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Links from GEO DataSets

Items: 20

1.

Expression data from MCF7 wt and MCF7/HER2-18 xenografts

(Submitter supplied) To investigate molecular mechanisms of resistance, we used two different in vivo xenograft models of estrogen receptor-positive (ER+) breast cancer, with or without HER2 over-expression (MCF7/HER2-18 and MCF7 wt, respectively). Mice with established tumors were assigned to the following treatment groups: continued estrogen supplementation (E2), estrogen deprivation (ED), ED plus tamoxifen (Tam), all with or without the EGFR tyrosine kinase inhibitor gefinitinib (G). more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
65 Samples
Download data: CEL
Series
Accession:
GSE8141
ID:
200008141
2.

Expression data from MCF7 wt xenografts

(Submitter supplied) To investigate molecular mechanisms of resistance, we used two different in vivo xenograft models of estrogen receptor-positive (ER+) breast cancer, with or without HER2 over-expression (MCF7/HER2-18 and MCF7 wt, respectively). Mice with established tumors were assigned to the following treatment groups: continued estrogen supplementation (E2), estrogen deprivation (ED), ED plus tamoxifen (Tam), all with or without the EGFR tyrosine kinase inhibitor gefinitinib (G). more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
14 Samples
Download data: CEL, XLS
Series
Accession:
GSE8140
ID:
200008140
3.

Expression data from MCF7/HER2-18 xenografts

(Submitter supplied) To investigate molecular mechanisms of resistance, we used two different in vivo xenograft models of estrogen receptor-positive (ER+) breast cancer, with or without HER2 over-expression (MCF7/HER2-18 and MCF7 wt, respectively). Mice with established tumors were assigned to the following treatment groups: continued estrogen supplementation (E2), estrogen deprivation (ED), ED plus tamoxifen (Tam), all with or without the EGFR tyrosine kinase inhibitor gefinitinib (G). more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
51 Samples
Download data: CEL, TXT
Series
Accession:
GSE8139
ID:
200008139
4.

Expression data from MCF7 xenografts

(Submitter supplied) In order to help determine the genes involved in resistance of breast cancer to endocrine therapy, we compared global gene expression profiles of tamoxifen-resistant MCF-7 WT xenograft tumors with E2-supplemented tumors. Keywords: two group comparison
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
7 Samples
Download data: CEL
Series
Accession:
GSE7327
ID:
200007327
5.

Gene expression profiles of PDX models with acquired resistance to endocrine treatments

(Submitter supplied) Acquired resistance to endocrine therapy occurs with high frequency in patients with luminal breast cancer (LBC). We report here the establishment of four patient-derived xenograft models of LBC with acquired resistance in vivo to tamoxifen and estrogen deprivation.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL11532
30 Samples
Download data: CEL
Series
Accession:
GSE55561
ID:
200055561
6.

Gene expression profiling of breast cancer cells with knockdown of PTEN

(Submitter supplied) Activation of the PI3K pathway in estrogen receptor α (ER)-positive (+) breast cancer is associated with reduced ER expression and activity, luminal B subtype, and poor outcome. PTEN is a negative regulator of the PI3K pathway typically lost in ER-negative (-) breast cancer. To clarify the effect of PTEN down-regulation on the response of ER+/HER2- breast cancer to endocrine therapy, we established reduced PTEN cell models using inducible knockdown. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL9052
2 Samples
Download data: FPKM_TRACKING
7.

AKT antagonist AZD5363 influences estrogen receptor function in endocrine resistant breast cancer and synergizes with fulvestrant (ICI182780) in vivo

(Submitter supplied) Phosphoinositide-3-kinase/protein-kinaseB/mammalian target of rapamycin (PI3K/AKT/mTOR) signalling plays an important role in breast cancer (BC). Its interaction with estrogen receptor (ER) signalling becomes more complex and inter-dependent with acquired endocrine resistance. Targeting mTOR combined with endocrine therapy has shown clinical utility, however, a negative feedback-loop exists downstream of PI3K/AKT/mTOR. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10558
12 Samples
Download data: TXT
Series
Accession:
GSE69893
ID:
200069893
8.

HOXB7 is an ERα cofactor in the activation of HER2 and multiple ER target genes leading to endocrine resistance

(Submitter supplied) Why breast cancers become resistant to tamoxifen despite continued expression of the estrogen receptor alpha (ERα) and what factors are responsible for high HER2 expression in these tumors remains an enigma. HOXB7 ChIP analysis followed by validation showed that HOXB7 physically interacts with ERα, and that the HOXB7-ERα complex enhances transcription of many ERα target genes including HER2. Investigating strategies for controlling HOXB7, our studies revealed that MYC, stabilized via phosphorylation mediated by EGFR-HER2 signaling, inhibits transcription of miRNA-196a, a HOXB7 repressor. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10558
4 Samples
Download data: TXT
Series
Accession:
GSE63607
ID:
200063607
9.

Time-resolved DNA methylation profiling of endocrine resistance in the T47D luminal A breast cancer cell line

(Submitter supplied) Endocrine therapy is the most used treatment for hormone receptor positive breast cancers. Despite the clear benefit of endocrine therapy for patients with ER+ breast cancer, resistance to treatment is a critical clinical issue affecting a large number of patients. While many studies have shown that genetics is an important factor in therapy resistance, recent publications have also reported that epigenetics might play a major role in the acquisition of resistance to endocrine therapies. more...
Organism:
Homo sapiens
Type:
Methylation profiling by genome tiling array
Platform:
GPL21145
40 Samples
Download data: TXT
Series
Accession:
GSE154626
ID:
200154626
10.

Antisense miRNA-221/222 (si221/222) and control inhibitor (GFP) treated fulvestrant-resistant breast cancer cells

(Submitter supplied) Full title: Expression data from antisense miRNA-221/222 (si221/222) and control inhibitor (GFP) treated fulvestrant-resistant breast cancer cells The expression of miR-221/222 were found to be upregulated in fulvestrant resistant breast cancer cells MCF7-FR compared to its drug-sensitive counterpart MCF7. To investigate the role of miR-221/222 in acquired resistance to fulvestrant, we lowered the level of miR-221/222 in MCF7-FR cells using miRNA inhibitors (antagomirs), and compared gene expression profiles before and after treatment.
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS4054
Platform:
GPL570
9 Samples
Download data: CEL
Series
Accession:
GSE19777
ID:
200019777
11.
Full record GDS4054

microRNA-221/222 knockdown effect on fulvestrant-resistant MCF7 breast cancer cells

Analysis of fulvestrant-resistant MCF7 cells transfected with antisense miRNA inhibitors targeting miR-221 and miR-222. miR-221/222 knockdown inhibits cell proliferation in fulvestrant-resistant MCF7-F cells. Results provide insight into the role of miR-221/222 in acquired resistance to fulvestrant.
Organism:
Homo sapiens
Type:
Expression profiling by array, transformed count, 3 genotype/variation sets
Platform:
GPL570
Series:
GSE19777
9 Samples
Download data: CEL
12.

Effect of MEL-18 knockdown on estrogen-sensitive MCF7 breast cancer cells

(Submitter supplied) Gene expression analysis of MEL-18-silenced MCF7 cell lines. MEL-18 is a component of the polycomb repressive complex (PRC)-1, which is a critical epigenetic modulator of stem cell regulation and normal and cancerous development. Accumulating studies have suggested that MEL-18 might act as a tumor suppressor in several human tumors, including breast cancer. Results provide insight into the functional role of MEL-18 in estrogen-dependent breast cancer.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10558
4 Samples
Download data: TXT
Series
Accession:
GSE64716
ID:
200064716
13.

RNA interference screening identifies the Insulin/IGF-1 receptor pathway as a mechanism of escape from hormone dependence in breast cancer

(Submitter supplied) A significant fraction of breast cancers exhibit de novo or acquired resistance to estrogen deprivation. A kinome-wide siRNA screen identified a role for Insulin Receptor (InsR) in the hormone-independent growth of ER+ breast cancer cells We used gene expression microarrays to identify genes and pathways that are altered by insulin stimulation of ER+ MCF-7 human breast cancer cells.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL13158
9 Samples
Download data: CEL, CHP
Series
Accession:
GSE28580
ID:
200028580
14.

Acquired HER2 mutations in ER+ metastatic breast cancer confer resistance to ER-directed therapies

(Submitter supplied) Estrogen receptor positive (ER+) breast cancers that develop resistance to therapies that target the ER are the most common cause of breast cancer death. Beyond mutations in ER, which occur in 25-30% of patients treated with aromatase inhibitors (AIs), our understanding of clinical mechanisms of resistance to ER-directed therapies remains incomplete. We identified activating HER2 mutations in metastatic biopsies from eight patients with ER+ metastatic breast cancer who had developed resistance to ER-directed agents, including AIs, tamoxifen, and fulvestrant. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
864 Samples
Download data: TXT
Series
Accession:
GSE121411
ID:
200121411
15.

Under conditions of hormonal adjuvant treatment the estrogen receptor apoprotein supports breast cancer cell cycling through the retinoic acid receptor α1 apoprotein

(Submitter supplied) Under conditions of hormonal adjuvant treatment the estrogen receptor apoprotein supports breast cancer cell cycling through the retinoic acid receptor α1 apoprotein. Basal proliferation persisted in estrogen-sensitive breast cancer cells grown in hormone depleted conditioned media without or with 4-hydroxytamoxifen (OH-Tam). Downregulating ER using siRNA inhibited basal proliferation by promoting cell cycle arrest. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS4065
Platform:
GPL570
12 Samples
Download data: CEL
Series
Accession:
GSE26298
ID:
200026298
16.
Full record GDS4065

Effect of estrogen receptor- or retinoic acid receptor-knockdown on estrogen-sensitive MCF7 breast cancer cells

Analysis of MCF7 cells transfected with control siRNA, estrogen receptor α (ER) siRNA or retinoic acid receptor α (RARα) siRNA. Basal proliferation of MCF7 cells was diminished by knocking down ER or RARα. Results provided insight into the molecular basis of basal proliferation.
Organism:
Homo sapiens
Type:
Expression profiling by array, count, 2 agent, 3 dose, 3 genotype/variation sets
Platform:
GPL570
Series:
GSE26298
12 Samples
Download data: CEL
17.

Dynamic changes in gene expression in vivo predict prognosis of tamoxifen-treated patients with breast cancer

(Submitter supplied) Tamoxifen is the most widely prescribed anti-estrogen treatment for patients with ER-positive breast cancer. However, there is still a need for biomarkers that reliably predict endocrine sensitivity in breast cancers and these may well be expressed in a dynamic manner. In this study we assessed gene expression changes at multiple time points (days 1, 2, 4, 7, 14) after tamoxifen treatment in the ER-positive ZR-75-1 xenograft model that displays significant changes in apoptosis, proliferation and angiogenesis within 2 days of therapy. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL506
32 Samples
Download data: TXT
Series
Accession:
GSE22386
ID:
200022386
18.

Differences in the Transcriptional Response to Fulvestrant and Estrogen Deprivation in ER-Positive Breast Cancer

(Submitter supplied) Aromatase inhibitors are first-line postmenopausal agents for estrogen receptor alpha (ERa)-positive breast cancer. However, there is considerable response heterogeneity and women frequently relapse. Estrogen deprivation does not completely arrest ERa activity, and transactivation of the unliganded receptor may continue through cross-talk with growth factor pathways. In contrast with aromatase inhibitors, the selective ER downregulator fulvestrant also abrogates ligand-independent ERa activity. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6884
76 Samples
Download data: TXT
Series
Accession:
GSE71791
ID:
200071791
19.

Genome wide analysis of PAX2 chromatin interaction in MCF-7 cell

(Submitter supplied) The aim of the study is to understand the role of the transcription factor PAX2 in estrogen receptor positive breast cancer cell line by using ChIP-seq. MCF-7-PAX2 stable cells were cultured in full media and treated with doxycycline (50ng/ml) for 16 hours to induce overexpression of PAX2-HA protein. Then cells were treated with 4-OH-tamoxifen (1μM) for 6 hours. All 3 treatments (Veh, Dox, DoxTam) were performed in duplicates. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL18573 GPL9052
7 Samples
Download data: NARROWPEAK
Series
Accession:
GSE140060
ID:
200140060
20.

Genome wide analysis of transcripts regulated by PAX2 and Tamoxifen in MCF-7 cells

(Submitter supplied) The aim of the study is to understand the role of the transcription factor PAX2 in estrogen receptor positive breast cancer cell line by using GRO-seq. MCF-7-PAX2 stable cells were cultured in full media and treated with doxycycline (50ng/ml) for 16 hours to induce overexpression of PAX2. Then cells were treated with 4-OH-tamoxifen (1μM) for 6 hours. All 4 treatments (Veh, Tam, Dox, DoxTam) were performed in duplicates. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
8 Samples
Download data: TXT
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