Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

43 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MRNA profiling by array of cartilage tumors

ABSTRACT: In this study, a series of 102 cartilage tumors was used to uncover the molecular diversity of chondrosarcomas through the profiling of mRNA, miRNA, DNA methylation, DNA copy number aberrations and point mutations. An integrated classification using multiple molecular dimensions revealed three major molecular features unraveling the diversity in clinical outcome of chondrosarcoma: a high mitotic state, regional 14q32 loss of expression and IDH mutations leading to genome-wide hypermethylation. These three robust and simple molecular features classify chondrosarcoma in subtypes with superior clinical value as compared to the current grading system.

ORGANISM(S): Homo sapiens

SUBMITTER: Elarouci Nabila

PROVIDER: E-MTAB-7264 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

High-throughput sequencing of miRNA of cartilage tumors

Project description:In this study, a series of 102 cartilage tumors was used to uncover the molecular diversity of chondrosarcomas through the profiling of mRNA, miRNA, DNA methylation, DNA copy number aberrations and point mutations. An integrated classification using multiple molecular dimensions revealed three major molecular features unraveling the diversity in clinical outcome of chondrosarcoma: a high mitotic state, regional 14q32 loss of expression and IDH mutations leading to genome-wide hypermethylation. These three robust and simple molecular features classify chondrosarcoma in subtypes with superior clinical value as compared to the current grading system.

2019-07-19 | E-MTAB-7265 | biostudies-arrayexpress

Methylation profiling by array of cartilage tumors

2019-07-19 | E-MTAB-7263 | biostudies-arrayexpress

Genotyping by array of cartilage tumors taken from human patients

2019-08-05 | E-MTAB-8213 | biostudies-arrayexpress

Gene expression profiling data following HIF-1α or HIF-2α knockdown in SW1353 cells

Project description:Chondrosarcomas, malignant cartilaginous neoplasms, are capable of transitioning to highly aggressive, metastatic, and treatment-refractory states, resulting in significant patient mortality. We aimed to uncover the transcriptional program directing such tumor progression in chondrosarcomas. Here, we conducted weighted correlation network analysis (WGCNA) to extract a characteristic gene module underlying chondrosarcoma malignancy. We identified hypoxia-inducible factor-2α (HIF-2α, encoded by EPAS1) as an upstream regulator that governs the malignancy gene module. HIF-2α was upregulated in high grade chondrosarcoma biopsies and HIF-2α gene amplification was associated with the poor prognosis of patients with chondrosarcoma. Using tumor xenograft mouse models, we demonstrated that HIF-2α confers chondrosarcomas the capacities required for tumor growth, local invasion, and metastasis. Pharmacological inhibition of HIF-2α in conjunction with the chemotherapy agents synergistically enhanced chondrosarcoma cell apoptosis and abolished malignant signatures of chondrosarcoma in mice. We expect that our insights into the pathogenesis of chondrosarcoma will provide guidelines for the development of novel molecular-targeted therapeutics for chondrosarcoma.

2020-08-21 | GSE156565 | GEO

Decoupling NAD+ metabolic dependency in chondrosarcoma by targeting the SIRT1–HIF-2α axis

Project description:Chondrosarcomas represent the second most common primary bone malignancy. Despite the vulnerability of chondrosarcoma cells to nicotinamide adenine dinucleotide (NAD+) depletion, targeting the NAD+ synthesis pathway remains challenging due to broad implications in biological processes. Here, we establish SIRT1 as a central mediator reinforcing the dependency of chondrosarcoma cells on NAD+ metabolism via HIF-2α-mediated transcriptional reprogramming. SIRT1 knockdown abolishes aggressive phenotypes of chondrosarcomas in orthotopically transplanted tumors in mice. Chondrosarcoma cells thrive under glucose starvation by accumulating NAD+ and subsequently activating the SIRT1–HIF-2α axis. Decoupling this link via SIRT1 inhibition unleashes apoptosis and suppresses tumor progression in conjunction with chemotherapy. Unsupervised clustering analysis identifies a high-risk chondrosarcoma patient subgroup characterized by the upregulation of NAD+ biosynthesis genes. Finally, SIRT1 inhibition abolishes HIF-2α transcriptional activity and sensitizes chondrosarcoma cells to doxorubicin-induced cytotoxicity, irrespective of underlying pathways to accumulate intracellular NAD+. We provide system-level guidelines to develop therapeutic strategies for chondrosarcomas.

2023-12-01 | GSE248490 | GEO

SNP array analysis on Maffucci tumours

2011-07-19 | GSE26674 | GEO

SNP array analysis on Maffucci tumours

Project description:Here we have used four enchondromas and two chondrosarcomas of Maffucci patients. We also had one normal sample available for paired analysis in one of the chondrosarcoma II. We did not find any LOH or coomon copy number variation in all Maffucci enchondromas while chondrosarcomas are genetically unstable. Affymetrix SNP 6.0 array was performed using 4 EC and 2CS of Maffucci patients. Illumina expression v3 array was possible to perform using only 1 EC and 2 CS due to rarity of the disease. For SNP array, we used 29 control samples submitted previously (GSE22965) to creat baseline.

2011-07-18 | E-GEOD-26674 | biostudies-arrayexpress

Single-cell RNA sequencing analysis reveals CHOP as an early marker for conventional chondrosarcoma

Project description:Chondrosarcoma is the malignant form of chondrogenic tumors that consist of cartilage producing cells. Chondrosarcoam can arise from benign chondrogenic lesion. Benign chondrogenic tumors are normally managed conservatively, while surgical intervention can improve clinical outcomes of patients with chondrosarcoma. Clinical decision making is mainly based on the grade of the chondrogenic tumor. However, interobserver viability is high. There is currently no clear molecular for the grading and clinical decision making. To tackle this clinical problem, we performed single-cell RNA sequencing on chondrosarcomas of different grades, an enchondroma, as well as a chondroblastic osteosarcoma and a fetal femur as comparison.

2024-01-18 | GSE184118 | GEO

Clonal evolution through loss of chromosomes and subsequent polyploidization in chondrosarcoma

Project description:Near-haploid chromosome numbers have been found in less than 1% of cytogenetically reported tumors, but seem to be more common in certain neoplasms including the malignant cartilage-producing tumor chondrosarcoma. By a literature survey of published karyotypes from chondrosarcomas we could confirm that loss of chromosomes resulting in hyperhaploid-hypodiploid cells is common and that these cells may polyploidize. Sixteen chondrosarcomas were investigated by single nucleotide polymorphism (SNP) array and the majority displayed SNP patterns indicative of a hyperhaploid-hypodiploid origin, with or without subsequent polyploidization. Except for chromosomes 5, 7, 19, 20 and 21, autosomal loss of heterozygosity was commonly found, resulting from chromosome loss and subsequent duplication of monosomic chromosomes giving rise to uniparental disomy. Additional gains, losses and rearrangements of genetic material, and even repeated rounds of polyploidization, may affect chondrosarcoma cells resulting in highly complex karyotypes. Loss of chromosomes and subsequent polyploidization was not restricted to a particular chondrosarcoma subtype and, although commonly found in chondrosarcoma, binucleated cells did not seem to be involved in these events.

2011-09-26 | GSE25985 | GEO

A multimodal treatment of carbon ions irradiation, miRNA-34 and mTOR inhibitor specifically control high-grade chondrosarcoma cancer stem cells

Project description:High-grade chondrosarcomas are chemo- and radio-resistant cartilage-forming tumors of bone that often relapse and metastase. Thus, new therapeutic strategies are urgently needed. Here we show that high-grade chondrosarcoma cells contain a population of radioresistant cancer stem cells that can be targeted by a combination of carbon-ion therapy, miR-34 mimic administration and/or rapamycin treatment that triggers FOXO3 and miR-34 over-expression. mTOR inhibition by rapamycin triggered FOXO3 and miR-34, leading to KLF4 repression. Our results show that particle therapy combined with molecular treatments effectively controls cancer stem cells and may overcome treatment resistance of high-grade chondrosarcoma.

2020-10-15 | GSE135371 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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