Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Extracellular niche and tumor microenvironment enhance the impact of KRAS inhibitors in pancreatic cancer models [DSP]

ABSTRACT: Extracellular niche and tumor microenvironment enhance the impact of KRAS inhibitors in pancreatic cancer models [DSP]

PROVIDER: PRJNA1049456 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR27118114_1.fastq.gz	Fastqsanger.gz
	SRR27118114_2.fastq.gz	Fastqsanger.gz
	SRR27118115_1.fastq.gz	Fastqsanger.gz
	SRR27118115_2.fastq.gz	Fastqsanger.gz
	SRR27118116_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 46

Similar Datasets

Extracellular niche and tumor microenvironment enhance the impact of KRAS inhibitors in pancreatic cancer models.

Project description:Extracellular niche and tumor microenvironment enhance the impact of KRAS inhibitors in pancreatic cancer models.

| PRJNA1049453 | ENA

Extracellular niche and tumor microenvironment enhance the impact of KRAS inhibitors in pancreatic cancer models [CRISPR]

Project description:Extracellular niche and tumor microenvironment enhance the impact of KRAS inhibitors in pancreatic cancer models [CRISPR]

| PRJNA1049457 | ENA

Extracellular niche and tumor microenvironment enhance the impact of KRAS inhibitors in pancreatic cancer models [scRNA-seq]

Project description:Extracellular niche and tumor microenvironment enhance the impact of KRAS inhibitors in pancreatic cancer models [scRNA-seq]

| PRJNA1049460 | ENA

Extracellular niche and tumor microenvironment enhance the impact of KRAS inhibitors in pancreatic cancer models [RNA-seq]

Project description:Extracellular niche and tumor microenvironment enhance the impact of KRAS inhibitors in pancreatic cancer models [RNA-seq]

| PRJNA1049461 | ENA

Extracellular niche and tumor microenvironment enhance the impact of KRAS inhibitors in pancreatic cancer models [DSP]

Project description:Pancreatic ductal adenocarcinoma (PDAC) is an aggressive disease for which new therapeutic interventions are needed. Here, we assessed the cellular response to pharmacological KRAS inhibition, targeting the central oncogenic factor in PDAC. In a panel of PDAC cell lines, pharmaceutical inhibition of the KRASG12D allele with MRTX1133 yields variable efficacy in the suppression of cell growth and downstream gene expression programs in 2D culture. CRISPR-Cas9 loss-of-function screens identified ITGB1 as a novel driver for enhanced therapeutic response that regulates mechanotransdcution signaling and YAP/TAZ expression, which is further confirmed by gene specific knockdowns and combinatorial drug synergy. Interestingly, MRTX1133 is considerably more efficacious in the context of 3D cell cultures. Moreover, MRTX1133 elicits a more pronounced cytostatic effect in controlling the in vivo tumor growth in PDAC patient-derived xenografts. In syngeneic models, KRASG12D inhibition leads to potent tumor regression that did not occur in immune-deficient hosts. Digital spatial profiling on tumor tissues indicates that MRTX1133-mediated KRAS inhibition enhances interferon-γ signaling and induces antigen presentation that modulates the tumor microenvironment. Further investigation on the immunological response using single-cell sequencing and multispectral imaging reveals that tumor regression is associated with suppression of neutrophils and influx of effector CD8+ T-cells. Thus, both tumor cell-intrinsic and extrinsic events contribute to response and credential KRASG12D inhibition as a promising strategy for a large percentage of PDAC tumors.

2024-01-24 | GSE249538 | GEO

CBFB-DSP-ChIPseq and YAP-DSP-ChIPseq

Project description:CBFB-DSP-ChIPseq and YAP-DSP-ChIPseq

| PRJNA982827 | ENA

Radiation combined with KRAS-MEK inhibitors enhances anticancer immunity in KRAS-mutated tumor models [LLC RNA-seq]

Project description:KRAS mutation is a common driver in solid tumors, and KRAS-mutated tumors are relatively resistant to radiotherapy. Therefore, we investigated the combined effect of radiation and KRAS-MEK inhibitors (AMG510 and trametinib) in KRAS-mutated tumors.

2022-10-01 | GSE209766 | GEO

Radiation combined with KRAS-MEK inhibitors enhances anticancer immunity in KRAS-mutated tumor models [CT26 RNA-seq]

2022-10-01 | GSE209765 | GEO