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Links from GEO DataSets

Items: 20

1.

Therapeutic efficacy of INX-315, a selective CDK2 inhibitor, in solid tumors [MCF7 ATACseq]

(Submitter supplied) We performed the Assay for Transposase-Accessible Chromatin with Sequencing (ATAC-Seq) on (i) parental MCF7 cells treated with control vehicle or abemaciclib (ii) abemaciclib- and abemaciclib/fulvestrant-resistant cells treated with control vehicle or INX-315.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
16 Samples
Download data: BW, NARROWPEAK
Series
Accession:
GSE243147
ID:
200243147
2.

Therapeutic efficacy of INX-315, a selective CDK2 inhibitor, in solid tumors

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL18573 GPL19057
130 Samples
Download data: BW
Series
Accession:
GSE243154
ID:
200243154
3.

Therapeutic efficacy of INX-315, a selective CDK2 inhibitor, in solid tumors [Gastric mouse (GA0103) RNAseq]

(Submitter supplied) We performed RNA sequencing on tumours harvested from GA0103 (gastric cancer) PDX treated for 40-50 days with either control vehicle or 100 mg/kg BID INX-315.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
8 Samples
Download data: CSV
Series
Accession:
GSE243153
ID:
200243153
4.

Therapeutic efficacy of INX-315, a selective CDK2 inhibitor, in solid tumors [OVCAR3 RNAseq]

(Submitter supplied) We performed RNA sequencing on OVCAR3 parental cells treated with either control vehicle for 4 days or 300 nM INX-315 for 7 days.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
6 Samples
Download data: CSV
Series
Accession:
GSE243152
ID:
200243152
5.

Therapeutic efficacy of INX-315, a selective CDK2 inhibitor, in solid tumors [OV5398PDX RNAseq]

(Submitter supplied) We performed RNA sequencing on tumors harvested from OV5398 (ovarian) PDX treated for 40-50 days with either control vehicle (PEG), 100 mg/kg BID INX-315 or 200 mg/kg QD INX315.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
11 Samples
Download data: CSV
Series
Accession:
GSE243151
ID:
200243151
6.

Therapeutic efficacy of INX-315, a selective CDK2 inhibitor, in solid tumors [MCF7 and T47D RNAseq]

(Submitter supplied) We performed RNA sequencing on T47D and MCF7 cells, both parental and abema- or abema/fulvestrant- resistant, treated with either control vehicle or 300 nM (MCF7) or 100 nM (T47D) INX-315 for 7 days
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
48 Samples
Download data: CSV
Series
Accession:
GSE243150
ID:
200243150
7.

Therapeutic efficacy of INX-315, a selective CDK2 inhibitor, in solid tumors [HER2mouse upfront RNAseq]

(Submitter supplied) We treated tumour-bearing MMTV-rtTA/tetO-HER2 female mice with either vehicle (veh), INX-315 (INX), Abemaciclib (LY) or both INX-315 and Abema in combination (LY.INX) for 7 days. Resistant tumors were collected and RNA sequencing performed
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
19 Samples
Download data: CSV
Series
Accession:
GSE243149
ID:
200243149
8.

Therapeutic efficacy of INX-315, a selective CDK2 inhibitor, in solid tumors [HER2mouse resistant RNAseq]

(Submitter supplied) We treated tumour-bearing MMTV-rtTA/tetO-HER2 female mice with 75 mg/kg Abemaciclib for ~4 weeks (or until point of resistance, where tumours have started to grow again). Mice were then divided into treatment groups, receiving vehicle (veh), INX-315 (INX), Abemaciclib (LY) or both INX-315 and Abema in combination (LY.INX). Resistant tumors were collected and RNA sequencing performed.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
22 Samples
Download data: CSV
Series
Accession:
GSE243148
ID:
200243148
9.

Expression data from LncRNA TROJAN knockdown breast cancer cells

(Submitter supplied) Background: Estrogen receptor-positive (ER+) breast cancers represent approximately two-thirds of all breast cancers and have a sustained risk of late disease recurrence. Cyclin-dependent kinase 4 and 6 (CDK4/6) inhibitors have shown significant efficacy in ER+ breast cancer. However, their effects are still limited by drug resistance. In this study, we aim to explore the role of long noncoding RNA TROJAN in ER+ breast cancer. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL17586
3 Samples
Download data: CEL
Series
Accession:
GSE148858
ID:
200148858
10.

Microarray gene expression data from MCF-7 and LetR cells

(Submitter supplied) Resistance to aromatase inhibitor (AI) treatment and combined CDK4/6 inhibitor (CDK4/6i) and endocrine therapy (ET) are crucial clinical challenges in treating estrogen receptor-positive (ER+) breast cancer. Understanding the resistance mechanisms and identifying reliable predictive biomarkers and novel treatment combinations to overcome resistance are urgently needed. Herein, we show that upregulation of CDK6, p-CDK2, and/or cyclin E1 is associated with adaptation and resistance to AI-monotherapy and combined CDK4/6i and ET in ER+ advanced breast cancer. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL17586
9 Samples
Download data: CEL, TXT, XLSX
Series
Accession:
GSE210399
ID:
200210399
11.

High CDK6 protects cells from fulvestrant-mediated apoptosis and is a predictor of resistance to fulvestrant in estrogen receptor-positive metastatic breast cancer

(Submitter supplied) Purpose: Resistance to endocrine therapy in estrogen receptor-positive (ER+) breast cancer remains a major clinical problem. Recently, the CDK4/6 inhibitor palbociclib combined with letrozole was approved for treatment of ER+ advanced breast cancer, and other CDK4/6 inhibitors are being investigated in combination with different endocrine treatments. However, the role of CDK4/6 in endocrine resistance and their potential as predictive biomarkers of endocrine treatment response remains undefined. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
26 Samples
Download data: CEL
Series
Accession:
GSE74391
ID:
200074391
12.

Gene expression and copy number analysis of OVCAR-3 and CDK2 resistant sublines

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Genome variation profiling by SNP array; Expression profiling by array
Platforms:
GPL6244 GPL13135
20 Samples
Download data: CEL, TXT
Series
Accession:
GSE48921
ID:
200048921
13.

Copy number analysis of OVCAR-3 and CDK2 resistant sublines

(Submitter supplied) Cyclin E1 (CCNE1) is amplified in various tumor types including high-grade serous ovarian cancer where it is associated with poor clinical outcome. We have demonstrate that suppression of the Cyclin E1 partner kinase, CDK2, induces apoptosis in a CCNE1 amplicon-dependent manner. Little is known of mechanisms of resistance to CDK inhibitors. We therefore generated OVCAR-3 sublines with reduced sensitivity to CDK2 inhibitors and profiled by SNP copy number microarrays.
Organism:
Homo sapiens
Type:
Genome variation profiling by SNP array
Platform:
GPL13135
6 Samples
Download data: TXT
Series
Accession:
GSE48920
ID:
200048920
14.

Gene expression analysis of OVCAR-3 and CDK2 resistant sublines

(Submitter supplied) Cyclin E1 (CCNE1) is amplified in various tumor types including high-grade serous ovarian cancer where it is associated with poor clinical outcome. We have demonstrate that suppression of the Cyclin E1 partner kinase, CDK2, induces apoptosis in a CCNE1 amplicon-dependent manner. Little is known of mechanisms of resistance to CDK inhibitors. We therefore generated OVCAR-3 sublines with reduced sensitivity to CDK2 inhibitors and profiled by gene expression microarrays.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6244
14 Samples
Download data: CEL
Series
Accession:
GSE48919
ID:
200048919
15.

Gene expression analyses of palbociclib treated ER+ breast cancer cell lines as assessed by RNA-seq

(Submitter supplied) The goal of this study is to measure gene expression changes resulting over time of palbociclib treatment of T47D, MCF7, and CAMA1 ER+ breast cancer cell lines.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
15 Samples
Download data: XLSX
16.

CDK4 phosphorylation status and rational use for combining CDK4/6 and BRAF/MEK inhibition in advanced thyroid carcinomas

(Submitter supplied) Despite overall good prognosis associated to thyroid cancer, poorly differentiated carcinomas (PDTC) and anaplastic carcinomas (ATC) represent major clinical challenges. We have shown that the presence of active T172-phosphorylated CDK4 predicts sensitivity to CDK4/6 inhibitory drugs (CDK4/6i) including palbociclib. Here, CDK4 phosphorylation was detected in all well-differentiated thyoid carcinomas (n=29), 19/20 PDTC, 16/23 ATC, and 18/21 thyroid cancer cell lines including 11 ATC-derived ones. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
16 Samples
Download data: TXT
Series
Accession:
GSE235468
ID:
200235468
17.

Estrogen receptor ChIP-seq in response to mTOR inhibition

(Submitter supplied) We have used ChIP-seq to profile binding of the estrogen receptor (ER) to chromatin in response to two mTOR inhibitors, i.e. everolimus (RAD001) and vistusertib (AZD2014). Two hours of treatment with these inhibitors significantly affected mTOR signaling, but surprisingly did not affect binding of ER to chromatin. This suggests that these mTOR inhibitors work through largely ER-independent mechanisms.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
24 Samples
Download data: NARROWPEAK
Series
Accession:
GSE103023
ID:
200103023
18.

Inhibition of CK1e potentiates the therapeutic efficacy of CDK4/6 inhibitor in breast cancer

(Submitter supplied) In this study, we found that combination treatment of breast cells with CK1 inihbitor (D 4476) and CDK4/6 inhibitor (Ribociclib) exhibited greatly enhanced therapeutic efficacy than CDK4/6 inhiitor single treatment
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
9 Samples
Download data: XLSX
19.

Expression data from primary breast tumors (Auckland)

(Submitter supplied) Frozen tissue specimens from primary breast tumors were collected and profiled using Affymetrix U133 plus 2 expression microarrays. A publication describing the generation of these data is not yet available. However, these data can be used alongside other Affymetrix breast tumour data sets to form large meta-cohorts for breast cancer research, as was done in Lasham et. al. J Natl Cancer Inst. 2012 Jan 18;104(2):133-146.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
107 Samples
Download data: CEL
Series
Accession:
GSE36771
ID:
200036771
20.

Unveiling the differential Senescence Phenotypes of MCF7 Cells Treated with Diverse Therapeutic Agents: A Comprehensive Transcriptome Analysis

(Submitter supplied) Therapeutic drugs are commonly used for treatment various cancers. However, despite to this purpose, Cancer treated by drugs undergoes senescence phenotypes and is known to acquire more aggressive ability. Futhermore, senescence can be induced vairous type of drug via differential mechanisms. Therefore, we analyzed to validate differential charateristics of senescence phenotypes compare between drugs.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL30209
12 Samples
Download data: XLSX
Series
Accession:
GSE229264
ID:
200229264
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