populations. Overall design: Cells were isolated from 4 human patients. A paired analysis was used to compare RANK-positive and RANK-negative cells within patients.
RANK ligand as a potential target for breast cancer prevention in BRCA1-mutation carriers.
No sample metadata fields
View SamplesBRCA1, a well-known breast and ovarian cancer susceptibility gene with multiple interacting partners, is predicted to have diverse biological functions. However, to date its only well-established role is in the repair of damaged DNA and cell cycle regulation. In this regard, the etiopathological study of low penetrant variants of BRCA1 provides an opportunity to uncover its other physiologically important functions. Using this rationale, we studied the R1699Q variant of BRCA1, a potentially moderate risk variant, and found that it does not impair DNA damage repair but abrogates the repression of miR-155, a bona fide oncomir. We further show that in the absence of functional BRCA1, miR-155 is up-regulated in BRCA1-deficient mouse mammary epithelial cells, human and mouse BRCA1-deficienct breast tumor cell lines as well as tumors. Mechanistically, we found that BRCA1 represses miR-155 expression via its association with HDAC2, which deacetylates H2A and H3 on the miR-155 promoter. Finally, we show that over-expression of miR-155 accelerates whereas the knockdown of miR-155 attenuates the growth of tumor cell lines in vivo. Taken together, our findings demonstrate a new mode of tumor suppression by BRCA1 and reveal miR-155 as a potential therapeutic target for BRCA1-deficient tumors.
Tumor suppressor BRCA1 epigenetically controls oncogenic microRNA-155.
Specimen part
View SamplesWe examined the functional significance of the R1699Q variant of human BRCA1 gene using a mouse ES cell-based assay.
Tumor suppressor BRCA1 epigenetically controls oncogenic microRNA-155.
Specimen part
View SamplesMicroglia are the resident myeloid-lineage cells in the central nervous system. Despite myriad observations of microglia associated with various tissue pathologies in degenerative disease, their function in and contributions to the pathophysiological processes remain unclear. It is particularly uncertain whether microglia act harmfully to contribute to worsening of degeneration, act beneficially to combat disease-related dysfunction, or perform functions that result in both outcomes. In this dataset, we report RNA sequencing results from mice that undergo inducible ALS/FTLD-like degeneration and subsequent recovery. The goals were to identify whether microglia show transcriptional signatures commensurate with the disease stage or if they remain constant throughout. Additionally, we sought to understand whether there was a particular transcriptional or functional signature associated with functional recovery in the mice. The latter could lead to an understanding of how microglia may be targeted to combat disease and enhance recovery following or during degeneration. Overall design: mRNA profiles from microglia sorted from whole-spinal cord taken from doxycycline (DOX) inducible NEFH-tTa/tetO-208-hTDP43 (rNLS8, (+/+)) mice. In these mice, removal of doxycycline from the diet (DOX-OFF) induces transgenic expression and degeneration and reintroduction (DOX-ON) suppresses expression and enables recovery. We report profiles from rNLS8 mice that were DOX-OFF for 2 weeks (N=8) or 6 weeks (N=7), or DOX-OFF for 6 weeks followed by DOX-ON for 1 week (N=9). We also report profiles from control samples that include: rNLS8 mice that were DOX-ON for 6 weeks (N = 6) as asymptomatic genetic controls and WT (-/-) littermates that were DOX-OFF for 2 weeks (N=4), 6 weeks (N=1), or DOX-OFF for 6 weeks followed by 1 week DOX-ON (N=3) as asymptomatic doxycycline controls.
Microglia-mediated recovery from ALS-relevant motor neuron degeneration in a mouse model of TDP-43 proteinopathy.
Sex, Specimen part, Cell line, Subject
View SamplesThe enzymes of the poly-ADP-ribose polymerase (PARP) super-family control many relevant cellular processes, but a precise understanding of their activities in different physiological or disease contexts is largely incomplete. We found that transcription of several PARP genes was dynamically regulated upon macrophage activation by several inflammatory stimuli. Specifically, PARP14 was strongly induced by endotoxin stimulation and translocated to the nucleus in stimulated cells. Quantitative mass spectrometry analysis showed that PARP14 bound to a group of interferon-stimulated gene (ISG)-encoded proteins, most with an unknown function, and it was required for their nuclear accumulation. Moreover, PARP14 depletion attenuated transcription of primary antiviral response genes regulated by the transcription factor IRF3, including Ifnb1, thus reducing IFNß production and activation of ISGs involved in the secondary antiviral response. Overall, these data hint at a role of PARP14 in the control of antimicrobial responses and specifically in nuclear activities of a subgroup of ISG-encoded proteins. Overall design: mRNA sequencing of differentially expressed genes in PARP14 WT and KO RAW 264.7 cells, upon: no treatment, LPS, Jak inhibitor or LPS plus Jak inhibitor treatment.
PARP14 Controls the Nuclear Accumulation of a Subset of Type I IFN-Inducible Proteins.
Specimen part, Cell line, Treatment, Subject
View SamplesThe enzymes of the poly-ADP-ribose polymerase (PARP) super-family control many relevant cellular processes, but a precise understanding of their activities in different physiological or disease contexts is largely incomplete. We found that transcription of several PARP genes was dynamically regulated upon macrophage activation by several inflammatory stimuli. Specifically, PARP14 was strongly induced by endotoxin stimulation and translocated to the nucleus in stimulated cells. Quantitative mass spectrometry analysis showed that PARP14 bound to a group of interferon-stimulated gene (ISG)-encoded proteins, most with an unknown function, and it was required for their nuclear accumulation. Moreover, PARP14 depletion attenuated transcription of primary antiviral response genes regulated by the transcription factor IRF3, including Ifnb1, thus reducing IFNß production and activation of ISGs involved in the secondary antiviral response. Overall, these data hint at a role of PARP14 in the control of antimicrobial responses and specifically in nuclear activities of a subgroup of ISG-encoded proteins. Overall design: mRNA sequencing of differentially expressed genes in PARP14 WT RAW 264.7 cells, with or without LPS treatment
PARP14 Controls the Nuclear Accumulation of a Subset of Type I IFN-Inducible Proteins.
Specimen part, Cell line, Treatment, Subject
View Samples