Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genomic landscape of Neutrophilic Leukemias of Ambiguous Diagnosis

ABSTRACT: Genomic landscape of Neutrophilic Leukemias of Ambiguous Diagnosis

PROVIDER: PRJNA528526 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Genomic landscape of Neutrophilic Leukemias of Ambiguous Diagnosis

Project description:Genomic landscape of Neutrophilic Leukemias of Ambiguous Diagnosis

| PRJNA528527 | ENA

Genomic landscape of neutrophilic leukemias of ambiguous diagnosis.

Project description: Not available

| S-EPMC6742922 | biostudies-literature

MicroRNA expression profiling of leukemias of ambiguous lineage

Project description:Classifying leukemias of ambiguous lineage as either acute myeloid leukemia or acute lymphoid leukemia using microRNA expression profiling

2013-05-07 | E-MTAB-1459 | biostudies-arrayexpress

Transcriptomic signature can distinguish chronic neutrophilic leukemia from ambiguous neutrophilic leukemias.

Project description: Not available

| S-EPMC12006112 | biostudies-literature

RNA-seq data of acute leukemias of ambiguous lineage (ALAL)

Project description:We generated RNA-seq data of 30 cases of acute leukemia of ambiguous lineage (ALAL), including both bilineal and biphenotypic patients, in order to develop methods to improve the diagnosis of this disease. First, we used an in-house pipeline to comprehensively detect genetic lesions in RNA-sequencing data. Second, we generated a machine learning (ML) classifier trained on compared ALAL gene expression profiles (GEPs) with representative AML (n=145), B-ALL (n=223) and T-ALL (n=85) cases.

2025-05-16 | E-MTAB-15145 | biostudies-arrayexpress

Ambiguous genetic codes

Project description:Crammed, ambiguous genetic codes

| PRJEB9019 | ENA

METTL3 Deficiency in Macrophage Aggravates Neutrophilic Asthma by Regulating ZBP1-NLRP3 Inflammasome Activation

Project description:N6-methyladenosine (m6A), the most abundant RNA modification, plays the essential role in the immune disorders. Yet, the role of m6A and its master regulator, methyltransferase-like 3 (METTL3) in asthma remain ambiguous. Here, we found that macrophage deficient in METTL3 aggravates the ovalbumin/lipopolysaccharide (OVA/LPS)-induced neutrophilic asthma. Subsequently, we observed that METTL3 deficiency facilitates NLRP3 but not AIM2 and NLRC4-dependent inflammasome activation and IL-1β secretion. Mechanistically, METTL3 deficiency enhanced NLRP3 inflammasome activation were dependent on upregulation of ZBP1 and TRAF1. Lastly, we elucidated that METTL3 negatively regulates ZBP1 expression through m6A modification dependence. In summary, the study unveils the function of m6A in regulating NLRP3 inflammasome activation in macrophage and identifies potential targets in therapeutic intervention of neutrophilic asthma.

2025-02-09 | GSE283939 | GEO

Epigenetic landscape of mixed phenotype leukemias

Project description:Leukemias with ambiguous lineage comprise a number of loosely defined entities, often without a clear mechanistic basis. Here, we investigated a group of such leukemias with a CpG Island Methylator Phenotype (CIMP), previously identified as CEBPA-silenced AML. Transcriptomics and epigenomics analyses revealed a hybrid myeloid/lymphoid epigenetic landscape, whereas genetic alterations were heterogenous. This suggests that CIMP leukemias are defined by their shared epigenetic profile rather than a common genetic lesion. Gene expression enrichment showed strong similarity with ETP-ALL and an early lymphoid progenitor cell of origin. Accordingly, integration of differential methylation and expression revealed widespread silencing of myeloid transcription factors (TFs), among which CEBPA was key for differentiation arrest. Hypermethylation also resulted in loss of CTCF binding, accompanied by a few changes in chromatin interactions involving critical TFs like KLF4. In conclusion, epigenetic dysregulation, and not genetic lesions, explain the mixed phenotype of a group of CIMP leukemias resembling ETP-ALL.

| EGAS00001007094 | EGA

The genomic landscape of core-binding factor acute myeloid leukemias.

Project description: Not available

| S-EPMC5508996 | biostudies-literature

IL-36 Amplifies Neutrophilic Lung Inflammation

Project description:IL-36, which belongs to the IL-1 superfamily, is increasingly linked to neutrophilic inflammation. Here, we performed single-cell RNA-seq on an acute LPS mouse model of lung inflammation to provide insights into the intercellular signaling pathways and mechanisms through which IL-36 promotes lung inflammation. We identified neutrophils as a source of IL-36 which provides a rationale for targeting IL-36 to improve treatment of a variety of neutrophilic lung diseases.

2021-01-25 | GSE159161 | 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