Similar studies for GEO DataSets (Select 200133714) - GEO DataSets

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Items: 20

Select item 2001337141.

Transcriptional profiling of BL/6 mice with alterations in Kras, Stk11, and/or Keap1/Nrf2.

(Submitter supplied) Transcriptional profiling of BL/6 mice harboring a mutant Kras allele, with or without knockouts of Stk11 and/or Keap1, or with expression of an Nfe2l2 transgene, Nrf2Tg. In lung adenocarcinoma (LUAD), stabilization of the transcription factor NRF2 through genomic alterations in KEAP1 and NFE2L2 occurs in roughly a quarter of patients, often in the context of STK11 tumor suppressor loss. In this study, we demonstrate that NRF2 activation in the context of concurrent KRAS mutation and STK11 loss promotes aggressive LUAD tumor behavior in both human and mouse preclinical models. more...

Organism:: Mus musculus

Type:: Expression profiling by array

Platform:: GPL18233
23 Samples

Download data: CEL

Series

Accession:: GSE133714

ID:: 200133714

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 2001938952.

KrasG12D/+ co-mutation alters the transcriptional landscape of lung adenocarcinoma

(Submitter supplied) The tumor microenvironment (TME) contains a rich source of nutrients that sustain cell growth and ultimately facilitate tumor progression. The availability of glucose and glutamine in the TME are essential for the development and activation of effector T cells that exert anti-tumor function. Recently, inhibition of glutaminase, the enzyme that hydrolyzes glutamine to glutamate, has garnered interest as an approach to both decrease tumor metabolism and growth, while increasing available glutamine in the TME for effector T cells. more...

Organism:: Mus musculus

Type:: Expression profiling by high throughput sequencing

Platform:: GPL19057
35 Samples

Download data: TXT

Series

Accession:: GSE193895

ID:: 200193895

PubMed Similar studies

Select item 2000720943.

KRAS mutation-associated gene expression, p53 and STK11 mutations, proliferation and immune surveillance in lung adenocarcinoma

(Submitter supplied) While mutations in the KRAS oncogene are amongst the most prevalent in human cancer, there are few successful treatments to target these tumors. It is also likely that heterogeneity in KRAS-mutant tumor biology significantly contributes to the response to therapy. We hypothesized that presence of commonly co-occurring mutations in STK11 and TP53 tumor suppressors may represent a significant source of heterogeneity in KRAS-mutant tumors. more...

Organism:: Homo sapiens

Type:: Expression profiling by array

Platform:: GPL15048
442 Samples

Download data: CEL

Series

Accession:: GSE72094

ID:: 200072094

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 2001228364.

Nrf2 activation promotes lung cancer metastasis by blocking degradation of Bach1

(Submitter supplied) Purpose: The goal of this study is to analyze the transcriptional pathways regulated by Fbxo22 and Keap1 in mouse lung adeno carcinoma cells. Methods: mouse lung adeno carcinoma cells either Keap1 wild type (KP) or mutant (KPK), have been transfected for 3 days with siRNA targeting Fbxo22. Knock down efficiency has been evaluated by western blot (using specific antibody for Fbxo22) and qPCR (using specific oligos for Fbxo22) . more...

Organism:: Mus musculus

Type:: Expression profiling by high throughput sequencing

Platform:: GPL17021
12 Samples

Download data: CSV

Series

Accession:: GSE122836

ID:: 200122836

PubMed Full text in PMC Similar studies SRA Run Selector

Select item 2001385715.

In vivo epigenetic CRISPR screen identifies Asf1a as an immunotherapeutic target in Kras-mutant lung adenocarcinoma

(Submitter supplied) Despite substantial progress in lung cancer immunotherapy, the overall response rate in KRAS-mutant lung adenocarcinoma (ADC) patients remains low. Combining standard immunotherapy with adjuvant approaches that enhance adaptive immune responsesâ€”such as epigenetic modulation of anti-tumor immunityâ€”is therefore an attractive strategy. To identify epigenetic regulators of tumor immunity, we constructed an epigenetic-focused sgRNA library, and performed an in vivo CRISPR screen in KrasG12D/P53-/- (KP) lung ADC model. more...

Organism:: Mus musculus; Homo sapiens

Type:: Genome binding/occupancy profiling by high throughput sequencing

Platforms:: GPL20301 GPL21103
10 Samples

Download data: BW

Series

Accession:: GSE138571

ID:: 200138571

PubMed Full text in PMC Similar studies SRA Run Selector

Select item 2001336046.

Single-cell transcriptomic profiling of mouse KrasG12DP53-/- (KP) lung tumors in response to tumor cell intrinsic Asf1a knockout (KO), anti-PD-1 or combination treatment (Asf1a KO + anti-PD-1).

(Submitter supplied) We performed single-cell RNA sequencing (scRNAseq) analysis on the mouse lung tissues from KP tumor-bearing mice treated with tumor cell intrinsic Asf1a KO, anti-PD-1 or combination treatment

Organism:: Mus musculus

Type:: Expression profiling by high throughput sequencing

Platform:: GPL21103
4 Samples

Download data: MTX, TSV

Series

Accession:: GSE133604

ID:: 200133604

PubMed Full text in PMC Similar studies SRA Run Selector

Select item 2001272327.

In vitro and in vivo epigenome-wide CRISPR screens in mouse KrasG12D/P53-/- (KP) lung adenocarcinoma model

(Submitter supplied) To systematically study the functions of epigenetic genes in controlling tumor progression and regulating anti-tumor immunity, we performed a series of in vitro and in vivo epigenome-wide CRISPR screens in mouse KP lung adenocarcinoma model. We constructed an epigenetic-focused sgRNA library, established KP-Cas9-library pools, and then performed in vitro and in vivo CRISPR screens. For in vitro screens, we compared the cell pools harvested at week 4 with the cells pools harvested at week 2 to check the functions of epigenetic genes in tumor cell proliferation. more...

Organism:: Mus musculus; synthetic construct

Type:: Other

Platforms:: GPL19604 GPL17021
54 Samples

Download data: TXT

Series

Accession:: GSE127232

ID:: 200127232

PubMed Full text in PMC Similar studies SRA Run Selector

Select item 2001272058.

RNA-seq to compare gene expression profiles between Asf1a WT and Asf1a KO cells

(Submitter supplied) KrasG12D/P53-/-(KP)-Cas9 single clone was transfected with ctrl vector, ctrl sgRNA-1, ctrl-sgRNA-2 or ctrl-sgRNA-3 and then selected by using 5ug/ml Blasticidin, to get the 4 ctrl lines; KP-Cas9 single clone was transfected with Asf1a sgRNA-1, sgRNA-2, sgRNA-3 and new sgRNA-1 and then selected by using 5ug/ml Blasticidin, and then picked up single clones with Asf1a KO. For each Asf1a sgRNA, we selected one clone for RNA seq, so totally we have 4 Asf1a KO clones for RNA seq.

Organism:: Mus musculus

Type:: Expression profiling by high throughput sequencing

Platform:: GPL17021
8 Samples

Download data: TXT

Series

Accession:: GSE127205

ID:: 200127205

PubMed Full text in PMC Similar studies SRA Run Selector

Select item 2002414829.

KEAP1 mutation in lung adenocarcinoma promotes immune evasion and immunotherapy resistance.

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:: Mus musculus

Type:: Expression profiling by high throughput sequencing

Platforms:: GPL21103 GPL24247
10 Samples

Download data

Series

Accession:: GSE241482

ID:: 200241482

PubMed Full text in PMC Similar studies

Select item 20024148110.

KEAP1 mutation in lung adenocarcinoma promotes immune evasion and immunotherapy resistance [scRNA-seq]

(Submitter supplied) Immune cells were isolated from the lungs of mice bearing KEAP1 mutant or wildtype tumors. We found that in KEAP1 mutant tumors there is a reduction in CD103 DCs and early activated T cells as well as an increase in exhausted CD8 T cells in comparison to WT controls.

Organism:: Mus musculus

Type:: Expression profiling by high throughput sequencing; Other

Platform:: GPL21103
4 Samples

Download data: RDS

Series

Accession:: GSE241481

ID:: 200241481

PubMed Full text in PMC Similar studies

Select item 20024148011.

KEAP1 mutation in lung adenocarcinoma promotes immune evasion and immunotherapy resistance [RNA-seq]

Organism:: Mus musculus

Type:: Expression profiling by high throughput sequencing

Platform:: GPL24247
6 Samples

Download data: TXT

Series

Accession:: GSE241480

ID:: 200241480

PubMed Full text in PMC Similar studies

Select item 20025016612.

KEAP1-mutant lung cancers weaken anti-tumor immunity and promote an M2-like macrophage phenotype.

(Submitter supplied) Considerable advances have been made in lung cancer therapies, but there is still an unmet clinical need to improve survival for lung cancer patients. Immunotherapies have improved survival, although only 20-30% of patients respond to these treatments. Interestingly, cancers with mutations in KEAP1, the negative regulator of the NRF2 cytoprotective pathway, are resistant to immune checkpoint inhibition and correlate with decreased immune cell infiltration. more...

Organism:: Mus musculus

Type:: Expression profiling by high throughput sequencing

Platform:: GPL24247
15 Samples

Download data: TXT

Series

Accession:: GSE250166

ID:: 200250166

PubMed Full text in PMC Similar studies

Select item 20023759213.

Glutamine antagonist DRP-104 suppresses tumor growth and enhances response to checkpoint blockade in KEAP1 mutant lung cancer

(Submitter supplied) Keap1 mutant lung tumors were injected into mice and once lung tumors formed the mice were treated with anti-PD1, DRP-104, or the combination of the drugs. Immune cells and tumor cells were isolated from the lungs and ExCITE-seq was performed.

Organism:: Mus musculus

Type:: Other

Platform:: GPL21103
2 Samples

Download data: CSV, MTX, TSV, TXT

Series

Accession:: GSE237592

ID:: 200237592

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Select item 20025592714.

Differential squamous cell fates elicited by NRF2 gain-of-function versus KEAP1 loss-of-function

(Submitter supplied) Clinical evidence has revealed that high-level activation of NRF2 caused by somatic mutations in NRF2 is frequently detected in esophageal squamous cell carcinoma (ESCC), whereas that by somatic mutations in KEAP1, a negative regulator of NRF2, is not. Here, we challenged to generate a mouse model of NRF2-activated ESCC using the cancer-derived NRF2L30F mutation and cancer-driver mutant Trp53R172H. Concomitant expression of NRF2L30F and Trp53R172H induced proliferation of squamous cell epithelia and resulted in NRF2-activated ESCC-like lesions. In contrast, while squamous cell-specific deletion of KEAP1 induced similar NRF2 hyper-activation, the loss-of-KEAP1 combined with Trp53R172H did not elicit the proliferation and formation of ESCC-like lesions. Instead, KEAP1-deleted cells disappeared from the esophageal epithelium over time by cell competition. These findings provide insights into the observation that somatic mutations are more frequently observed in NRF2 than in KEAP1, and the mouse model developed here will be instrumental in elucidating the mechanistic basis leading to NRF2-activated ESCC.

Organism:: Mus musculus

Type:: Expression profiling by high throughput sequencing

Platform:: GPL28457
25 Samples

Download data: TXT

Series

Accession:: GSE255927

ID:: 200255927

PubMed Similar studies

Select item 20024012015.

Genome-Wide CRISPR Screen Identifies Multiple Synthetic Lethal Targets That Enhance KRAS (G12C) Inhibitor Efficacy

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:: Mus musculus; Homo sapiens

Type:: Other; Expression profiling by high throughput sequencing

Platforms:: GPL24676 GPL24247 GPL20301
65 Samples

Download data: MTX, TSV, TXT

Series

Accession:: GSE240120

ID:: 200240120

PubMed Full text in PMC Similar studies

Select item 20024011816.

Genome-Wide CRISPR Screen Identifies Multiple Synthetic Lethal Targets That Enhance KRAS (G12C) Inhibitor Efficacy [scRNA-seq]

(Submitter supplied) KRAS G12C inhibitors (G12Ci) alone and in various combinations are being tested in multiple tumors with over-activation of the RAS/ERK pathway. KRAS plays a critical role in normal cell signaling; hence, G12Cis could influence the signaling pathways. We found that several novel pathways including Hippo pathways are upregulated upon MRTX849 treatment. Our results argue for testing KRAS G12C and TEAD inhibitor combinations in NSCLC patients.

Organism:: Homo sapiens

Type:: Expression profiling by high throughput sequencing

Platform:: GPL20301
3 Samples

Download data: MTX, TSV

Series

Accession:: GSE240118

ID:: 200240118

PubMed Full text in PMC Similar studies

Select item 20024011317.

Genome-Wide CRISPR Screen Identifies Multiple Synthetic Lethal Targets That Enhance KRAS (G12C) Inhibitor Efficacy [RNA-seq-mm10]

Organism:: Mus musculus

Type:: Expression profiling by high throughput sequencing

Platform:: GPL24247
14 Samples

Download data: TXT

Series

Accession:: GSE240113

ID:: 200240113

PubMed Full text in PMC Similar studies

Select item 20024011118.

Genome-Wide CRISPR Screen Identifies Multiple Synthetic Lethal Targets That Enhance KRAS (G12C) Inhibitor Efficacy [RNA-seq-human]

(Submitter supplied) Transcriptomic analysis of NSCLC cells either under MRTX849 treatment or Ctrl (DMSO) to identify key pathways causing resistance.

Organism:: Homo sapiens

Type:: Expression profiling by high throughput sequencing

Platform:: GPL24676
12 Samples

Download data: TXT

Series

Accession:: GSE240111

ID:: 200240111

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 20024011019.

Genome-Wide CRISPR Screen Identifies Multiple Synthetic Lethal Targets That Enhance KRAS (G12C) Inhibitor Efficacy [CRISPR]

(Submitter supplied) KRAS G12C inhibitors (G12Ci) alone and in various combinations are being tested in multiple tumors with over-activation of the RAS/ERK pathway. KRAS plays a critical role in normal cell signaling; hence, G12Cis has been reported to create resistance. We found several novel pathways, including Hippo pathways, are enriched from significant dropouts upon MRTX849 treatment. Our results argue for testing KRAS G12C and TEAD inhibitor combinations in NSCLC patients.