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Links from GEO DataSets

Items: 10

1.
Full record GDS5029

SW480 KRAS-mutant colorectal cancer cell line response to dual inhibition of tankyrase and MEK: time course

Analysis of SW480 cancer cells treated with tankyrase inhibitor, MEK inhibitor, or both, for up to 16hrs. Dual inhibition of TNKS and MEK led to tumor regression. Results provide insight into molecular mechanisms underlying the synergistic effects of TNKS and MEK inhibitors in KRAS-mutant cancers.
Organism:
Homo sapiens
Type:
Expression profiling by array, count, 5 protocol, 3 time sets
Platform:
GPL570
Series:
GSE55624
18 Samples
Download data: CEL
DataSet
Accession:
GDS5029
ID:
5029
2.

Inhibiting tankyrases sensitizes KRAS mutant cancer cells to MEK inhibitors by FGFR2 feedback signaling

(Submitter supplied) Tankyrases (TNKS) play roles in Wnt signaling, telomere homeostasis and mitosis, offering attractive targets for anti-cancer treatment. Using unbiased combination screening in a large panel of cancer cell lines, we have identified a strong synergy between TNKS and MEK inhibitors in KRAS mutant cancer cells. Our study uncovers a novel function of TNKS in the relief of a feedback loop induced by MEK inhibition on FGFR2 signaling pathway. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS5029
Platform:
GPL570
18 Samples
Download data: CEL
Series
Accession:
GSE55624
ID:
200055624
3.

Epithelial-to-mesenchymal transition defines feedback activation of receptor tyrosine kinase signaling induced by MEK inhibition in KRAS mutant lung cancer

(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
Series
Accession:
GSE79235
ID:
200079235
4.

Synergistic activity and heterogeneous acquired resistance of combined MDM2 and MEK inhibition in KRAS mutant cancers

(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
5.

Transcriptomic analysis of T84 colon carcinoma cell line treated with trametinib, JQ1 or their combination

(Submitter supplied) T84 cells were treated with DMSO, 30nM trametinib (MEKi), 1µM JQ1 (BRD4i) or the combination of trametinib and JQ1 (combo) for 24h.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
12 Samples
Download data: XLSX
6.

Transcriptomic analysis of trametinib-resistant HCT116 colorectal carcinoma cells compared to the parental control cells

(Submitter supplied) HCT116 cells were treated with with increasing concentrations of trametinib over 2 months. Drug-resistant clones emerged and were cultured in the presence of 30 nmol/L trametinib. These cells exhibited a greater than 10-fold increase in the GI50 for trametinib compared to the parental cell line. RNA-seq of the resistant clone HCT116_R4 versus the parental cells identified differentially expressed genes potentially involved in resistance.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
6 Samples
Download data: TXT, XLSX
7.

4 NSCLC cell lines treated with GDC-0973, AZ-628 or a combination of both

(Submitter supplied) RNA was purified cancer cell lines. The "SAMPLE_ID" sample characteristic is a sample identifier internal to Genentech. The ID of this project in Genentech's ExpressionPlot database is PRJ0013114
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
48 Samples
Download data: TSV
Series
Accession:
GSE108464
ID:
200108464
8.

RNA-seq analysis of human pancreas cell line SU8686 treated with DOT1L inhibitor (SGC0946) or DMSO

(Submitter supplied) To understand the pathway alteration associated with DOT1L inhibition, we performed RNA-seq analysis of DOT1L inhibitor treated human pancreas cell line SU8686. We reported the changed pathways.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
6 Samples
Download data: XLS
Series
Accession:
GSE139070
ID:
200139070
9.

Combined MEKi (GDC-0973) and WNT (G007-LK) treatment in APC and KRAS mutant HCT-15 cell line

(Submitter supplied) We report RNAseq data from HCT-15 cells were treated wih control(DMSO), GDC-0973, G007-LK and combined GDC-0973 and G007-LK treatmetn for 24 hours.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
12 Samples
Download data: TXT
10.

RUNX2/CBFB modulates the response to MEK inhibitors through activation of receptor tyrosine kinases in KRAS mutant colorectal cancer

(Submitter supplied) Investigation of the transcriptional consequences of RUNX2 and CBFB loss in the presence and absence of the MEK inhibitor selumetinib in LoVo ERN1 knockout KRAS mutant colorectal cancer cells.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
6 Samples
Download data: TSV
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