Cdca7l acts as a male-specific oncogene in astrocytoma and glioblastoma, and can transform primary astrocyte growth in soft agar. We stably overexpressed Cdca7l in mouse primary astrocytes and compared gene expression to primary astrocytes expressing empty vector control in male and female cell to identify gene expression differences between male and female cells and between Cdca7l-overexpressing and normal primary astrocytes.
No associated publication
Sex, Specimen part
View SamplesCdca7l is expressed higher in male astrocytoma/GBM than female tumors or normal cells, and knockdown of Cdca7l blocks growth of male tumor cells, but not female tumor cells. We stably depleted Cdca7l in mouse astrocytoma cells and compared gene expression to control astrocytoma cells expressing non-targeting scrambled shRNA in male and female cells and to wild type primary astrocytes to identify gene expression differences between male and female cells and between Cdca7l-depleted, scrambled shRNA control cells and wild type primary astrocytes.
No associated publication
Sex
View SamplesCDCA7L is expressed higher in male astrocytoma/GBM than female tumors or normal cells, and knockdown of CDCA7L blocks growth of male tumor cells, but not female tumor cells. We stably depleted CDCA7L in human GBM cells and compared gene expression to control GBM cells expressing non-trageting scrambled shRNA in male and female cells to identify gene expression differences between male and female cells and between CDCA7L-depleted and scrambled shRNA control cells.
No associated publication
Sex
View SamplesTo understand molecular mechanisms by which reducing Id2 rescues impaired erythropoiesis and hematopoietic progenitor cell development in Gfi-1-/- mice, we compared gene expression in Gfi-1-/-;Id2+/- and Gfi-1-/- BMC using Affymetrix microarray.
Gfi-1 regulates the erythroid transcription factor network through Id2 repression in murine hematopoietic progenitor cells.
Specimen part
View SamplesIdentification of genes up-regulated in ALK-positive and EGFR/KRAS/ALK-negative lung adenocarcinomas.
Identification of genes upregulated in ALK-positive and EGFR/KRAS/ALK-negative lung adenocarcinomas.
Sex, Age, Specimen part
View SamplesGene expression data were obtained from 130 pediatric AML patients who were enrolled on the AML99 study conducted by the Japanese Childhood AML Cooperative Study Group.
No associated publication
No sample metadata fields
View SamplesPoorly differentiated type synovial sarcoma (PDSS) is a variant of synovial sarcoma characterized by predominantly round or short-spindled cells. Although accumulating evidence from clinicopathological studies suggests a strong association between this variant of synovial sarcoma and poor prognosis, little has been reported on the molecular basis of PDSS. To gain insight into the mechanism(s) that underlie the emergence of PDSS, we analyzed the gene expression profiles of 34 synovial sarcoma clinical samples, including 5 cases of PDSS, using an oligonucleotide microarray. In an unsupervised analysis, the 34 samples fell into 3 groups that correlated highly with histological subtype, namely, monophasic, biphasic, and poorly differentiated types. PDSS was characterized by down-regulation of genes associated with neuronal and skeletal development and cell adhesion, and up-regulation of genes on a specific chromosomal locus, 8q21.11. This locus-specific transcriptional activation in PDSS was confirmed by reverse transcriptase (RT)-PCR analysis of 9 additional synovial sarcoma samples. Our results indicate that PDSS tumors constitute a distinct genetic group based on expression profiles.
Gene expression profiling of synovial sarcoma: distinct signature of poorly differentiated type.
Sex, Specimen part
View SamplesOsteosarcoma patients with development of pulmonary metastasis have still poorer prognosis in spite of aggressive treatment. However, molecular mechanism of metastasis is still unknown.
Reduced argininosuccinate synthetase is a predictive biomarker for the development of pulmonary metastasis in patients with osteosarcoma.
Sex, Age
View SamplesAberrant DNA methylation is induced at specific promoter CpG islands (CGIs) in contrast with mutations. The specificity is influenced by genome architecture and epigenetic factors, but their relationship is still unknown. In this study, we isolated promoter CGIs susceptible and resistant to aberrant methylation induction during prostate and breast carcinogenesis. The effect of genome architecture was more evident for promoter CGIs susceptible in both of the two tissues than for promoter CGIs susceptible only in one tissue. Multivariate analysis of promoter CGIs with tissue-nonspecific susceptibility showed that genome architecture, namely a remote location from SINE (OR=5.98; 95% CI=2.33-15.34) and from LINE (OR=2.08; 95% CI=1.03-4.21), was associated with increased susceptibility, independent of epigenetic factors such as the presence of RNA polymerase II (OR=0.09; 95% CI=0.02-0.48) and H3K27me3 (OR=3.28; 95% CI=1.17-9.21). These results showed that methylation susceptibility of promoter CGIs is determined both by genome architecture and epigenetic factors, independently.
Effects of genome architecture and epigenetic factors on susceptibility of promoter CpG islands to aberrant DNA methylation induction.
Cell line
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Forced expression of the histone demethylase Fbxl10 maintains self-renewing hematopoietic stem cells.
Specimen part
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