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Links from GEO DataSets

Items: 20

1.

Comprehensive molecular characterization of lung tumors implicates AKT and MYC signaling in adenocarcinoma to squamous cell transdifferentiation

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Methylation profiling by high throughput sequencing
Platforms:
GPL20301 GPL24676
81 Samples
Download data: BW
Series
Accession:
GSE226070
ID:
200226070
2.

Comprehensive molecular characterization of lung tumors implicates AKT and MYC signaling in adenocarcinoma to squamous cell transdifferentiation [RNA-seq]

(Submitter supplied) To investigate molecular changes occurring during lung adenocarcinoma to squamous carcinoma transformation.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
43 Samples
Download data: TXT
Series
Accession:
GSE226069
ID:
200226069
3.

Comprehensive molecular characterization of lung tumors implicates AKT and MYC signaling in adenocarcinoma to squamous cell transdifferentiation [EPIC]

(Submitter supplied) To investigate molecular changes occurring during lung adenocarcinoma to squamous carcinoma transformation.
Organism:
Homo sapiens
Type:
Methylation profiling by high throughput sequencing
Platforms:
GPL24676 GPL20301
38 Samples
Download data: BW
Series
Accession:
GSE226068
ID:
200226068
4.

Patient-derived xenograft models of non-small cell lung cancer for evaluating targeted drug sensitivity and resistance

(Submitter supplied) Background: Patient-derived xenograft (PDX) models are a useful tool in cancer biology research. However, the number of lung cancer PDXs is limited Results: In the present study, we successfully established ten PDXs, including three adenocarcinoma (AD), six squamous cell carcinoma (SQ) and one large cell carcinoma (LA), from 30 patients with non-small cell lung cancer (NSCLC) (18 AD, 10 SQ, and 2 LA), mainly in SHO mice (Crlj:SHO-PrkdcscidHrhr). more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
12 Samples
Download data: TXT
5.

Targeting the CDK4/6-Rb pathway enhances response to PI3K inhibition in PIK3CA mutant lung squamous cell carcinoma

(Submitter supplied) The purpose of this study is to examine the efficacy of combined PI3K and CDK4/6 inhibition in lung squamous cell carcinoma (LUSC). LUSC patient-derived xenografts (PDX) are used as preclinical models for this study as they are clinically relevant models and have been shown to recapitulate patient tumor hisology, molecular features and drug response. We have demonstrated using the 1x1x1 drug design that PIK3CA mutation predicts response to PI3K inhibitors. more...
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by array
Platform:
GPL14951
9 Samples
Download data: TXT
Series
Accession:
GSE109679
ID:
200109679
6.

Multi-omics Analysis reveals novel therapeutic vulnerabilities in lung cancer

(Submitter supplied) Non-small cell lung cancer (NSCLC) comprises the majority (~85%) of all lung tumors, with lung adenocarcinoma (LUAD) and squamous cell carcinoma (LUSC) being the most frequently diagnosed histological subtypes. Currently, multi-modal omics profiles had been carried out in NSCLC, but no studies reported yet a systems biology approach to provide a complete picture of molecular perturbations specifically for LUAD and LUSC.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
58 Samples
Download data: XLS
7.

Gene expression signatures for lung adenocarcinoma

(Submitter supplied) We used whole genome microarray expression profiling as a discovery platform to identify genes through 7 pairs lung adenocarcinoma tissues and normal tissues
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL13497
14 Samples
Download data: TXT, XLSX
Series
Accession:
GSE140797
ID:
200140797
8.

Lineage-specific intolerance to oncogenic drivers restricts histological transformation

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL24247 GPL17021
42 Samples
Download data: BROADPEAK
Series
Accession:
GSE248207
ID:
200248207
9.

Lineage-specific intolerance to oncogenic drivers restricts histological transformation [ATAC-Seq]

(Submitter supplied) Lung adenocarcinoma (LUAD) and small cell lung cancer (SCLC) are thought to originate from different epithelial cell types in the lung. Intriguingly, LUAD can histologically transform into SCLC following treatment with targeted therapies. Here we designed models to follow the conversion of LUAD to SCLC and found the barrier to histological transformation converges on tolerance to Myc, which we implicate as a lineage-specific driver of the pulmonary neuroendocrine cell. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL17021
15 Samples
Download data: BROADPEAK, TXT
Series
Accession:
GSE248206
ID:
200248206
10.

Lineage-specific intolerance to oncogenic drivers restricts histological transformation [scRNA-Seq]

(Submitter supplied) Lung adenocarcinoma (LUAD) and small cell lung cancer (SCLC) are thought to originate from different epithelial cell types in the lung. Intriguingly, LUAD can histologically transform into SCLC following treatment with targeted therapies. Here we designed models to follow the conversion of LUAD to SCLC and found the barrier to histological transformation converges on tolerance to Myc, which we implicate as a lineage-specific driver of the pulmonary neuroendocrine cell. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
27 Samples
Download data: H5AD
Series
Accession:
GSE248202
ID:
200248202
11.

USP13 Drives Lung Squamous Cell Carcinoma via Switching Lung Club Cell Lineage Plasticity

(Submitter supplied) Lung squamous cell carcinoma (LUSC) is associated with high mortality and limited targeted therapies. USP13 is one of the most amplified genes in LUSC, and yet its role in lung cancer is largely unknown. Here, we establish a novel mouse model of LUSC by overexpressing USP13 in KrasG12D/+; Trp53flox/flox background (KPU). KPU model faithfully recapitulates the key pathohistological, molecular features, and cellular pathways of human LUSC. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21493
24 Samples
Download data: CSV
Series
Accession:
GSE244847
ID:
200244847
12.

∆Np63 executes an oncogenic program through the regulation of a common landscape of super-enhancer associated genes in non-small cell lung cancer

(Submitter supplied) Distinct lung stem cells give rise to lung adenocarcinoma (ADC) and squamous cell carcinoma (SCC). ΔNp63 guides development of these cells through regulation of terminal differentiation; however, its mechanistic role in lung cancer development has remained elusive. We utilized a ΔNp63-specific conditional knockout mouse model and found that ∆Np63 maintains lung ADC and SCC by keeping lung stem cells in quiescence. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL17021 GPL21103
21 Samples
Download data: TDF, TXT
Series
Accession:
GSE131671
ID:
200131671
13.

Whole-transcriptome analysis of tumor tissues of lung adenocarcinoma reveals molecular changes under the influence of IFN-γ

(Submitter supplied) IFN-γ is a critical cytokine which regulates both innate and adaptive immune. Ample evidences have elucidated the mechanisms of IFN-γ mediated antitumor effects, including driving T Helper Type 1 (Th1) polarization, activating cytotoxic lymphocyte (CTL) and natural killer T cells, upregulating major histocompatibility complex class I expression (MHC Class I) in tumor cells, and inhibiting tumor cells proliferation, inducing tumor cells apoptosis. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL21185
12 Samples
Download data: TXT
Series
Accession:
GSE99995
ID:
200099995
14.

Identification of a unique subtype of lung squamous cell carcinoma defined by SOX2 and a neural differentiation factor BRN2

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platform:
GPL18573
51 Samples
Download data: BED
Series
Accession:
GSE137461
ID:
200137461
15.

Identification of a unique subtype of lung squamous cell carcinoma defined by SOX2 and a neural differentiation factor BRN2 [RNA-seq]

(Submitter supplied) Lineage-specific transcriptional regulators control differentiation states not only during normal development but also during cancer evolution. By investigating super-enhancer landscape of lung squamous cell carcinoma (LUSC), we identified a unique ‘neural’ subtype defined by Sox2 and a neural lineage factor Brn2. Robust protein-protein interaction and genomic co-occupancy of these factors indicated their transcriptional cooperation in this ‘neural’ LUSC in contrast to the cooperation of Sox2 and p63 in the classical LUSC. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
8 Samples
Download data: TXT
16.

Identification of a unique subtype of lung squamous cell carcinoma defined by SOX2 and a neural differentiation factor BRN2 [ChIP-seq]

(Submitter supplied) Lineage-specific transcriptional regulators control differentiation states not only during normal development but also during cancer evolution. By investigating super-enhancer landscape of lung squamous cell carcinoma (LUSC), we identified a unique ‘neural’ subtype defined by Sox2 and a neural lineage factor Brn2. Robust protein-protein interaction and genomic co-occupancy of these factors indicated their transcriptional cooperation in this ‘neural’ LUSC in contrast to the cooperation of Sox2 and p63 in the classical LUSC. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
43 Samples
Download data: BED
Series
Accession:
GSE137459
ID:
200137459
17.

Simvastatin overcomes resistance to tyrosine kinase inhibitors in patient-derived, oncogene-driven lung adenocarcinoma models

(Submitter supplied) There is an unmet clinical need to develop novel strategies to overcome resistance to tyrosine kinase inhibitors (TKIs) in patients with oncogene-driven lung adenocarcinoma (LUAD). Statins is a class of drugs that act as competitive inhibitors of 3-hydroxy-3-methyl-glutaryl-CoA reductase (HMGCR). The objective of this study was to determine if simvastatin could overcome TKI resistance using the vivo LUAD models. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
4 Samples
Download data: TXT
Series
Accession:
GSE249807
ID:
200249807
18.

CDC7 inhibition impairs neuroendocrine transformation in lung and prostate tumors through MYC degradation

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
68 Samples
Download data
Series
Accession:
GSE252569
ID:
200252569
19.

CDC7 inhibition impairs neuroendocrine transformation in lung and prostate tumors through MYC degradation III

(Submitter supplied) Neuroendocrine (NE) transformation is a mechanism of resistance to targeted therapy in lung and prostate adenocarcinomas leading to poor prognosis. Upregulation of the cell cycle kinase CDC7 occurred in tumors undergoing NE transformation, after TP53/RB1 co-inactivation, leading to induced sensitivity to the CDC7 inhibitor simurosertib. CDC7 inhibition suppressed NE transdifferentiation and extended response to targeted therapy in in vivo models of NE transformation by inducing the proteasome-mediated degradation of MYC, implicated in stemness and histological transformation. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
42 Samples
Download data: TXT
Series
Accession:
GSE252568
ID:
200252568
20.

CDC7 inhibition impairs neuroendocrine transformation in lung and prostate tumors through MYC degradation II

(Submitter supplied) Neuroendocrine (NE) transformation is a mechanism of resistance to targeted therapy in lung and prostate adenocarcinomas leading to poor prognosis. Upregulation of the cell cycle kinase CDC7 occurred in tumors undergoing NE transformation, after TP53/RB1 co-inactivation, leading to induced sensitivity to the CDC7 inhibitor simurosertib. CDC7 inhibition suppressed NE transdifferentiation and extended response to targeted therapy in in vivo models of NE transformation by inducing the proteasome-mediated degradation of MYC, implicated in stemness and histological transformation. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
14 Samples
Download data: TXT
Series
Accession:
GSE252567
ID:
200252567
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