Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Polyclonal interactions overcome fitness barriers in Apc-driven intestinal tumorigenesis

ABSTRACT: Polyclonal interactions overcome fitness barriers in Apc-driven intestinal tumorigenesis

PROVIDER: PRJNA1139121 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR29927700_1.fastq.gz	Fastqsanger.gz
	SRR29927700_2.fastq.gz	Fastqsanger.gz
	SRR29927701_1.fastq.gz	Fastqsanger.gz
	SRR29927701_2.fastq.gz	Fastqsanger.gz
	SRR29927702_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 126

Similar Datasets

Polyclonal interactions overcome fitness barriers in Apc-driven intestinal tumorigenesis

Project description:Loss-of-function mutations in the tumour suppressor APC are an initial step in intestinal tumorigenesis. APC-mutant intestinal stem cells (ISCs) outcompete their wild type neighbours through the secretion of Wnt antagonists, accelerating the fixation and subsequent rapid clonal expansion of mutants. Reports of polyclonal intestinal tumours in patients and mouse models appear at odds with this process. Here we combine multicolour lineage tracing with chemical mutagenesis in mice to show that a large proportion of intestinal tumours have a multiancestral origin. Polyclonal tumours retain a structure comprising subclones with distinct Apc mutations and transcriptional states, driven predominantly by differences in KRAS and MYC signalling. These pathway level changes are accompanied by profound cancer stem cell phenotypic differences. Importantly, these findings are confirmed by introducing an oncogenic Kras mutation that results in predominantly monoclonal tumour formation. Further, polyclonal tumours have accelerated growth dynamics suggesting a link between polyclonality and tumour progression. Together, these findings demonstrate the role of interclonal interactions in promoting tumorigenesis through non-cell autonomous pathways dependent on the differential activation of oncogenic pathways between clones.

2024-08-30 | GSE272850 | GEO

Project description:Polyclonal interactions overcome fitness barriers in Apc-driven intestinal tumorigenesis

| PRJNA1141743 | ENA

Development of gene expression signatures for identifying novel factors that can overcome age-associated reprogramming barriers

Project description:To investigate the molecular features underlying senescence and rejuvenation during aged cell reprogramming and identify novel factors that can overcome age-associated barriers, we compared gene expression for reprogramming intermediates on D8 of tail-tip fibroblasts (TTFs) from young Wild Type (WT), old WT, and old p16 knockout (KO) mice. We collected TTFs from young WT, old WT, and old p16 KO mice and reprogrammed the cells by introducing four reprogramming factors, including Oct4, Sox2, Klf4, and c-Myc. Gene expression of reprogramming intermediates on D8 were compared. Two independent experiments were performed using different mice donors for each experiment.

2016-03-31 | E-GEOD-79747 | biostudies-arrayexpress

Development of gene expression signatures for identifying novel factors that can overcome age-associated reprogramming barriers

2016-03-31 | GSE79747 | GEO

Polyclonality overcomes fitness barriers in Apc-driven tumorigenesis.

Project description:Loss-of-function mutations in the tumour suppressor APC are an initial step in intestinal tumorigenesis1,2. APC-mutant intestinal stem cells outcompete their wild-type neighbours through the secretion of Wnt antagonists, which accelerates the fixation and subsequent rapid clonal expansion of mutants3-5. Reports of polyclonal intestinal tumours in human patients and mouse models appear at odds with this process6,7. Here we combine multicolour lineage tracing with chemical mutagenesis in mice to show that a large proportion of intestinal tumours have a multiancestral origin. Polyclonal tumours retain a structure comprising subclones with distinct Apc mutations and transcriptional states, driven predominantly by differences in KRAS and MYC signalling. These pathway-level changes are accompanied by profound differences in cancer stem cell phenotypes. Of note, these findings are confirmed by introducing an oncogenic Kras mutation that results in predominantly monoclonal tumour formation. Further, polyclonal tumours have accelerated growth dynamics, suggesting a link between polyclonality and tumour progression. Together, these findings demonstrate the role of interclonal interactions in promoting tumorigenesis through non-cell autonomous pathways that are dependent on the differential activation of oncogenic pathways between clones.

| S-EPMC11525183 | biostudies-literature

Apc

Project description:Drosophila melanogaster Apc, APC-like, is differentially expressed in 20 experiment(s);

| FBgn0015589 | ExpressionAtlas

Apc

Project description:Drosophila melanogaster Apc, APC-like, is expressed in 5 baseline experiment(s);

| FBgn0015589 | ExpressionAtlas

Apc and ApcKras

Project description:Apc and ApcKras

| PRJNA673353 | ENA

Apc

Project description:Rattus norvegicus Apc, APC regulator of WNT signaling pathway [Source:RGD Symbol;Acc:2123], is differentially expressed in 17 experiment(s);

| ENSRNOG00000020423 | ExpressionAtlas

Apc

Project description:Rattus norvegicus Apc, APC regulator of WNT signaling pathway [Source:RGD Symbol;Acc:2123], is expressed in 6 baseline experiment(s);

| ENSRNOG00000020423 | ExpressionAtlas

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