Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

KRAS allelic imbalance drives a MAPK dependent tumour initiation programme inefficient at rewiring the tumour microenvironment to provoke metastasis

ABSTRACT: KRAS allelic imbalance drives a MAPK dependent tumour initiation programme inefficient at rewiring the tumour microenvironment to provoke metastasis

PROVIDER: PRJNA797286 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR17621169_1.fastq.gz	Fastqsanger.gz
	SRR17621169_2.fastq.gz	Fastqsanger.gz
	SRR17621170_1.fastq.gz	Fastqsanger.gz
	SRR17621170_2.fastq.gz	Fastqsanger.gz
	SRR17621171_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 50

Similar Datasets

KRAS allelic imbalance drives a MAPK dependent tumour initiation programme inefficient at rewiring the tumour microenvironment to provoke metastasis

Project description:Murine small intestinal tumours, adjacent normal tissues and tumour organoids, following Kras mutation under the control of VilCreER, alone or in combination with p53 and Notch mutation, in the presence or absence of a wild type Kras allele.

2022-01-17 | GSE193703 | GEO

Adipocytes disrupt the translational programme of Acute Lymphoblastic Leukaemia to favour tumour survival and persistence

Project description:Adipocytes disrupt the translational programme of Acute Lymphoblastic Leukaemia to favour tumour survival and persistence

| PRJNA637296 | ENA

KRAS allelic imbalance drives tumour initiation yet suppresses metastasis in colorectal cancer in vivo.

Project description: Not available

| S-EPMC10762264 | biostudies-literature

Adipocytes disrupt the translational programme of Acute Lymphoblastic Leukaemia to favour tumour survival and persistence [BM-MSC]

Project description:Adipocytes disrupt the translational programme of Acute Lymphoblastic Leukaemia to favour tumour survival and persistence [BM-MSC]

| PRJNA637302 | ENA

Adipocytes disrupt the translational programme of Acute Lymphoblastic Leukaemia to favour tumour survival and persistence [Nalm-6]

Project description:Adipocytes disrupt the translational programme of Acute Lymphoblastic Leukaemia to favour tumour survival and persistence [Nalm-6]

| PRJNA633808 | ENA

Early fibrotic niches establish tumour-permissive microenvironments

Project description:Pathologic transformation represents a critical yet poorly defined window during which mutant epithelial stem cells actively construct the microenvironment that enables tumour initiation. Here, using integrated single-cell, spatial, and functional analyses, we define the earliest multicellular events that license this transition following oncogenic activation in the lung. KrasG12D-mutant alveolar type II cells rapidly adopt regenerative-like states that act as signalling hubs, orchestrating coordinated stromal and immune reprogramming while enhancing epithelial plasticity. Through secretion of Amphiregulin (Areg), mutant epithelial cells activate EGFR signalling in adjacent fibroblasts, inducing a fibrotic, injury-like programme. Reprogrammed fibroblasts, in turn, expand and reprogramme alveolar macrophages, amplifying inflammatory signalling and reinforcing epithelial plasticity. These reciprocal interactions establish a self-sustaining epithelial–stromal–immune circuit that generates a tumour-permissive niche prior to malignant outgrowth. Disruption of the Areg–EGFR axis prevents early niche formation and abrogates tumour initiation. Conservation of this programme in KRASG12D-inducible human alveolar organoids and early-stage lung adenocarcinoma tissues identifies epithelial–microenvironment communication as a therapeutically actionable vulnerability and suggests that intercepting niche formation may prevent progression to treatment-resistant disease.

2026-02-25 | GSE310335 | GEO

Allelic imbalance in CALR somatic mutagenesis.

Project description: Not available

| S-EPMC4430307 | biostudies-literature

Allelic imbalance in human breast cancer.

Project description: Not available

| S-EPMC5355213 | biostudies-literature

Synaptic and transcriptomic features of fear matrix pyramidal neurons predict inefficient fear extinction

Project description:Trauma-related disorders arise from inefficient fear extinction and have immeasurable social and economic costs. Here, we characterized mouse phenotypes that spontaneously show individual differences in adaptive or maladaptive fear extinction and, before the traumatic experience, we found that specific morphological, electrophysiological and transcriptomic patterns of fear matrix pyramidal neurons predispose to trauma-related disorders. Finally, by using an optogenetic approach we showed the possibility to rescue the inefficient fear extinction activating fear matrix infralimbic pyramidal neurons

2023-06-02 | GSE209572 | GEO

The developmental programme for genesis of the entire kidney is recapitulated in Wilms tumour

Project description:Expression profiling of Wilms tumour samples, which identified molecular signatures of the ureteric bud and collecting duct as well as those of the proximal and distal tubules in triphasic histology tumours. These observations indicate Wilms tumours can arise from a precursor cell capable of generating the entire kidney, such as the cells of the intermediate mesoderm from which both the metanephric mesenchym and ureteric bud are derived.

2017-12-31 | E-MTAB-3516 | biostudies-arrayexpress

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