GEO DataSets

(Submitter supplied) Oncogenic KRAS is found in more than 25% of lung adenocarcinomas, the major histologic subtype of non–small cell lung cancer (NSCLC), and is an important target for drug development. To this end, we generated four NSCLC lines with stable knockdown selective for oncogenic KRAS. As expected, stable knockdown of oncogenic KRAS led to inhibition of in vitro and in vivo tumor growth in the KRAS-mutant NSCLC cells, but not in NSCLC cells that have wild-type KRAS (but mutant NRAS). more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

15 Samples

Download data: CEL

(Submitter supplied) There are currently no effective targeted therapies for KRAS mutant cancers. Therapeutic strategies that combine MEK inhibitors with agents that target apoptotic pathways may be a promising therapeutic approach. We investigated combining MEK and MDM2 inhibitors as a potential treatment strategy for KRAS mutant non-small cell lung cancers and colorectal carcinomas that harbor wild-type TP53. The combination of pimasertib (MEK inhibitor) + SAR405838 (MDM2 inhibitor) was synergistic and induced the expression of PUMA and BIM, led to apoptosis and growth inhibition in vitro, and tumor regression in vivo. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL16791

198 Samples

Download data: TXT

(Submitter supplied) Mutant KRAS (mut-KRAS) is present in 30% of all human cancers and plays a critical role in cancer cell growth and resistance to therapy. There is evidence from colon cancer that mut-KRAS is a poor prognostic factor and negative predictor of patient response to molecularly targeted therapy. However, evidence for such a relationship in non small cell lung cancer (NSCLC) is conflicting. KRAS mutations are primarily found at codons 12 and 13, where different base changes lead to alternate amino acid substitutions that lock the protein in an active state. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL6244

22 Samples

Download data: CEL

(Submitter supplied) RNA seq data of PDX2 treated with vehicle of SHP099 --> to check senescence and SASP gene expression signatures

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL16791

12 Samples

Download data: XLSX

(Submitter supplied) KRAS-mutant non-small cell lung cancer (NSCLC) is one of the main subtypes across lung cancers. Despite the enormous studies on KRAS-mutant NSCLC, new therapeutic targets need to be identified because current therapies are insufficient. Here we show the tumor promoting function of PIERCE1 in the KRAS-mutant NSCLC. Mechanistically, PIERCE1 depletion inhibits cell growth and AKT phosphorylation (pAKT) at S473, particularly in KRAS-mutant lung cancer. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL16699

8 Samples

Download data: TXT

(Submitter supplied) To determine the difference of gene expression profile in epithelial and mesenchymal KRAS mutant lung cancers, epithelial NCI-H358 cells were treated with TGFβ1 (4 ng/mL) or PBS for 14 days in order to induce epithelial to mesenchymal transition (EMT). Gene expression was determined in NCI-H358 cells before and after EMT induction. In addition, in order to investigate the effect of a MEK inhibitor trametinib on gene expression, mesenchymal NCI-H1792 cells were treated with 50 nM trametinib for 48 hours. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL17077

8 Samples

Download data: TXT

(Submitter supplied) To identify the gene expression changes in NRAS mutant cell line SKMEL-103, KRAS mutant cell line AsPC1 and HRAS mutant cell line RH-36 upon BAY 11-7082 treatment, we analyzed these cell line with either control DMSO or BAY 11-7082 treatment via RNA sequencing.

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL16791

18 Samples

Download data: TXT

(Submitter supplied) Mutations in the NRAS oncogene are present in up to 20% of melanoma. Here, we show that interferon alpha-inducible protein 6 (IFI6) is necessary for NRASQ61K-induced transformation and melanoma growth. IFI6 was transcriptionally upregulated by NRASQ61K, and knockdown of IFI6 resulted in DNA replication stress due to dysregulated DNA replication via E2F2. This stress consequentially inhibited cellular transformation and melanoma growth via senescence or apoptosis induction depending on the RB and p53 pathway status of the cells. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL10558

12 Samples

Download data: TXT

(Submitter supplied) Prostate cancer cell lines grow in full serum under standard conditions were profiled on Agilent-014698 Human Genome CGH Microarray 105A. Digestion, labeling, hybridization and data analysis of genomic DNA were performed according to the Agilent Technologies (Santa Clara, CA) protocol version 6.0 for 105 K arrays.

Organism:

Homo sapiens

Type:

Genome variation profiling by genome tiling array

Platform:

GPL9075

11 Samples

Download data: TXT

(Submitter supplied) Activation of the Ras/Erk pathway upregulates expression of the Kruppel-like Factor 5 (KLF5) transcription factor, and KLF5 is a downstream mediator of Ras oncogenic signaling. Specifically, in bladder and colon cancer cell lines KLF5 upregulates the Ras-pathway target gene cyclin D1, and facilitates entry into the S phase of the cell cycle. Ras mutations are common in lung cancer, but a role for KLF5 in lung tumorigenesis has not been defined. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

9 Samples

Download data: CEL

(Submitter supplied) From ~1,700 non-small cell lung cancer specimens collected at the MD Anderson Cancer Center over the years 1997 to 2005, we selected 914 tumors with detailed clinical and pathological information. We extracted RNA and DNA from frozen tissues using histology quality control from 700 cases. RNA was examined for quality using Agilent Bioanalyzer and RNA integrity number (RIN) was obtained for all specimens. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL6884

275 Samples

Download data: TXT

(Submitter supplied) We have developed cdk4/hTERT-immortalized normal human bronchial epithelial cells (HBECs) to study lung cancer pathogenesis. By studying the oncogenic effect of common lung cancer alterations (p53, KRAS, and c-MYC) we demonstrate the ability of this model to characterize the stepwise transformation of bronchial epithelial cells to full malignancy. Using HBECs derived from multiple individuals we found: 1) the combination of five genetic alterations (p53, KRASV12, c-MYC, CDK4 and hTERT) is sufficient for full tumorigenic conversion of HBECs; 2) high levels of KRASV12 are required for full malignant transformation of HBECs, however these levels also stimulate oncogene-induced senescence; 3) RAS-induced senescence is largely bypassed with loss of p53 function; 4) over-expression of c-MYC greatly enhances malignancy but only in the context of sh-p53+KRASV12; 5) HBECs from different individuals vary in their sensitivity to transformation by these oncogenic manipulations; 6) serum-induced epithelial-to-mesenchymal transition (EMT) increases in vivo tumorigenicity; 7) genetically-identical clones of transformed HBECs exhibit pronounced differences in tumor growth, histology, and differentiation as well as sensitivity to standard platinum-based chemotherapies; and 8) an mRNA signature derived from tumorigenic and non-tumorigenic clones is predictive of outcome in lung cancer patients. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL10558

15 Samples

Download data: TXT

(Submitter supplied) 3 Cell lines from Apc, p53 (AP) GEMMs were compared to 12 cell lines from Apc, Kras, p53 (AKP) GEMMs. Mouse 430 2.0 arrays were used to determine genomic expression differences between the two genotypes (AP and AKP).

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

15 Samples

Download data: CEL, TXT

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

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL25483

24 Samples

Download data: CEL

(Submitter supplied) HOXC10 overexpression modifies the therapeutic response to combined MEK and BRD4 inhibitors We performed microarray analysis of cells expressing LACZ or HOXC10 treated with MEK and BRD4 inhibition in combination for 24 hours, prior to the induction of cell death, to analyze transcriptional changes that might be mechanistic drivers of the therapeutic effect.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL25483

12 Samples

Download data: CEL

(Submitter supplied) MEK and BRD4 inhibitors induce cell death of subset of KRAS-mutant lung tumors in vitro and in vivo We performed microarray analysis of MEK and BRD4 inhibition alone and in combination 24 hours after treatment, prior to the induction of cell death, to analyze transcriptional changes that might be mechanistic drivers of the therapeutic effect

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL25483

12 Samples

Download data: CEL

(Submitter supplied) Lung cancer is the leading cause of cancer deaths. Tumor heterogeneity, which hampers development of targeted therapies, was herein deconvoluted via single cell RNA sequencing in aggressive human adenocarcinomas (carrying Kras-mutations) and comparable murine model. We identified a tumor-specific, mutant-KRAS-associated subpopulation which is conserved in both human and murine lung cancer. We previously reported a key role for the oncogene BMI-1 in adenocarcinomas. more...

Organism:

Homo sapiens; Mus musculus

Type:

Expression profiling by high throughput sequencing

Platforms:

GPL18573 GPL24268 GPL27138

31 Samples

Download data: CSV, TSV, TXT

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

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing; Non-coding RNA profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL18573

39 Samples

Download data: BED, BW

(Submitter supplied) By integrating chromatin and transcriptome analyses of ChIp-seq and Cap Analysis of Gene Expression sequencing (CAGE-seq), we showed that the presence of an active promoter and an enhancer at the KIMAT1 and HIF1A-As2 promoter region.

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL18573

3 Samples

Download data: BED, BW

(Submitter supplied) In our study, we valided the important oncogeneic roles of KIMAT1 and HIF1A-As2 in non-small cell lung cancer. We used custom designed GapmeRs to silence the KIMAT1 and HIF1A-As2 in H1299 and performed small RNA-seq. 214 and 233 microRNAs were regulated by KIMAT1 and HIF1A-As2, respectively.

Organism:

Homo sapiens

Type:

Non-coding RNA profiling by high throughput sequencing

Platform:

GPL18573

9 Samples

Download data: XLSX