Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single cell RNA sequencing profiles on whole tumors from a Kras/Rnf43 genetically engineered mouse model of pancreatic adenocarcinoma

ABSTRACT: Single cell RNA sequencing profiles on whole tumors from a Kras/Rnf43 genetically engineered mouse model of pancreatic adenocarcinoma

PROVIDER: PRJNA780878 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR16957200_1.fastq.gz	Fastqsanger.gz
	SRR16957200_2.fastq.gz	Fastqsanger.gz
	SRR16957201_1.fastq.gz	Fastqsanger.gz
	SRR16957201_2.fastq.gz	Fastqsanger.gz
	SRR16957202_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 20

Similar Datasets

Single cell RNA sequencing profiles on whole tumors from a Kras/Rnf43 genetically engineered mouse model of pancreatic adenocarcinoma

Project description:We report single cell RNA sequencing of pancreatic enzymatically digested whole, fresh tumors from a genetically engineered mouse model (GEMM) of pancreatic adenocarcinoma. This GEMM consists of pancreas specific expression of oncogenic Kras (Kras-G12D) in addition of homozygous deletion of the ring finger domain (catalytic domain) of Rnf43. This GEMM is termed 'KRC'.

2022-03-23 | GSE188946 | GEO

RNAseq of genetically engineered mouse model (GEMM) tumors

Project description:We report the expression profiling of lung adenocarcinoma tumors arising from genetically engineered mice with activation of KRAS(K) and loss of either SMARCA4 (S), p53(P) or both.

2018-06-17 | GSE94927 | GEO

Transcriptomic characterization of sotorasib-resistant tumors in Kras-G12C/Trp53-driven LUAD in genetically engineered mice

Project description:To characterize sotorasib resistance in lung adenocarcinomas (LUAD), we generated genetically engineered mice (Kras-G12C, Trp53-KO) and compared the transcriptional profiles of untreated and sotorasib-resistant tumors

2023-03-05 | GSE204752 | GEO

Transcriptional response to PORCN inhibition using an orthotopic model of RNF43 mutant pancreatic adenocarcinoma (HPAF-II)

Project description:Timecourse RNA-seq of response to PORCN inhibition, using ETC-159, in an orthotopic model of RNF43 mutant pancreatic adenocarcinoma (HPAF-II).

2018-12-04 | GSE118041 | GEO

Transcriptional response to PORCN inhibition using a subcutaneous model of RNF43 mutant pancreatic adenocarcinoma (HPAF-II)

Project description:SRP136970 - PRJNA448481 - RNA-seq of response to PORCN inhibition, using ETC-159,in a subcutanenous model of RNF43 mutant pancreatic adenocarcinoma (HPAF-II).

2018-12-04 | GSE118179 | GEO

Single Cell RNA seq of Genetically Engineered Mouse Models of Pancreatic Adenocarcinoma

Project description:Single Cell RNA seq of Genetically Engineered Mouse Models of Pancreatic Adenocarcinoma

| PRJNA516878 | ENA

Transcriptional response to PORCN inhibition using an in vitro model of RNF43 mutant pancreatic adenocarcinoma (HPAF-II)

Project description:SRP136961 - PRJNA448457 - RNA-seq of response to PORCN inhibition, using ETC-159, in vitro of RNF43 mutant pancreatic adenocarcinoma (HPAF-II).

2018-12-04 | GSE118190 | GEO

Alveolar differentiation drives resistance to KRAS inhibition in lung adenocarcinoma [scRNA-seq]

Project description:Lung adenocarcinoma (LUAD), commonly driven by KRAS mutations, is responsible for 7% of all cancer mortality. The first allele-specific KRAS inhibitors were recently approved in LUAD, but clinical benefit is limited by intrinsic and acquired resistance. LUAD predominantly arises from alveolar type 2 (AT2) cells, which function as facultative alveolar stem cells by self-renewing and replacing alveolar type 1 (AT1) cells. Using genetically engineered mouse models, patient-derived xenografts, and patient samples we found inhibition of KRAS promotes transition to a quiescent AT1-like cancer cell state in LUAD tumors. Similarly, suppressing Kras induced AT1 differentiation of wild-type AT2 cells upon lung injury. The AT1-like LUAD cells exhibited high growth and differentiation potential upon treatment cessation, whereas ablation of the AT1-like cells robustly improved treatment response to KRAS inhibitors. Our results uncover an unexpected role for KRAS in promoting intra-tumoral heterogeneity and suggest targeting alveolar differentiation may augment KRAS-targeted therapies in LUAD.

2023-11-01 | GSE246481 | GEO

Alveolar differentiation drives resistance to KRAS inhibition in lung adenocarcinoma [RNA-seq]

2023-11-01 | GSE246480 | GEO

RNA-seq of genetically engineered mouse microglia

Project description:RNA-seq of genetically engineered mouse microglia sorted into populations.

2022-04-06 | GSE196174 | GEO