Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Acute myeloid leukemia cells resist chemotherapy through a transient senescence-like state [PDX]

ABSTRACT: Acute myeloid leukemia cells resist chemotherapy through a transient senescence-like state [PDX]

PROVIDER: PRJNA610898 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11260700_1.fastq.gz	Fastqsanger.gz
	SRR11260700_2.fastq.gz	Fastqsanger.gz
	SRR11260701_1.fastq.gz	Fastqsanger.gz
	SRR11260701_2.fastq.gz	Fastqsanger.gz
	SRR11260702_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 186

Similar Datasets

Acute myeloid leukemia cells resist chemotherapy through a transient senescence-like state [PDX]

Project description:In acute myeloid leukemias (AML), chemotherapy is frequently followed by disease relapse, yet the mechanism by which AML reemerges is not fully understood. We hypothesized that chemotherapy induces senescence-like dormancy that facilitates survival to genotoxic exposure, allowing AML cells to endure treatment in a transiently dormant state while retaining potential for leukemic repopulation. Here, we show that primary AML cells exhibit hallmark senescence features following treatment with cytarabine (AraC), including growth arrest, increased cellular granularity, senescence-associated-β-galactosidase (SA-β-gal) activity, and senescence-associated transcriptomic alterations. Induction of AraC-induced premature senescence was regulated by the ATR kinase activity and mediated stress-survival. High-throughput single cell RNA (scRNA)-seq analysis of primary AML cells ex vivo and in vivo following chemotherapy suggest active transcriptional programming towards senescent-like dormancy instead of enrichment for leukemia stem cells (LSCs). scRNA-seq of sorted AraC-induced premature senescent AML cells demonstrated a heterogenous population including a fraction of cells with simultaneous expression of dormancy- and senescence-associated gene signatures. Xenotransplantation of AraC-induced premature senescent AML cells into mice demonstrated that senescent-like AML cells maintain leukemia-repopulating potential. Altogether, we propose a mechanism of AML relapse whereby AML cells tolerate chemotherapy via acquisition of a transient senescent-like state.

2021-03-14 | GSE146592 | GEO

Acute myeloid leukemia cells resist chemotherapy through a transient senescence-like state

Project description:Acute myeloid leukemia cells resist chemotherapy through a transient senescence-like state

| PRJNA610828 | ENA

Acute myeloid leukemia cells resist chemotherapy through a transient senescence-like state [Array]

Project description:Acute myeloid leukemia cells resist chemotherapy through a transient senescence-like state [Array]

| PRJNA610835 | ENA

Acute myeloid leukemia cells resist chemotherapy through a transient senescence-like state [RNA-seq]

Project description:Acute myeloid leukemia cells resist chemotherapy through a transient senescence-like state [RNA-seq]

| PRJNA605820 | ENA

Acute myeloid leukemia cells resist chemotherapy through a transient senescence-like state [scRNA-seq]

Project description:Acute myeloid leukemia cells resist chemotherapy through a transient senescence-like state [scRNA-seq]

| PRJNA610895 | ENA

Acute myeloid leukemia cells resist chemotherapy through a transient senescence-like state [Array]

2021-03-14 | GSE146542 | GEO

Acute myeloid leukemia cells resist chemotherapy through a transient senescence-like state [RNA-seq]

2021-03-14 | GSE145061 | GEO

Acute myeloid leukemia cells resist chemotherapy through a transient senescence-like state [scRNA-seq]

2021-03-14 | GSE146590 | GEO

Acute myeloid leukemia cells resist chemotherapy through a transient senescence-like state

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

2021-03-14 | GSE146544 | GEO

The Wnt/β-catenin and RAS-ERK Pathways were Activated in Tissues of Chemotherapy-Resistant Gastric Cancer PDX Tumor

Project description:Chemotherapy resistance and disease recurrence remains major causes of gastric cancer patient mortality. We describe possible relationship between Wnt/b-catenin and RAS/ERK pathways in GC patients and acquired-resistant GC PDX tumors against FOLFOX, 5-fluorouracil-based chemotherapy. RNA sequencing analysis also demonstrates that Wnt/b-catenin pathway is an actionable target pathway for overcoming the chemotherapy resistance. These provide that an approach targeting both Wnt/b-catenin and RAS/ERK pathways could be novel therapeutic strategy in GC resistant to standard chemotherapy.

2019-05-26 | GSE128967 | 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