Alterations in gene expression following knockdown of thioredoxin 1 (TR1) with stable viral transduction
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Philip Moos
PROVIDER: E-GEOD-56519 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:This experiment was to determine if we could observe changes in gene expression following the attenuation of one of the primary redox regulators of cells - thioredoxin reductase 1. The experiment was set up with two cell lines that expressed different basal levels of TR1. LOX cells represent an aggressive melanoma in xenograft models and are high expressors of TR1 while SK Mel-28 cells represent a non-aggressive melanoma in xenografts adn are low expressors of TR1.
2015-04-28 | GSE56519 | GEO
Project description:Melanoma is one of the most aggressive and treatment-resistant cancers. It represents the most life-threatening neoplasm of the skin, and its incidence has been increasing for the last three decades. Melanoma evolves from the local transformation of melanocytes to primary tumors, which can metastasize to multiple organs. Brain metastases represent one of the most significant causes of death in cutaneous melanoma patients. Despite aggressive multi-modality threapy, patients with melanoma brain metastasis have a median survival of less than a year, with a majority of these patients dying as a result of their intracranial disease. To identify alterations in gene expression related to brain metastasis, we used Affymetrix expression arrays to assess differentially expressed genes in melanocytes, lymph node metastases, and brain metastases. Total RNA from twenty-two specimens representing normal melanocytes (n=3), melanoma lymph node metastasis (n=12), and melanoma brain metastasis (n=7) was extracted and analyzed by Affymetrix expression arrays. Melanocytes specimens were used as control samples. Melanocytes were acquired from Invitrogen (LifeTechnologies). Metastatic melanoma specimens were taken from different patients, established as cell lines in the John Wayne Cancer Institute. Early passages (less than 6) were used to perform expression analysis.
2013-09-19 | E-GEOD-44660 | biostudies-arrayexpress
Project description:Melanoma is one of the most aggressive and treatment-resistant cancers. It represents the most life-threatening neoplasm of the skin, and its incidence has been increasing for the last three decades. Melanoma evolves from the local transformation of melanocytes to primary tumors, which can metastasize to multiple organs. Brain metastases represent one of the most significant causes of death in cutaneous melanoma patients. Despite aggressive multi-modality threapy, patients with melanoma brain metastasis have a median survival of less than a year, with a majority of these patients dying as a result of their intracranial disease. We aimed to find brain metastasis-specific molecular markers. To identify alterations in DNA methylation related to brain metastasis, we used Illumina 450K BeadChips to assess differentially methylated regions in melanocytes, primary melanomas, lymph node metastases, and brain metastases. Bisulphite-converted DNA from 40 specimens was hybridised to the Illumina Infinium 450k Human Methylation BeadChip.
2013-09-19 | E-GEOD-44661 | biostudies-arrayexpress
Project description:Melanoma is one of the most aggressive and treatment-resistant cancers. It represents the most life-threatening neoplasm of the skin, and its incidence has been increasing for the last three decades. Melanoma evolves from the local transformation of melanocytes to primary tumors, which can metastasize to multiple organs. Brain metastases represent one of the most significant causes of death in cutaneous melanoma patients. Despite aggressive multi-modality threapy, patients with melanoma brain metastasis have a median survival of less than a year, with a majority of these patients dying as a result of their intracranial disease. To identify alterations in gene expression related to brain metastasis, we used Affymetrix expression arrays to assess differentially expressed genes in melanocytes, lymph node metastases, and brain metastases.
2013-09-19 | GSE44660 | GEO
Project description:Melanoma is one of the most aggressive and treatment-resistant cancers. It represents the most life-threatening neoplasm of the skin, and its incidence has been increasing for the last three decades. Melanoma evolves from the local transformation of melanocytes to primary tumors, which can metastasize to multiple organs. Brain metastases represent one of the most significant causes of death in cutaneous melanoma patients. Despite aggressive multi-modality threapy, patients with melanoma brain metastasis have a median survival of less than a year, with a majority of these patients dying as a result of their intracranial disease. We aimed to find brain metastasis-specific molecular markers. To identify alterations in DNA methylation related to brain metastasis, we used Illumina 450K BeadChips to assess differentially methylated regions in melanocytes, primary melanomas, lymph node metastases, and brain metastases.
2013-09-19 | GSE44661 | GEO
Project description:Pappalardo2016 - PI3K/AKT and MAPK Signaling
Pathways in Melanoma Cancer
This model is described in the article:
Computational Modeling of
PI3K/AKT and MAPK Signaling Pathways in Melanoma Cancer.
Pappalardo F, Russo G, Candido S,
Pennisi M, Cavalieri S, Motta S, McCubrey JA, Nicoletti F, Libra
M.
PLoS ONE 2016; 11(3): e0152104
Abstract:
Malignant melanoma is an aggressive tumor of the skin and
seems to be resistant to current therapeutic approaches.
Melanocytic transformation is thought to occur by sequential
accumulation of genetic and molecular alterations able to
activate the Ras/Raf/MEK/ERK (MAPK) and/or the PI3K/AKT (AKT)
signalling pathways. Specifically, mutations of B-RAF activate
MAPK pathway resulting in cell cycle progression and apoptosis
prevention. According to these findings, MAPK and AKT pathways
may represent promising therapeutic targets for an otherwise
devastating disease.Here we show a computational model able to
simulate the main biochemical and metabolic interactions in the
PI3K/AKT and MAPK pathways potentially involved in melanoma
development. Overall, this computational approach may
accelerate the drug discovery process and encourages the
identification of novel pathway activators with consequent
development of novel antioncogenic compounds to overcome tumor
cell resistance to conventional therapeutic agents. The source
code of the various versions of the model are available as S1
Archive.
This model is hosted on
BioModels Database
and identified by:
MODEL1609190000.
To cite BioModels Database, please use:
BioModels Database:
An enhanced, curated and annotated resource for published
quantitative kinetic models.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2024-09-02 | BIOMD0000000666 | BioModels
Project description:Cutaneous melanoma is an aggressive type of skin cancer with a complex genetic landscape caused by the malignant transformation of melanocytes. The study aimed at providing an in-silico network model based on the systematic profiling of the melanoma-associated genes considering germline mutations, somatic mutations, and genome-wide association studies (GWAS) signals (collectively melanoma risk genes). A protein-protein interaction network (melanoma risk network) was constructed using the melanoma risk genes to describe the functional landscape in which the melanoma genes operate within the cellular milieu. A significant portion of the melanoma risk network showed differential expression when SK-MEL-28 human melanoma cells were exposed to the phytochemicals harmine and berberine chloride reinforcing the hypothesis that network modelling may represent an alternative screening approach to prioritize potentially active compounds.
2023-11-01 | GSE246383 | GEO
Project description:CD4(+) type 1 T regulatory (Tr1) cells are induced in the periphery and have a pivotal role in promoting and maintaining tolerance. The absence of surface markers that uniquely identify Tr1 cells has limited their study and clinical applications. By gene expression profiling of human Tr1 cell clones, we identified the surface markers CD49b and lymphocyte activation gene 3 (LAG-3) as being stably and selectively coexpressed on mouse and human Tr1 cells. We showed the specificity of these markers in mouse models of intestinal inflammation and helminth infection and in the peripheral blood of healthy volunteers. The coexpression of CD49b and LAG-3 enables the isolation of highly suppressive human Tr1 cells from in vitro anergized cultures and allows the tracking of Tr1 cells in the peripheral blood of subjects who developed tolerance after allogeneic hematopoietic stem cell transplantation. The use of these markers makes it feasible to track Tr1 cells in vivo and purify Tr1 cells for cell therapy to induce or restore tolerance in subjects with immune-mediated diseases. The transcriptome of human Tr1 cell clones to that of TH0 cell clones either unstimulated or stimulated for 6 and 16 h. Tr1 and TH0 cell clones were isolated from peripheral blood of 2 Healthy Donors (HDs). mRNA from T cell clones unstimulated (t0, n=4 Tr1 cell clones and n=10 TH0 cell clones) or stimulated with immobilized anti-CD3 and soluble anti-CD28 mAbs (6h and 16h, n=4 Tr1 cell clones and n=5 TH0 cell clones) was isolated. Differential expression of 28869 genes was investigated by whole transcript Affymetric chips.
2013-12-20 | E-GEOD-53514 | biostudies-arrayexpress
Project description:Expression profiles of aggressive versus non-aggressive ovarian, breast, melanoma, and prostate cancer cell lines Expression profiles of aggressive versus non-aggressive ovarian, breast, melanoma, and prostate cancer cell lines was determined. 231MFP, C8161, SKOV3, DU145, and PC3 are aggressive and MCF7, MUM2C, OVCAR3, and LNCaP are non-aggressive cancer cells. We are not comparing across all of the cell lines--just between C8161 and MUM2C, SKOV3 and OVCAR3, 231MFP and MCF7, and LNCaP/DU145/PC3. Therefore the normalization strategies used are different. We have not used the same normalization strategy
2011-08-09 | E-GEOD-28846 | biostudies-arrayexpress
Project description:Purpose: To identify gene expression patterns in ex vivo isolated human Tr1 cells. Method: RNA sequencing of total mRNA. Results: Differential gene expression of Tr1 and non-Tr1 CD4+ T memory cells. Conclusions: ex vivo type 1 regulatory T cells have a distinct gene expression profile compared to non-Tr1 CD4+ T cell memory cells.
2021-07-02 | GSE169761 | GEO