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GSE30074
Homo sapiens
30 Downloadable Samples
Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Pediatric medulloblastoma is considered a highly heterogeneous disease, and a new strategy of risk stratification to optimize therapeutic outcomes is required. We aimed to investigate a new risk-stratification approach based on expression profiles of medulloblastoma cohorts. We analyzed gene expression profiles of 30 primary medulloblastomas and detected strong evidence that poor survival outcome was significantly associated with mRNA expression profiles of 17p loss. However, it was not supported in independent cohorts from previously published data (n=100). We speculated that this controversy might come from complex conditions of two important prognostic determinants, loss of tumor suppressors (chromosome 17p) and high expression of oncogenes, c-myc (MYC) or N-myc (MYCN). Simultaneous consideration of these two factors led to a new subgrouping of patients, exhibiting obviously different survival expectancies between the subgroups. Patients with up-regulated WNT signalings were always pre-defined as an independent subgroup, which ultimately removed confounding effect arising from contradictory outcome, favorable prognosis of WNT medulloblastomas despite their high MYC/MYCN expression level. We also found that age is a significant prognostic marker after adjusting for 17p and MYC/MYCN status. Diminished survival in age <3 years was more substantial in groups with high expression of MYC/MYCN or 17p loss, indicating survival outcome might be coordinately affected by these three factors. We suggest a more tailored and easily applicable subgrouping system based on expression profiles of chromosome 17p and MYC/MYCN, while separating WNT medulloblastoma as an independent subgroup, which could provide the basis for a novel risk-stratification strategy in pediatric medulloblastoma.
Publication Title
Prognostic classification of pediatric medulloblastoma based on chromosome 17p loss, expression of MYCC and MYCN, and Wnt pathway activation.
Sample Metadata Fields
Sex, Specimen part
View Samples- Homo sapiens
- 11 Downloadable Samples
- Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)
Description
Study of HP1 Knock Down on gene expression and splicing regulation in Human HeLa cells
Publication Title
Histone H3 lysine 9 trimethylation and HP1γ favor inclusion of alternative exons.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 8 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
To understand the link between invasion behavior and the steps of metastasis formation, we isolated invasive subpopulations from MDA-MB-231 cells in vitro using matrigel coated boyden chambers. Whole genome transcriptional profiling was used to characterize the expression changes uniquely related to invasive abilities of these cells.
Publication Title
Invading basement membrane matrix is sufficient for MDA-MB-231 breast cancer cells to develop a stable in vivo metastatic phenotype.
Sample Metadata Fields
Cell line
View Samples- Xenopus laevis
- 20 Downloadable Samples
- Affymetrix Xenopus laevis Genome 2.0 Array (xlaevis2)
Description
The transcription factors Pax3 and Zic1 are among the earliest genes activated at the neural plate border. Pax3 and Zic1 in combination promote neural crest fate, while Zic1 alone regulate cranial placode progenitor formation. We used microarrays to identify the global repertoire of genes activated by these facors individually or in combination to gain insights into the molecular mechanisms underlying cell fate decision at the neural plate border.
Publication Title
Identification of Pax3 and Zic1 targets in the developing neural crest.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Homo sapiens
- 3 Downloadable Samples
- Affymetrix Human Gene 2.0 ST Array (hugene20st)
Description
SOCS1 plays a role in cellular senescence. Knocking down SOCS1 in senescence induced by the STAT5 oncogene results in senescence bypass by preventing p53 activation
Publication Title
SOCS1 regulates senescence and ferroptosis by modulating the expression of p53 target genes.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 1 Downloadable Sample
- Affymetrix Human Gene 2.0 ST Array (hugene20st)
Description
The expression of the forkhead transcription factor CHES1, also known as FOXN3, is reduced in many types of cancers. In vitro, CHES1 expression suppresses cell proliferation in tumor cell lines but not in normal cells. Conversely shRNA-mediated depletion of CHES1 increases tumor cell proliferation.
Publication Title
CHES1/FOXN3 regulates cell proliferation by repressing PIM2 and protein biosynthesis.
Sample Metadata Fields
Cell line
View Samples- Mus musculus
- 6 Downloadable Samples
NextSeq 500
Description
RNA-SEQ of mutants B cell for IgH 3''RR and Emu Overall design: CD43- splenic B-cells from wt, Eµ-deficient or 3''RR deficient mice, non stimulated (NS) or stimulated (S) with 5mg/ml LPS.
Publication Title
E<sub>μ</sub> and 3'RR IgH enhancers show hierarchic unilateral dependence in mature B-cells.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 4 Downloadable Samples
- NextSeq 500
Description
The IgH 3' regulatory region (3'RR) controls class switch recombination (CSR) and somatic hypermutation (SHM) in B cells. The mouse 3'RR contains four enhancer elements with hs1,2 flanked by inverted repeated sequences and the center of a 25-kb palindrome bounded by two hs3 enhancer inverted copies (hs3a and hs3b). hs4 lies downstream of the palindrome. Evolution maintained in mammals this unique palindromic arrangement suggesting that it is functionally significant. We report that deconstructing the palindromic IgH 3'RR strongly impacts its function even when enhancers are preserved. CSR and IgH transcription appear poorly dependent from the 3'RR architecture and are more or less preserved provided 3'RR enhancers are present. By contrast, an “architectural effect” significantly lowers VH germline transcription, AID recruitment and SHM. In conclusion, this work indicates that the IgH 3'RR does not simply pile up enhancer units but also optimally expose them into a functional architecture of crucial importance. Overall design: RNAseq analysis of B-cell splenocytes with (S=stimulated) or without (R=resting) LPS activation from wt, delta2leftPAL, and deltaIRIS mice.
Publication Title
Deciphering the importance of the palindromic architecture of the immunoglobulin heavy-chain 3' regulatory region.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 86 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Patients with oral preneoplastic lesion (OPL) have high risk of developing oral cancer. Although certain risk factors such as smoking status and histology are known, our ability to predict oral cancer risk remains poor. The study objective was to determine the value of gene expression profiling in predicting oral cancer development. Gene expression profile was measured in 86 of 162 OPL patients who were enrolled in a clinical chemoprevention trial that used the incidence of oral cancer development as a prespecified endpoint. The median follow-up time was 6.08 years and 35 of the 86 patients developed oral cancer over the course. Gene expression profiles were associated with oral cancer-free survival and used to develope multivariate predictive models for oral cancer prediction.
Publication Title
Gene expression profiling predicts the development of oral cancer.
Sample Metadata Fields
Sex, Age, Race
View Samples- Mus musculus
- 8 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
This work was designed to determine the role of the vascular endothelial growth factor A (VEGF) isoforms during early neuroepithelial development in the mammalian central nervous system (CNS), specifically in the forebrain. An emerging model of interdependence between neural and vascular systems includes VEGF, with its dual roles as a potent angiogenesis factor and neural regulator. Although a number of studies have implicated VEGF in CNS development, little is known about the role that the different VEGF isoforms play in early neurogenesis. We used a mouse model of disrupted VEGF isoform expression that eliminates the predominant brain isoform, VEGF164, and expresses only the diffusible form, VEGF120. We tested the hypothesis that VEGF164 plays a key role in controlling neural precursor populations in developing cortex. We used microarray analysis to compare gene expression differences between wild type and VEGF120 mice at E9.5, the primitive stem cell stage of the neuroepithelium. We quantified changes in PHH3-positive nuclei, neural stem cell markers (Pax6 and nestin) and the Tbr2-positive intermediate progenitors at E11.5 when the neural precursor population is expanding rapidly. Absence of VEGF164 (and VEGF188) leads to reduced proliferation without an apparent effect on the number of Tbr2-positive cells. There is a corresponding reduction in the number of mitotic spindles that are oriented parallel to the ventricular surface relative to those with a vertical or oblique angle. These results support a role for the VEGF isoforms in supporting the neural precursor population of the early neuroepithelium.
Publication Title
Vascular endothelial growth factor (VEGF) isoform regulation of early forebrain development.
Sample Metadata Fields
Specimen part
View Samples