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Links from GEO DataSets

Items: 20

1.

CBX5 loss drives EGFR inhibitor resistance and results in therapeutically actionable vulnerabilities in lung cancer

(Submitter supplied) The study evaluated the differential gene expression in CBX5 knockdown cells compared to control shRNA expressed HCC827 cells. Briefly, human lung cancer HCC827 cells stably expressing either CBX5 shRNAs or control shRNA were analysed for gene expression.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
9 Samples
Download data: TXT
2.

RNA-seq of PC9 cells tolerant to gefitinib

(Submitter supplied) EGFR inhibitors (EGFRi) are effective against EGFR mutant lung cancers. The efficacy of these drugs however is mitigated by the outgrowth of resistant cells, most often driven by a secondary acquired mutation in EGFR, T790M. We recently demonstrated that T790M can arise de novo during treatment (Hata et al., Nature Medicine 2016); it follows that one potential therapeutic strategy to thwart resistance would be identifying and eliminating these cells (referred to as drug tolerant cells (DTCs)) prior to acquiring secondary mutations like T790M. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
5 Samples
Download data: CSV
Series
Accession:
GSE117610
ID:
200117610
3.

Effect of 35d and curcumin treatment on gene expression in GR6 cells

(Submitter supplied) To investigate gene expression changes by 35d and curcumin, we treated 1 uM 35d and curcumin for 24h in GR6 cells. We then performed gene expression profiling analysis using data obtained from RNA-seq of untreated and treated cells
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
3 Samples
Download data: TXT
Series
Accession:
GSE215786
ID:
200215786
4.

Long non-coding RNA CRNDE Involved in Resistance to EGFR tyrosine kinase inhibitor in EGFR-mutant Lung Cancer via eIF4A3/MUC1/EGFR Signal.

(Submitter supplied) Introduction: Overcoming of acquired resistance to EGFR-tyrosine kinase inhibitors (EGFR-TKIs) is an intractable obstacle for many clinical oncologists. The mechanisms of resistance to EGFR-TKIs are very complex. Long non-coding RNAs (lncRNAs) may play an important role in cancer development and metastasis. However, the biological process between lncRNAs and drug resistance to EGFR mutated lung cancer largely unknown. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL20844
6 Samples
Download data: TXT
Series
Accession:
GSE163913
ID:
200163913
5.

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 responses—such as epigenetic modulation of anti-tumor immunity—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
6.

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
7.

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
8.

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
9.

Epithelial-to-mesenchymal transition antagonizes response to targeted therapies in lung cancer by suppressing BIM

(Submitter supplied) Purpose: Epithelial-to-mesenchymal transition (EMT) confers resistance to a number of targeted therapies and chemotherapies. However, it has been unclear why EMT promotes resistance, thereby impairing progress to overcome it. Experimental Design: We have developed several models of EMT-mediated resistance to EGFR inhibitors (EGFRi) in EGFR mutant lung cancers to evaluate a novel mechanism of EMT-mediated resistance. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
2 Samples
Download data: BED
Series
Accession:
GSE106896
ID:
200106896
10.

Gene Expression Regulation by Lung Cancer Oncogenes

(Submitter supplied) To characterize gene expression changes induced by oncogenes implicated in human lung adenocarcinoma, we analyzed the whole transcriptome of NIH3T3 cells expressing mutant EGFR (exon 19 deletion) or wild-type EGFR. Expression levels of several genes from this list were validated by quantitative RT-PCR using the same RNA samples.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL10787
4 Samples
Download data: TXT
Series
Accession:
GSE104494
ID:
200104494
11.

MUSASHI-2 RNA binding protein confers resistance to an epidermal growth factor receptor-tyrosine kinase inhibitor Osimertinib in lung adenocarcinoma

(Submitter supplied) Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) are effective in non-small cell lung cancer (NSCLC) patients harboring EGFR mutations. However, due to the acquired resistance to EGFR-TKIs, even third generation Osimertinib, the patients suffer poor prognosis. The resistance mechanisms are still not fully understood. Here, we demonstrate that increased expression of MUSASHI-2 (MSI2), an RNA binding protein, is novel mechanisms for resistance to EGFR-TKIs. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL21185
16 Samples
Download data: TXT
Series
Accession:
GSE168280
ID:
200168280
12.

Single-cell Transcriptome Analysis Revealed that EGFR Mutation Leads to a Suppressive Tumor Immune Microenvironment in Lung Adenocarcinoma

(Submitter supplied) We analyzed 40,799 single cells from nine samples and found that in EGFR-mutant LUAD, tumor cells generated an immunosuppressive microenvironment by releasing cytokines to attract suppressive immune cells such as myeloid-derived suppressor cells (MDSCs) directly or indirectly by interacting with macrophages, dendritic cells, or other cell types. By contrast, EGFR wild-type LUAD had a greater ability to recruit immunocompetent T cells such as TRMs and Th1 cells, thus driving a proinflammatory microenvironment.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
9 Samples
Download data: TSV, TXT
Series
Accession:
GSE171145
ID:
200171145
13.

Targeting 14-3-3ζ overcomes resistance to EGFR-TKIs in lung adenocarcinoma via BMP2/Smad/ID1 signaling

(Submitter supplied) 14-3-3ζ has been found to promote the proliferation, metastasis and chemoresistance of cancer cells in several cancers including lung adenocarcinoma; however, its significance in epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) resistance remains unknown. Our work uncovers a hitherto unappreciated role of 14-3-3ζ in EGFR-TKI resistance. We determined global gene expression profiling in EGFR-TKI-resistant H1975 cells using microarray analysis.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL15207
6 Samples
Download data: CEL
Series
Accession:
GSE156435
ID:
200156435
14.

Acquired resistance to PRMT5 inhibition and the consequent collateral sensitivity to paclitaxel are both Stmn2 dependent

(Submitter supplied) Drug resistance is a major hurdle for the efficacy of cancer therapies. Protein arginine methyltransferase 5 (PRMT5) is an epigenetic regulator that is upregulated in most tumor types, and PRMT5 inhibitors (PRMT5i) are now in clinical trials. Here we describe the first model of resistance to PRMT5 inhibition, using cell lines derived from murine Kras-G12D;p53-null lung adenocarcinomas (LUAD). Initially, PRMT5 inhibition induced proliferation defects and apoptosis, but eventually we were able to generate numerous independent PRMT5i resistant lines. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
15 Samples
Download data: TXT
Series
Accession:
GSE157715
ID:
200157715
15.

Establishment of EGFR-inhibitor resistant triple negative breast cancer models from patient derived xenografts

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
9 Samples
Download data
Series
Accession:
GSE189325
ID:
200189325
16.

Establishment of EGFR-inhibitor resistant triple negative breast cancer models from patient derived xenografts [scRNA-seq]

(Submitter supplied) Aim: The goals of this study were to identify transcriptomic changes that arise in basal-like breast cancer cells during the development of resistance to epidermal growth factor receptor inhibitors (EGFRi) and to identify drugs that are cytotoxic once EGFRi resistance occurs. Methods: Human patient-derived xenografts (PDXs) were grown in immunodeficient mice and were treated with a set of EGFRi; the EGFRi erlotinib was selected for more expansive in vivo studies. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
2 Samples
Download data: CLOUPE, MTX, TSV
Series
Accession:
GSE189324
ID:
200189324
17.

Establishment of EGFR-inhibitor resistant triple negative breast cancer models from patient derived xenografts [Bulk RNA-seq]

(Submitter supplied) Aim: The goals of this study were to identify transcriptomic changes that arise in basal-like breast cancer cells during the development of resistance to epidermal growth factor receptor inhibitors (EGFRi) and to identify drugs that are cytotoxic once EGFRi resistance occurs. Methods: Human patient-derived xenografts (PDXs) were grown in immunodeficient mice and were treated with a set of EGFRi; the EGFRi erlotinib was selected for more expansive in vivo studies. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
7 Samples
Download data: TSV
Series
Accession:
GSE189257
ID:
200189257
18.

Study the differential gene expression of different lung cancer EGFR mutants in NIH3T3 cells

(Submitter supplied) Oncogenic mutations in the EGFR gene account for 15-20% of lung adenocarcinoma (LUAD) cases. However, the mechanism for EGFR driven tumor development and growth is not fully understood. Here, using a mRNA expression profiling-based approach we identified betacellulin (BTC) as one the gene upregulated by oncogenic EGFR in a MAP kinase-dependent manner. BTC protein expression was markedly increased in LUAD patient samples compared to normal lung tissue, with higher expression in EGFR-mutant LUAD. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
15 Samples
Download data: TXT
Series
Accession:
GSE101399
ID:
200101399
19.

Effect of gene expression changes after Erlotinib and CCR6 inhibitor treatment on PC9 and PC9GR cells

(Submitter supplied) Comparative gene expression profile analysis of RNA-seq data for PC9 GR cells after compound treatment.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
10 Samples
Download data: TXT
Series
Accession:
GSE244730
ID:
200244730
20.

Transcriptional control of HP1a by the RNA binding proteins RBMX/L1 maintain chromatin state in myeloid leukemia

(Submitter supplied) RNA binding proteins (RBPs) are key arbiters of post-transcriptional regulation that have been found to be dysregulated in hematological malignancies. Here, we identify the RBP RBMX and its retrogene RBMXL1 to be required for murine and human myeloid leukemogenesis. RBMX/L1 are overexpressed in acute myeloid leukemia (AML) primary patients compared to healthy individuals, and RBMX/L1 loss delayed leukemia development. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL20301
21 Samples
Download data: TXT, XLSX
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