Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

12 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A novel epigenetic regulated gene and involved in phenotypic switch classifies primary melanomas depending on the aggressiveness grade (gene expression)

ABSTRACT: Loss of methylation of a GTPase-activating protein in melanoma mediates higher proliferation, lower migration, and agressiveness of primary melanomas. Gene wide expression analysis of melanoma and breast primary and metastatic related tumorigenic cell lines.

ORGANISM(S): Homo sapiens

SUBMITTER: Antonio Gómez

PROVIDER: E-GEOD-46521 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

A novel epigenetic regulated gene and involved in phenotypic switch classifies primary melanomas depending on the aggressiveness grade

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-05-11 | E-GEOD-46522 | biostudies-arrayexpress

A novel epigenetic regulated gene and involved in phenotypic switch classifies primary melanomas depending on the aggressiveness grade (Illumina)

Project description:Loss of methylation of a GTPase-activating protein in melanoma mediates higher proliferation, lower migration, and aggressiveness of primary melanomas. Sequencing of bisulfite converted DNA and array based analysis of melanoma, breast, and colon primary and metastatic related tumorigenic cell lines.

2015-05-11 | E-GEOD-46419 | biostudies-arrayexpress

A novel epigenetic regulated gene and involved in phenotypic switch classifies primary melanomas depending on the aggressiveness grade (Illumina)

Project description:Loss of methylation of a GTPase-activating protein in melanoma mediates higher proliferation, lower migration, and aggressiveness of primary melanomas.

2015-05-11 | GSE46419 | GEO

A novel epigenetic regulated gene and involved in phenotypic switch classifies primary melanomas depending on the aggressiveness grade (gene expression)

Project description:Loss of methylation of a GTPase-activating protein in melanoma mediates higher proliferation, lower migration, and agressiveness of primary melanomas.

2015-05-11 | GSE46521 | GEO

A novel epigenetic regulated gene and involved in phenotypic switch classifies primary melanomas depending on the aggressiveness grade

Project description:This SuperSeries is composed of the SubSeries listed below.

2015-05-11 | GSE46522 | GEO

RNA-sequencing of Fes KO and WT melanomas

Project description:Publication abstract: An incomplete view of the (epi)genetic events that drive melanoma initiation and progression has been a major barrier to rational development of effective therapeutics and prognostic diagnostics for melanoma patients. Recent approaches that integrate human melanoma genomic and transcriptomic data provide unprecedented opportunities to discover oncogenic melanoma drivers. One limitation, however, is that human melanoma genome exhibits a radically altered cytogenetic profile. There is therefore the need for biologically-meaningful approaches to identify and validate lesions that drive melanomagenesis. We combined comparative oncogenomic approaches with mouse modeling to identify new cancer genes/pathways that drive melanoma progression. Spontaneously acquired genetic alterations such as copy-number alterations and specific mutations in mouse tumors of defined genetic origin were identified and used to prioritize relevant lesions from the complex human melanoma genomes. This integrated effort confirmed the importance of several genes and pathways previously implicated in melanoma and identified new putative melanoma tumor suppressor genes. Genetic ablation of one such gene, c-Fes, cooperated with BRafv600E to accelerate melanomagenesis in mice. This comparative oncogenomic approach has therefore helped discover a series of novel melanoma tumor suppressor genes, including c-FES, with prognostic and therapeutic relevance in human melanoma.

2017-06-21 | GSE83580 | GEO

Peripheral positioning of lysosomes supports melanoma aggressiveness

Project description:Emerging evidences suggest that both function and position of organelles are pivotal for tumor cell dissemination. Among them, lysosomes stand out as they integrate metabolic sensing with gene regulation and secretion of proteases. Yet, how lysosomes function is linked to their position and thereby control metastatic progression remains elusive. Here, we analyzed lysosome subcellular distribution in micropatterned patient-derived melanoma cells and found that lysosome spreading scales with their aggressiveness. Peripheral lysosomes promote invadopodia-based matrix degradation and invasion of melanoma cells which is directly linked to their lysosomal and cell transcriptional programs. When controlling lysosomal positioning using chemo-genetical heterodimerization in melanoma cells, we demonstrated that perinuclear clustering impairs lysosomal secretion, matrix degradation and invasion. Impairing lysosomal spreading in a zebrafish metastasis model significantly reduces invasive outgrowth. Our study provides a mechanistic demonstration that lysosomal positioning controls cell invasion, illustrating the importance of organelle adaptation in carcinogenesis.

2023-07-31 | E-MTAB-13165 | biostudies-arrayexpress

Combinatorial treatment with PARP and MAPK inhibitors to overcome phenotype switch-driven drug resistance in advanced melanoma

Project description:Metastatic melanoma is either intrinsically resistant or rapidly acquires resistance to targeted drugs such as MAPK inhibitors (MAPKi). Here, using a drug screen targeting chromatin regulators in patient-derived 3D melanoma cell cultures, we discovered that PARP inhibitors are capable of restoring MAPKi sensitivity. This synergy was found to be independent of DNA damage repair pathways and was effective both in vitro and in vivo in patients-derived xenografts. Strikingly, through integrated transcriptomic, proteomic and epigenomic analysis, we discovered that PARPi induces lysosomal autophagy which was accompanied by enhanced mitochondrial lipid metabolism that, ultimately, increased antigen presentation and sensitivity to T-cell cytotoxicity. Moreover, we also found that PARP inhibitors regulated EMT-like phenotype switching by dampening the mesenchymal phenotype via transcriptomic and epigenetic rearrangements. This, in turn, redirected melanoma cells towards a proliferative and, thus, MAPKi-sensitive state. Our study provides a scientific rational for treating patients with PARPi in combination with MAPKi to annihilate acquired therapy resistance.

2023-09-08 | PXD038822 | Pride

Comparative genomic hybridization of human primary melanomas

Project description:Malignant melanoma is an aggressive heterogeneous disease for which new biomarkers for diagnosis and clinical outcome are needed. We investigated by array-CGH the presence of DNA gains and losses to provide better genomic profile of primary malignant melanoma and to explore the possibility to distinguish metastatic from non metastatic melanomas using this technology. High resolution array-CGH (Agilent Technologies, Palo Alto, CA), with more than 40.000 probes, has been used to analyze 20 frozen tissues of vertical growth phase primary melanoma with a minimum follow-up time of 36 months. Eight patients developed nodal metastatic disease and twelve did not. For results validation, 83 additional melanoma samples with similar clinical characteristics were analysed by FISH. DNA copy number aberrations (CNA) were observed in 19 out of 20 cases. The most frequent changes were complete or partial losses in chromosomes 9 (12 cases, 60%) and 10 (9 cases, 45%), partial gains or trisomies of chromosome 7 (10 cases, 50%); and monosomy of chromosome 19 (7 cases, 35%). Sixty-four recurrent aberrant regions (SORIs) were precisely delimited and used as variables for clustering. Unsupervised Cluster analysis allowed the segregation of samples into two genomic groups that naturally fitted with the metastatic condition of the cases. Four of these aberrant regions were chosen for their biological interest and were confirmed as aberrant using FISH technique on fixed paraffin embedded tissues. Conclusion: Supervised classification allowed obtaining aberrations useful to separate samples with different clinical outcome. Obtained results are useful to improve the knowledge about melanoma tumorigenesis but unfortunately cannot be used as a marker for metastatic progression. Experiment Overall Design: Comparative experiment: pheripheral blood pool of ten healthy female donors: CONTROL vs. 20 Primary Vertigal Growth Phase Melanoma samples.

2009-01-14 | E-GEOD-11109 | biostudies-arrayexpress

Beta-catenin Controls Metastasis in Braf-activated Pten-inactivated Melanomas

Project description:Malignant melanoma is characterized by frequent metastasis, however specific changes that regulate this process have not been clearly delineated. Although it is well known that Wnt signaling is frequently dysregulated in melanoma, the functional implications of this observation are unclear. By modulating beta-catenin levels in a mouse model of melanoma that is based on melanocyte-specific Pten loss and BrafV600E mutation, we demonstrate that beta-catenin is a central mediator of melanoma metastasis to lymph node and lung. In addition to altering metastasis, beta-catenin levels control tumor differentiation and regulate both MAPK/Erk and PI3K/Akt signaling. Highly metastatic tumors with beta-catenin stabilization are very similar to a subset of human melanomas; together these findings establish Wnt signaling as a metastasis regulator in melanoma. MoGene-1_0-st-v1: Four samples total. Two biological replicates of uncultured Pten/Braf murine melanomas and two biological replicates of uncultured Pten/Braf/Bcat-STA murine melanomas. MoEx-1_0-st-v1: Two samples total. Dissociated tumor and FACS-enriched Pten/Braf and Pten/Braf/Bcat-STA murine melanoma.

2011-10-12 | E-GEOD-32907 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data