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Homo sapiens
60 Downloadable Samples
Affymetrix Clariom S Human array (clariomshuman)
Description
Actinic keratosis is a common skin disease that may progress to invasive squamous cell carcinoma. Ingenol mebutate has demonstrated efficacy in field treatment of actinic keratosis. However, molecular mechanisms on ingenol mebutate response are not yet fully understood.
Publication Title
Identification of differentially expressed genes in actinic keratosis samples treated with ingenol mebutate gel.
Sample Metadata Fields
Specimen part, Disease, Disease stage, Subject
View Samples- Homo sapiens
- 12 Downloadable Samples
- Affymetrix CytoScan HD Array (cytoscanhdarray), Affymetrix Human Gene 2.0 ST Array (hugene20st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Transcriptome and cytogenetic profiling analysis of matched in situ/invasive cutaneous squamous cell carcinomas from immunocompetent patients.
Sample Metadata Fields
Sex, Age, Specimen part, Disease stage, Subject
View Samples- Homo sapiens
- 12 Downloadable Samples
- Affymetrix Human Gene 2.0 ST Array (hugene20st)
Description
Although most cutaneous squamous cell carcinomas (cSCC) develop from actinic keratoses (AK), the key events for this evolution remain unclear. We have combined the results of different genomic and expression array platforms on matched samples of sun-exposed skin, AK and cSCC from ten immunocompetent patients, with the objective of better understanding the mechanisms involved in this progression. Gene expression analysis and copy number alterations were assessed using GeneChip Human Gene 2.0 ST Array (Affymetrix) and CytoScan HD Cytogenetics Solution (Affymetrix) platforms, respectively. Integration of genome and transcriptome results was evaluated using the DR-Integrator tool. Additional studies (qPCR, immunohistochemistry and Western blot) were performed for selected genes. Twenty-two genes showed a progressive expression spectrum from clinically normal sun-exposed skin samples to cSCC. FOSL1 and BNC1 encode transcription factors whose expression was increased in cSCC in the expression array and the qPCR. By immunohistochemistry, FOSL1 showed an intense staining at the invasive front of cSCC samples and BNC1 expression varied from a nuclear location (sun-exposed skin) to a cytoplasmic location (cSCC). Western blot analyses confirmed the enhancement of FOSL1 and BNC1 expression. Additionally, the smallest overlapping regions of genomic imbalance (SORIs) involving at least 3 of the samples of each group (sun-exposed skin, AK or cSCC) were selected. One of the SORIs was a deletion in the p24.1 band of chromosome 3, shared by 7 of the cSCC. A strong correlation in the integration analysis was found for NEK10, a gene contained in the previously mentioned SORI. Loss of NEK10 expression in cSCC was confirmed by immunohistochemistry and western blot analyses. In conclusion, our findings suggest that FOSL1 may play a role in promoting the cSCC invasion ability. We have also identified two additional genes, NEK10 and BNC1, which could also act as tumor drivers.
Publication Title
Transcriptome and cytogenetic profiling analysis of matched in situ/invasive cutaneous squamous cell carcinomas from immunocompetent patients.
Sample Metadata Fields
Sex, Age, Specimen part, Disease stage, Subject
View Samples- Homo sapiens
- 2 Downloadable Samples
- Affymetrix Human Gene 2.0 ST Array (hugene20st)
Description
Cutaneous squamous cell carcinoma (cSCC) is the second most common malignancy in humans and approximately 5% metastasize, usually to regional lymph nodes. Epigenetic regulation of gene expression may allow tumoral cells to acquire new functions in order to escape from the primary tumor. The aim of this study was to investigate the expression and function of proteins of the Polycomb family of epigenetic regulators in the metastatic process of cSCC. A higher expression of RING1B and EZH2 was detected by immunohistochemistry in a series of primary cSCC tumors that metastasized (MSCC) when compared to non metastasizing cSCC (non MSCC). Stable downregulation of RING1B and EZH2 in cSCC cells results in enhanced expression of inflammatory cytokines and activation of the NFB signaling pathway. Accordingly, non MSCC display higher levels of membranous pS176 IKK and their stroma is enriched in neutrophils and eosinophils when compared to MSCC. In vitro, hematopoietic cells exhibit a substantial migratory response to supernatants from Polycomb depleted cSCC cells. Altogether these data indicate that RING1B and EZH2 repress the innate inflammatory cSCC function and impair tumor immunosurveillance and suggest that patients with high risk cSCC could benefit from clinical therapies addressed to harness the immune response.
Publication Title
The Polycomb proteins RING1B and EZH2 repress the tumoral pro-inflammatory function in metastasizing primary cutaneous squamous cell carcinoma.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 4 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Low levels of the cell cycle regulator p27Kip1 are associated with a worse outcome in many tumor types. We report here a new regulatory role of p27Kip1 as a transcriptional regulator. In association with transcriptional factors such as ETS and E2F4 and co-repressors like p130, HDACs and mSin3A, p27 binds to promoters of multiple genes leading to their repression. The p27-target genes participate in RNA processing, translation, respiration and cell cycle. Remarkably, p27-target genes are over-expressed in different human tumors in tight association with a poor clinical prognosis. We also observed a clear correlation between low levels of p27 and over-expression of p27-target genes in tumors. Overall, our findings indicate new tumor suppressor roles of p271 as a transcriptional regulator of genes relevant for oncogenesis.
Publication Title
p27Kip1 represses transcription by direct interaction with p130/E2F4 at the promoters of target genes.
Sample Metadata Fields
Specimen part
View Samples
GSE17063- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Aims/hypothesis Due to their ability to regulate various signalling pathways (cytokines, hormones, growth factors), the suppressor of cytokine signalling (SOCS) proteins are thought to be promising therapeutic targets for metabolic and inflammatory disorders. Hence, their role in vivo has to be precisely determined.
Publication Title
Constitutive expression of suppressor of cytokine signalling-3 in skeletal muscle leads to reduced mobility and overweight in mice.
Sample Metadata Fields
Specimen part, Subject
View Samples- Gallus gallus
- 4 Downloadable Samples
- Affymetrix Chicken Genome Array (chicken)
Description
We determined gene expression profiles which were induced in the chick chorio-allantoic membrane 24 h after application of recombinant human VEGF.
Publication Title
Impaired angiogenesis and tumor development by inhibition of the mitotic kinesin Eg5.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 8 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
In March 2006, murine Bone Marrow Stromal Cells (BMSC) were flown in the Soyuz 12S to the International Space Station to investigate the effects of microgravity on their osteogenic potential in a three-dimensional environment. BMSC were grown in porous bioceramic Skelite disks ( 9 mm x T 1.2 mm). The constructs were exposed to microgravity for ca. 8 days, then fixed for RNA extraction. While the flight experiment was performed in fully automated hardware inside the KUBIK incubator, one group of control samples were incubated inside manually operated hardwares (flight control), and the other control group was incubated under routine laboratory conditions (lab control). The altered gene expression profile was analyzed by Mouse Gene 1.0 ST array (Affymetrix) representing whole-transcript coverage. Each one of the 28853 genes is represented on the array by approximately 26 probes spread across the full length of the gene, providing a more complete and more accurate picture of gene expression than the 3 based expression array design.
Publication Title
Activation of nervous system development genes in bone marrow derived mesenchymal stem cells following spaceflight exposure.
Sample Metadata Fields
Specimen part, Disease
View Samples- Homo sapiens
- 3 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
For this study we selected a gene, -synuclein (SNCA), that is consistently under-expressed in MCF7 cells and breast tumors. Following transfection with an SNCA expression construct, two stable MCF7 clones (named MCF7-SNCA #1 and 2) were selected and examined for expression differences relative to the parental MCF7 cells.
Publication Title
Cancer develops, progresses and responds to therapies through restricted perturbation of the protein-protein interaction network.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 8 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Endocrine therapies targeting the proliferative effect of 17-estradiol (17E2) through estrogen receptor (ER) are the most effective systemic treatment of ER-positive breast cancer. However, most breast tumors initially responsive to these therapies develop resistance through a molecular mechanism that is not yet fully understood. The long-term estrogen-deprived (LTED) MCF7 cell model has been proposed to recapitulate acquired resistance to aromatase inhibitors (AIs) in postmenopausal women. To elucidate this resistance, genomic, transcriptomic and molecular data were integrated into the time course of MCF7-LTED adaptation. Dynamic and widespread genomic changes were observed, including amplification of the ESR1 locus consequently linked to an increase in ER. Dynamic transcriptomic profiles were also observed that correlated significantly with genomic changes and were influenced by transcription factors known to be involved in acquired resistance or cell proliferation (e.g. IRF1 and E2F1, respectively) but, notably, not by canonical ER transcriptional function. Consistently, at the molecular level, activation of growth factor signaling pathways by EGFR/ERBB/AKT and a switch from phospho-Ser118 (pS118)- to pS167-ER were observed during MCF7-LTED adaptation. Evaluation of relevant clinical settings identified significant associations between MCF7-LTED and breast tumor transcriptome profiles that characterize ER-negative status, early response to letrozole and recurrence after tamoxifen treatment. This study proposes a mechanism for acquired resistance to estrogen deprivation that is coordinated across biological levels and independent of canonical ER function.
Publication Title
Biological reprogramming in acquired resistance to endocrine therapy of breast cancer.
Sample Metadata Fields
Specimen part, Cell line
View Samples