We have identified the causal genes, which is MYB36, of ionome mutants.
The MYB36 transcription factor orchestrates Casparian strip formation.
Specimen part
View SamplesThis series represents 180 lymph-node negative relapse free patients and 106 lymph-node negate patients that developed a distant metastasis.
Gene-expression profiles to predict distant metastasis of lymph-node-negative primary breast cancer.
No sample metadata fields
View SamplesActivated T cells inhibit neurogenesis in adult animal brain and cultured human fetal neural stem cells (NSC). However, the role of inhibition of neurogenesis in human neuroinflammatory diseases is still uncertain because of the difficulty in obtaining adult NSC from patients. Recent developments in cell reprogramming suggest that NSC may be derived directly from adult fibroblasts. We generated NSC from adult human peripheral CD34+ cells by transfecting the cells with Sendai virus constructs containing Sox-2, Oct3/4, C-MyC and Klf-4. The derived NSC could be differentiated to astroglia and action potential firing neurons. Co-culturing NSC with activated autologous T cells or treatment with recombinant granzyme B caused inhibition of neurogenesis as indicated by decreased NSC proliferation and neuronal differentiation. Thus, we have established a unique autologous in vitro model to study the pathophysiology of neuroinflammatory diseases that has potential for usage in personalized medicine.
Derivation of neural stem cells from human adult peripheral CD34+ cells for an autologous model of neuroinflammation.
Specimen part
View SamplesTo determine the global effects of ASCT2 inhibition, we used next generation sequencing to determine mRNA expression changes in PC-3 cells treated with BenSer or GPNA for 48 h. Overall design: Examination of two different ASCT2 inhibitors BenSer and GPNA in prostate cancer cell line PC-3.
Targeting ASCT2-mediated glutamine uptake blocks prostate cancer growth and tumour development.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
C9ORF72 GGGGCC Expanded Repeats Produce Splicing Dysregulation which Correlates with Disease Severity in Amyotrophic Lateral Sclerosis.
Specimen part, Subject
View SamplesThe rediscovery of estrogen receptor (ESR1) mutations in metastatic breast cancer is current clinical scenario. We have modeled the three most frequent ESR1 mutations using stable lentiviral vectors in human breast cancer cell lines, and determined that they confer relative resistance to tamoxifen (Tam) in a cell-type specific manner due to distinct epigenetic changes. Resistance was only observed with concomitant engagement and activation of the insulin growth factor signaling pathway (IGF1R). The ESR1 mutants also exhibited enhanced binding with insulin growth factor receptor beta (IGF1R). The selective estrogen degrader, fulvestrant, significantly reduced the anchorage-independent growth of ESR1 mutant-expressing cells, while the combination treatment with the mTOR inhibitor everolimus, restored Tam sensitivity. Since we detected relatively high frequencies of these three mutations in primary breast tumors, our results suggest that clinical targeted sequencing of both primary and metastatic tumors may be justified and comination therapies considered.
ESR1 mutations affect anti-proliferative responses to tamoxifen through enhanced cross-talk with IGF signaling.
Cell line, Treatment
View SamplesObjective: An intronic GGGGCC-repeat expansion of C9ORF72 is the most common genetic variant of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia. The mechanism of neurodegeneration is unknown, but a direct effect on RNA processing mediated by RNA foci transcribed from the repeat sequence has been proposed.
C9ORF72 GGGGCC Expanded Repeats Produce Splicing Dysregulation which Correlates with Disease Severity in Amyotrophic Lateral Sclerosis.
Specimen part, Subject
View SamplesAstrocyte dysfunction impacts their normal function, including neuronal support, thereby contributing to neurodegenerative pathologies including Alzheimer's disease (AD). Therefore to understand the role of astrocytes in the pathogenesis of age-related disorders we analysed the gene expression profile of astrocytes with respect to Alzheimer-type pathology.
Microarray analysis of the astrocyte transcriptome in the aging brain: relationship to Alzheimer's pathology and APOE genotype.
Specimen part
View SamplesRNA sequencing in NIH-3T3 cells Overall design: Transcriptome analysis for three biological replicates of pLX307, SOS1 WT, SOS1 N233Y, and KRAS G12V cells
Identification and Characterization of Oncogenic <i>SOS1</i> Mutations in Lung Adenocarcinoma.
Cell line, Subject
View SamplesHuman peripheral blood mononuclear cells were cultured in presence of H37Ra strain at 37oC, 5%CO2. Cellular aggregates were collected at 24h, and RNA extracted and hybridized to Affymetrix microarrays (HG-U133). Raw data from microarray experiments was analyzed with dCHIP and SAM programs to determine the significance of changes at the biological context.
Microarray analysis of the in vitro granulomatous response to Mycobacterium tuberculosis H37Ra.
Specimen part
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