Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNAseq of 3LL-ΔΝRAS lung tumours treated with SHP2 or/and KRAS inhibitors

ABSTRACT: Intravenous-induced 3LL-ΔNRAS tumour bearing mice were treated with RMC-4550 or/and RMC-4998 for 7 days and isolated for RNAseq.

ORGANISM(S): Mus musculus

PROVIDER: GSE254755 | GEO | 2024/02/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

RNAseq of 3LL-ΔΝRAS lung tumours treated with SHP2 or/and KRAS inhibitors

Project description:RNAseq of 3LL-ΔΝRAS lung tumours treated with SHP2 or/and KRAS inhibitors

| PRJNA1071622 | ENA

SMARCB1 regulates a TFCP2L1-MYC transcriptional switch promoting renal medullary carcinoma transformation and ferroptosis resistance. [RNAseq]

Project description:Renal medullary carcinoma (RMC) is an aggressive tumour driven by bi-allelic loss of SMARCB1 and tightly associated with sickle cell trait. However, the cell-of-origin and oncogenic mechanism remain poorly understood. Using single-cell sequencing of human RMC, we defined transformation of thick ascending limb (TAL) cells into an epithelial-mesenchymal gradient of RMC cells associated with loss of renal epithelial transcription factors TFCP2L1, HOXB9 and MITF and gain of MYC and NFE2L2-associated oncogenic and ferroptosis resistance programs. We describe the molecular basis for this transcriptional switch that is reversed by SMARCB1 re-expression repressing the oncogenic and ferroptosis resistance programs leading to ferroptotic cell death. Ferroptosis resistance links TAL cell survival with the high extracellular medullar iron concentrations associated with sickle cell trait, an environment propitious to the mutagenic events associated with RMC development. This unique environment may explain why RMC is the only SMARCB1-deficient tumour arising from epithelial cells, differentiating RMC from rhabdoid tumours arising from neural crest cells.

2023-03-06 | GSE180999 | GEO

RNAseq from cuticles of tumor free (w1118) and tumor bearing Drosophila larvae (MARCM RasV12, scrib1) tumour-bearing Drosophila larvae

Project description:To investigate which factors might be driving the cachectic muscle wasting observed in our larval models bearing RasV12, scrib1 tumors, we performed RNA sequencing (RNAseq) on the cuticles of wild type and RasV12, scrib1 tumour-bearing larvae. Pathway and gene ontology analysis revealed significant deregulation of stress and starvation response genes, metabolic genes, and inflammation and immune regulatory genes within cachectic muscle of tumour bearing larvae.

2021-06-17 | GSE178332 | GEO

SMARCB1 regulates a TFCP2L1-MYC transcriptional switch promoting renal medullary carcinoma transformation and ferroptosis resistance.. [scRNAseq]

2023-03-06 | GSE181000 | GEO

SMARCB1 regulates a TFCP2L1-MYC transcriptional switch promoting renal medullary carcinoma transformation and ferroptosis resistance. [ChIPseq and Cut&Tag]

2023-03-06 | GSE180998 | GEO

Progression of KRas^G12D;Rosa26-MYC tumours to invasive disease

Project description:The aim of the study was to investigate gene expression tumour progression of KRas*/MYC driven lung tumours from adenocarcinoma in situ to invasive disease.

2018-06-01 | E-MTAB-6432 | biostudies-arrayexpress

The Q61H mutation decouples KRAS from upstream regulation and renders cancer cells resistant to SHP2 inhibitors.

Project description:Cancer cells bearing distinct KRAS mutations exhibit variable sensitivity to SHP2 inhibitors (SHP2i). Here we show that cells harboring KRAS Q61H are uniquely resistant to SHP2i, and investigate the underlying mechanisms using biophysics, molecular dynamics, and cell-based approaches. Q61H mutation impairs intrinsic and GAP-mediated GTP hydrolysis, and impedes activation by SOS1, but does not alter tyrosyl phosphorylation. Wild-type and Q61H-mutant KRAS are both phosphorylated by Src on Tyr32 and Tyr64 and dephosphorylated by SHP2, however, SHP2i does not reduce ERK phosphorylation in KRAS Q61H cells. Phosphorylation of wild-type and Gly12-mutant KRAS, which are associated with sensitivity to SHP2i, confers resistance to regulation by GAP and GEF activities and impairs binding to RAF, whereas the near-complete GAP/GEF-resistance of KRAS Q61H remains unaltered, and high-affinity RAF interaction is retained. SHP2 can stimulate KRAS signaling by modulating GEF/GAP activities and dephosphorylating KRAS, processes that fail to regulate signaling of the Q61H mutant.

| S-EPMC8560773 | biostudies-literature

RNAseq from cuticles of tumor free (w1118) and tumor bearing Drosophila larvae (MARCM RasV12, scrib1) tumour-bearing Drosophila larvae

Project description:RNAseq from cuticles of tumor free (w1118) and tumor bearing Drosophila larvae (MARCM RasV12, scrib1) tumour-bearing Drosophila larvae

| PRJNA738503 | ENA

RNAseq Expression data for mouse liver, Phenobarbital exposed livers and resulting liver tumours.

Project description:Through the analysis of mouse liver tumours promoted by distinct routes (DEN exposure alone, DEN exposure plus non-genotoxic insult with phenobarbital and non-alcoholic fatty liver disease); we report that the cancer associated hyper-methylated CGI events in mice are also predicated by silent promoters that are enriched for both the DNA modification 5-hydroxymethylcytosine (5hmC) and the histone modification H3K27me3 in normal liver. During cancer progression these CGIs undergo hypo-hydroxymethylation, prior to subsequent hyper-methylation; whilst retaining H3K27me3. A similar loss of promoter-core 5hmC is observed in Tet1 deficient mouse livers indicating that reduced Tet1 binding at CGIs may be responsible for the epigenetic dysregulation observed during hepatocarcinogenesis. Consistent with this reduced Tet1 protein levels are observed in mouse liver tumour lesions. As in human, DNA methylation changes at CGIs do not appear to be direct drivers of hepatocellular carcinoma progression in mice. Instead dynamic changes in H3K27me3 promoter deposition are strongly associated with tumour-specific activation and repression of transcription. Our data suggests that loss of promoter associated 5hmC in diverse liver tumours licences DNA methylation reprogramming at silent CGIs during cancer progression. We carry out paired end , strand specific RNAseq prior to sequencing on Illumina Hiseq 2500 to report on the transcriptional landscape in replicate control mouse livers (n=2), 12 week Phenobarbital exposed livers (n=2)and resulting (35 week PB) liver tumours (n=3).

2016-05-17 | E-GEOD-77729 | biostudies-arrayexpress

LAKTP_MTO orthotopic primary caecum tumours from Galunisertib-treated C57BL/6J mice

Project description:Mouse tumour organoids (MTOs) derived from a compound mutant (LAKTP) intestinal cancer model were orthoptopically transplanted into syngeneic C57BL/6J mice. Tumour-bearing mice were treated with TGF-beta inhibitor Galunisertib or vehicle control. Whole tumour mRNA was extracted from primary tumours and expression profiling was performed with the objective to characterize the tumour microenvironment (TME). As a TGF-beta-activated TME has been associated to a poor prognosis and the CRC consensum molecular subtype CMS4, and the mouse model was found to have such an activated TME, we used the array data to classify these tumours in this mouse model system as CMS4-like. Furthermore, treatment with TGF-beta inhibitor reduced the fibroblast- and T cell-specific TGF-beta response signatures, also associated to poor prognosis in human CRC. This treatment was associated to a strong reduction/prevention of liver metastasis, as well as a reduction of primary tumour (and local carcinomatosis) size.

2018-02-12 | GSE103562 | 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