Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ABSTRACT: Multiomic single-cell sequencing of skin and blister fluid from patients with severe cutaneous adverse drug reactions.

PROVIDER: PRJNA1070820 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other
	SRR27776500_1.fastq.gz	Fastqsanger.gz
	SRR27776500_2.fastq.gz	Fastqsanger.gz
	SRR27776502_1.fastq.gz	Fastqsanger.gz
	SRR27776502_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 169

Similar Datasets

Multiomic single-cell sequencing of skin and blister fluid from patients with severe cutaneous adverse drug reactions.

Project description:Severe cutaneous adverse reactions (SCAR) are rare but life-threatening drug reactions mediated by human leukocyte antigen (HLA) class I-restricted CD8+ T-cells. To obtain an unbiased assessment of SCAR cellular immunopathogenesis, we performed single-cell (sc) transcriptome, surface proteome, and TCR sequencing (5' scRNA-TCR-CITE-seq, 10x Genomics) on unaffected skin, affected skin, and blister fluid from diverse SCAR patients.

2024-09-18 | GSE275871 | GEO

Expression data from skin of patients with adverse drug reactions (ADRs)

Project description:ADRs are immune mediated skin reactions of diverse severity and etiology. The patho-mechanisms are however not well understood. We used a gene expression array for the comparison of the gene expression profile of 2 cutaneous adverse drug reactions (MPR and AGEP) to normal skin.

2019-02-01 | GSE121421 | GEO

Homo sapiens

Project description:Identification of drug-specific public TCR driving severe cutaneous adverse reactions

| PRJNA550004 | ENA

Single cell RNA-sequencing reveals molecular signatures that distinguish allergic from irritant contact dermatitis

Project description:Allergic and irritant contact dermatitis can be challenging to distinguish. We used single cell RNA sequencing (scRNA-seq) and insterstitial fluid proteomic analysis to compare suction blister biopsy skin samples from human volunteers with induced allergic and irritant contact dermatitis reactions.

2024-09-15 | GSE267929 | GEO

Expression data from skin of patients with adverse drug reactions (ADRs)

Project description:Expression data from skin of patients with adverse drug reactions (ADRs)

| PRJNA497293 | ENA

PBMS cells from SJS/TEN

Project description:Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are life-threatening adverse drug reactions characterized by massive epidermal necrosis, in which the specific danger signals involved remain unclear. Here we show that blister cells from skin lesions of SJS-TEN primarily consist of cytotoxic T lymphocytes (CTLs) and natural killer (NK) cells, and both blister fluids and cells were cytotoxic. Gene expression profiling identified granulysin as the most highly expressed cytotoxic molecule, confirmed by quantitative PCR and immunohistochemistry. Granulysin concentrations in the blister fluids were two to four orders of magnitude higher than perforin, granzyme B or soluble Fas ligand concentrations, and depleting granulysin reduced the cytotoxicity. Granulysin in the blister fluids was a 15-kDa secretory form, and injection of it into mouse skin resulted in features mimicking SJS-TEN. Our findings demonstrate that secretory granulysin is a key molecule responsible for the disseminated keratinocyte death in SJS-TEN and highlight a mechanism for CTL- or NK cell—mediated cytotoxicity that does not require direct cellular contact.

2008-12-04 | GSE13727 | GEO

SJS blister cells

2008-12-04 | GSE13726 | GEO

Transcription profiling of human Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis patients blister cells from skin lesions reveals these consist of cytotoxic T cells annd NK cells

Project description:Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis; (TEN) are life-threatening adverse drug reactions characterized; by massive epidermal necrosis, in which the specific danger; signals involved remain unclear. Here we show that blister; cells from skin lesions of SJS-TEN primarily consist of cytotoxic; T lymphocytes (CTLs) and natural killer (NK) cells, and both; blister fluids and cells were cytotoxic. Gene expression profiling; identified granulysin as the most highly expressed cytotoxic; molecule, confirmed by quantitative PCR and immunohistochemistry. Granulysin concentrations in the blister fluids; were two to four orders of magnitude higher than perforin,; granzyme B or soluble Fas ligand concentrations, and depleting; granulysin reduced the cytotoxicity. Granulysin in the blister; fluids was a 15-kDa secretory form, and injection of it into; mouse skin resulted in features mimicking SJS-TEN. Our; findings demonstrate that secretory granulysin is a key molecule; responsible for the disseminated keratinocyte death in SJS-TEN; and highlight a mechanism for CTL- or NK cellâmediated; cytotoxicity that does not require direct cellular contact. Experiment Overall Design: Blood samples were obtained from 5 different patients with SJS/TEN. The peripheral blood mononuclear cells (PBMCs) were isolated from the whole blood samples by Ficoll-Isopaque (Pharmacia Fine Chemicals) density gradient centrifugation. Total RNA from PBMC was isolated using the RNeasy kit (Qiagen). The 28S and 18S ribosomal RNA peak ratios were determined using microfluidics technology (Agilent). RNA was subjected to reverse transcription using the Superscript II kit (Invitrogen), and the cleaned cRNA was then hybridized to an Affymetrix human genome U133 plus 2.0 array.

2009-01-13 | E-GEOD-13727 | biostudies-arrayexpress

Transcriptomic study from total RNA extract from reconstructed Human Epidermis (RHE) at 3 time points and quatriplicats under Afatinib (100 nm) exposure versus vehicle

Project description:Effect of EGFR inhibitors on the epidermis Epidermal Growth Factor inhibitors (EGFRi) used in oncology therapy modify the keratinocyte differentiation processes, impairing proper skin barrier formation and leading to Cutaneous Adverse Drug Reactions (CADR). To uncover the molecular signatures associated with CADRs, we applied phospho-proteomic and transcriptomic assays on Reconstructed Human Epidermis (RHE) tissues exposed to a therapeutically relevant concentration of afatinib, a second EGFRi generation. Following drug exposure, we observed an increased expression of gene families involved in keratinocyte differentiation, senescence, oxidative stress and alterations in the epidermal immune-related markers. Furthermore, our results show that afatinib may interfere with Vitamin D3 (VD3) metabolism, acting via CYP27A1 and CYP24A1 to regulate calcium concentration through the PI3K/AKT pathway. Consequently, basal layer keratinocytes switch from a pro-proliferating to a pro-differentiative program, characterized by upregulation of biomarkers associated with increased keratinization, cornification, Th2 response and decreased innate immunity. Such effects may increase the skin susceptibility to cutaneous penetration of irritants and pathogens.

2022-02-23 | GSE167246 | GEO

38-502:BRAFTOVI/MEKTOVI Combination Therapy Specified Drug Use Survey(CRC)

Project description:Primary outcome(s): [Safety]Occurrence status of adverse drug reactions and infections, Occurrence status of adverse drug reactions corresponding to specified safety concerns, Factors that are considered to affect safety Specified safety concerns: Cutaneous malignancies, palmar-plantar erythrodysaesthesia syndrome, eye disorders, cardiac dysfunction, hypertension, rhabdomyolysis, hepatic dysfunction, and haemorrhage [Efficacy]Antitumor effect and overall survival (OS)

| 2613085 | ecrin-mdr-crc

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