Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome-wide expression profile in FH-deficient vs FH-competent cells

ABSTRACT: Genome-wide expression profile in FH-deficient vs FH-competent cells

PROVIDER: PRJNA310748 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR3142950.fastq.gz	Fastqsanger.gz
	SRR3142960.fastq.gz	Fastqsanger.gz
	SRR3142970.fastq.gz	Fastqsanger.gz
	SRR3142980.fastq.gz	Fastqsanger.gz
	SRR3142990.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 470

Similar Datasets

Genome-wide expression profile in FH-deficient (UOK262) vs FH-competent (UOK262pFH) human cells derived from metastatsis to the mediastinum of a HLRCC patient

Project description:Comparison of the transcriptome of human kideny cancer cells either wild-type for FH or FH-deficient. The UOK262 cells were isolated from mediastinum metastasis of a HLRCC patient (Yang et al. Cancer Genetics and Cytogenetics, Volume 196, Issue 1, 1 January 2010, Pages 45–55). FH function was restored in the UOK262 by re-expressing the FH transcript from an exogenous plasmid.

2016-09-22 | GSE77538 | GEO

Genome-wide expression profile in FH-deficient vs FH-competent cells

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

2016-09-22 | GSE77542 | GEO

HIRA loss transforms FH deficient cells

Project description:HIRA loss transforms FH deficient cells

| PRJNA838360 | ENA

HIRA loss transforms FH deficient cells [ChIP-Seq]

Project description:Fumarate Hydratase (FH) is a mitochondrial enzyme that catalyses the reversible hydration of fumarate to malate in the TCA cycle. Germline mutations of FH lead to HLRCC, a cancer syndrome characterised by a highly aggressive form of renal cancer(1). Although HLRCC tumours metastasise rapidly, FH-deficient mice develop premalignant cysts in the kidneys, rather than carcinomas(2). How Fh1-deficient cells overcome these tumour suppressive events during transformation is unknown. Here, we perform a genome-wide CRISPR/Cas9 screen to identify genes that, when ablated, enhance the proliferation of Fh1-deficient cells. We found that the depletion of the HIRA enhances proliferation and invasion of Fh1-deficient cells in vitro and in vivo. Mechanistically, Hira loss enables the activation of MYC and its target genes, increasing nucleotide metabolism specifically in Fh1-deficient cells, independent of its histone chaperone activity. These results are instrumental for understanding mechanisms of tumorigenesis in HLRCC and the development of targeted treatments for patients.

2022-10-29 | GSE203056 | GEO

Comprehensive molecular profiling of FH-deficient renal cell carcinoma identifies molecular subtypes and novel therapeutic targets

Project description:Conducting an in-depth exploration of the multi-omics landscape of Fumarate Hydratase (FH)-deficient renal cell carcinoma (RCC), the study aimed to unravel the intricate molecular mechanisms underlying this rare and aggressive form of renal cancer. Analyzing 126 patients with FH-deficient RCC, we identified distinct variant spectrum of FH gene, with truncating mutation correlated with adverse prognostic factors and a worse response to immune checkpoint blockade. The identification of three molecular subtypes with diverse clinical/genomic characteristics and varying response to systemic treatment further enriched the understanding of the heterogeneous tumor microenvironment (particularly immune-related) in FH-deficient RCC, and suggested potential therapeutic targets. These findings offer a basis for molecular stratification, shedding light on the tailored therapeutic strategies in improving treatment response of FH-deficient RCC.

2025-03-06 | GSE291073 | GEO

HIRA loss transforms FH deficient cells [RNA-Seq]

Project description:Purpose: Identifying transcriptional changes led by Hira loss in FH deficient cells Methods: RNA was extracted from the cell lines using QIAGEN kit folloging the manufacturer instructions. RNA concentrator kit was used to guarantee RNA quality. Results/Conclusion: We identified MYC/E2F1 signatures as the top upregulated ones controlling the oncogenic events occuring in Fh1 and Hira deficient cells.

2022-10-29 | GSE201992 | GEO

The effect of FH mutations on fibroid expression profile, normal myometrium vs. FH-mutant fibroids.

Project description:A series of gene expression measurements of uterine fibroids with mutated fumarate hydratase (FH) gene and normal myometrium. Keywords: other

2005-12-20 | GSE2724 | GEO

HIRA loss transforms FH deficient cells [RNA-Seq]

Project description:HIRA loss transforms FH deficient cells [RNA-Seq]

| PRJNA833945 | ENA

HIRA loss transforms FH deficient cells [ChIP-Seq]

Project description:HIRA loss transforms FH deficient cells [ChIP-Seq]

| PRJNA838364 | ENA

Distinct succinate modifying products are clinically diagnostic and prognostic biomarkers for fumarate hydratase deficient renal cell carcinoma

Project description:<p>Germline or somatic loss-of-function of fumarate hydratase (FH) predisposes patients to an aggressive form of renal cell carcinoma (RCC). Since other than tumor resection, there is no effective therapy for FH-deficient RCC, a competent method for early diagnosis and for early detection of recurrent and metastatic disease is an unmet clinical need. Currently, at best, an annual MRI scan is offered, though typically, MRI is used for symptomatic patients only. Therefore, finding specific and sensitive biomarkers suitable for routine and simple screens is crucial for improving the clinical outcome of these patients. Taking advantage of the robust metabolic rewiring that occurs in FH-deficient cells, we performed a large-scale study of plasma metabolomics comparing FH-deficient RCC patients to no-tumor control individuals or to wildtype FH RCC patients. Our results indicated two fumarate-derived metabolites, succinyl-adenosine and succinic-cysteine, to be outstanding plasma biomarkers for early diagnosis, with a positive predictive value of more than 90%. Furthermore, using pre-clinical and biochemical studies, we identified the enzymatic mechanisms by which these biomarkers are produced in and around the tumors. </p>

2022-08-12 | MTBLS3628 | MetaboLights

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