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GSE144909
Homo sapiens
4 Downloadable Samples
Illumina HumanHT-12 V4.0 expression beadchip
Description
A significant proportion of differentially expressed genes were associated with extracellular matrix organization and extracellular structure organization.
Publication Title
LAMA4 upregulation is associated with high liver metastasis potential and poor survival outcome of Pancreatic Cancer.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Homo sapiens
- 4 Downloadable Samples
Illumina HiSeq 2000
Description
gene expression of human gastric carcinoma cell line NCI-N87 under quercetin treatment
Publication Title
No associated publication
Sample Metadata Fields
Sex, Specimen part, Cell line
View Samples- Homo sapiens
- 6 Downloadable Samples
- Illumina HiSeq 4000
Description
No description.
Publication Title
No associated publication
Sample Metadata Fields
Sex, Specimen part, Cell line
View Samples- Homo sapiens
- 1 Downloadable Sample
- IlluminaHiSeq1000
Description
In addition to BCR, various rare fusion partners for the ABL1 gene have been reported in leukemia. We have identified the fusion gene SNX2-ABL1 in a pediatric case of acute lymphoblastic leukemia (ALL), which has only once previously been reported in an adult patient. Cytogenetic analysis detected this fusion gene arising from a t(5;9)(q22;q34) translocation. ALL cells carrying a SNX2-ABL1 fusion exhibited a BCR-ABL1+ALL-like gene expression profile. The patient poorly responded to dasatinib but partially responded to imatinib. Treatment using tyrosine kinase inhibitors requires further investigation to optimize the genotype-based treatment stratification for patients with SNX2-ABL1 fusion.
Publication Title
No associated publication
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 1 Downloadable Sample
- IlluminaHiSeq1000
Description
In addition to BCR, various rare fusion partners for the ABL1 gene have been reported in leukemia. We have identified the fusion gene SNX2-ABL1 in a pediatric case of acute lymphoblastic leukemia (ALL), which has only once previously been reported in an adult patient. Cytogenetic analysis detected this fusion gene arising from a t(5;9)(q22;q34) translocation. ALL cells carrying a SNX2-ABL1 fusion exhibited a BCR-ABL1+ALL-like gene expression profile. The patient poorly responded to dasatinib but partially responded to imatinib. Treatment using tyrosine kinase inhibitors requires further investigation to optimize the genotype-based treatment stratification for patients with SNX2-ABL1 fusion.
Publication Title
No associated publication
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 6 Downloadable Samples
- Illumina HiSeq 2500
Description
The impact of the transcriptome-wide alternative splicing on proteomic-wide protein subcellular localization was investigated by analyzing RNA-Seq data.
Publication Title
No associated publication
Sample Metadata Fields
Sex, Specimen part, Disease, Cell line
View Samples- Homo sapiens
- 9 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Combined overexpression of miR-125b with miR-99a and/or miR-100 induced VCR resistance in ETV6-RUNX1-positive leukemic cells Reh.
Publication Title
MiR-125b, miR-100 and miR-99a co-regulate vincristine resistance in childhood acute lymphoblastic leukemia.
Sample Metadata Fields
Disease, Cell line
View Samples- Homo sapiens
- 18 Downloadable Samples
- Illumina HiSeq 4000
Description
The most frequent genetic alterations in melanoma are gain-of-function mutations in BRAF, which result in addiction to the RAF-MEK-ERK signaling pathway. Despite success of RAF and MEK inhibitors in treating BRAFV600 mutant tumors, a major challenge is the inevitable emergence of drug resistance, which often involves reactivation of the MAPK pathway. Interestingly, resistant tumors are often sensitive to drug withdrawal, suggesting that hyperactivation of the MAPK pathway is not tolerated. To further characterize this phenomenon, we generated isogenic models of inducible MAPK hyperactivation in BRAFV600E melanoma cells by overexpression of ERK2. Using this model system, we demonstrated that supra-physiological levels of MAPK signaling led to cell death, which was reversed by MAPK inhibitors. Whereas MAPK pathway inhibition led to cell stasis in BRAFV600E melanoma cells, MAPK hyperactivation induced cytotoxicity. Furthermore, complete tumor regression was observed in an ERK2 overexpressing xenograft model. To identify mediators of MAPK hyperactivation- induced cell death, we conducted a large-scale pooled screen which showed that only shRNAs against BRAF and MAP2K1 rescued loss of cell viability. This suggested that no single downstream ERK2 effector was required, consistent with pleiotropic effects on multiple cellular stress pathways. Intriguingly, the detrimental effect of MAPK hyperactivation could be partially attributed to secreted factors, and more than 100 differentially secreted proteins were identified. The effect of ERK2 overexpression was highly context dependent, as RAS/RAF mutant but not RAS/RAF wildtype melanoma were sensitive to this perturbation. This vulnerability to MAPK hyperactivation raises the possibility of a novel therapeutic approach for RAS/RAF mutant cancers.
Publication Title
No associated publication
Sample Metadata Fields
Sex, Specimen part, Disease, Cell line, Treatment
View Samples- Homo sapiens
- 4 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
We established gene expression profiles of diagnostic bone marrow samples of monozygotic twins with acute lymphoblastic leukemia. We established technical duplicates for each twin.
Publication Title
Prenatal origin of separate evolution of leukemia in identical twins.
Sample Metadata Fields
Sex, Specimen part, Disease, Disease stage
View Samples- Homo sapiens
- 26 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
One of the most important features of tumor microenvironment, imposing adverse effect on patient prognosis, is low oxygen tension. There are two types of hypoxia that may occur within tumor mass: chronic and cycling. Preliminary studies point at cycling hypoxia as being more relevant in induction of aggressive phenotype of tumor cells and radioresistance though little is known about the molecular mechanism of this phenomenon. Analysis of gene expression profile of human prostate (PC-3), ovarian (SK-OV-3) and melanoma (WM793B) cancer cells to expermental cycling (interchanging conditions of 1% and 21% oxygen) or chronic (1% oxygen) for 72 hours. Gene expression profiles were analyzed using U133 Plus 2.0 Array (Affymetrix) oligonucleotide microarrays. Data analysis revealed that globally gene expression profiles induced by the two types of hypoxia are similar and they strongly depend on the cell type.However, cycling hypoxia changes expression of lower number of genes in comparison to chronic one ( 3767 vs. 5954 probesets (p<0.001)) and to lower extent (lower fold changes). Analysis of hypoxia-regulated gene lists obtained using Random Variance Model t-test identified 253 probe sets (FC>2, p<0.001) common to all three cell lines, though no universal (changed throughout all analyzed cell lines) genes specifically influanced only by cycling hypoxia was selected. On the other hand, we identified such genes within particular one or two cell lines. Among them those related with EGF pathway seemed to be overrepresented (i.e. EPHA2, AREG, and HBEGF) and together with PLAU and IL-8 were mostly validated by Q-PCR.
Publication Title
Global gene expression profiling in three tumor cell lines subjected to experimental cycling and chronic hypoxia.
Sample Metadata Fields
Specimen part, Cell line
View Samples