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Links from GEO DataSets

Items: 18

1.

Multi-treatment models for breast cancer

(Submitter supplied) RNA seq analysis of multiple treatments and their effects on in vitro breast cancer models
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
24 Samples
Download data: CSV, TXT
2.

Combined Targeting of Estrogen Receptor alpha and XPO1 prevent Akt activation, remodel metabolic pathways and induce autophagy to overcome tamoxifen resistance

(Submitter supplied) Majority of breast cancer specific deaths in women with ERα (+) tumor occur due to metastases that are resistant to endocrine therapy. There is a critical need for novel therapeutic approaches to resensitize recurrent ERα (+) tumors to endocrine therapies. The objective of this study was to elucidate mechanisms of improved effectiveness of combined targeting of ERα and XPO1, a nuclear transport protein in overcoming endocrine resistance. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
12 Samples
Download data: TXT
3.

NAD+ Metabolism Generates a Metabolic Vulnerability in Endocrine-Resistant Metastatic Breast Tumors

(Submitter supplied) Approximately 70% of human breast cancers express estrogen receptor-α (ERα), providing a potential target for endocrine therapy. However, 30%–40% of patients with ER+ breast cancer still experience recurrence and metastasis, with a 5-year relative overall survival rate of 24%. In this study, we identified NAMPT, an important enzyme in nicotinamide adenine dinucleotide (NAD+) metabolism, to be increased in metastatic breast cancer (MBC) cells treated with Fulv. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
28 Samples
Download data: TXT
Series
Accession:
GSE233062
ID:
200233062
4.

Targeting Metabolic Adaptations in the Breast Cancer–Liver Metastatic Niche Using Dietary Approaches to Improve Endocrine Therapy Efficacy

(Submitter supplied) Estrogen receptor–positive (ERþ) metastatic tumors contribute to nearly 70% of breast cancer–related deaths. Most patients with ERþ metastatic breast cancer (MBC) undergo treatment with the estrogen receptor antagonist fulvestrant as standard of care. Yet, among such patients, metastasis in liver is associated with reduced overall survival compared with other metastasis sites. The factors underlying the reduced responsiveness of liver metastases to ER targeting agents remain unknown, impeding the development of more effective treatment approaches to improve outcomes for patients with ERþ liver metastases. more...
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL25526
4 Samples
Download data: CSV, JPG, JSON, MTX, PNG, TIFF, TSV
Series
Accession:
GSE236681
ID:
200236681
5.

Targeting metabolic adaptations in the breast cancer–liver metastatic niche using dietary approaches to improve endocrine therapy efficacy

(Submitter supplied) Estrogen receptor-positive (ER+) metastatic tumors contribute to nearly 70% of breast cancer-related deaths. Most patients with ER+ metastatic breast cancer (MBC) undergo treatment with the estrogen receptor agonist fulvestrant (Fulv) as standard of care. Yet, among such patients, metastasis in liver is associated with reduced overall survival compared to other metastasis sites. The factors underlying the reduced responsiveness of liver metastases to ER agonists remain unknown, impeding the development of more effective treatment approaches to improve outcomes for patients with ER+ liver metastases. more...
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL11154 GPL16512
44 Samples
Download data: BW, CSV, TXT
Series
Accession:
GSE184156
ID:
200184156
6.

RNA-seq analysis of ESR1 mutations in T47D and MCF7 cell lines

(Submitter supplied) Purpose: Transcriptome analysis of ESR1 mutant cells was performed via sequencing total RNA in T47D and MCF7 cell lines containing Y537S and D538G mutations.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
48 Samples
Download data: CSV
7.

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
8.

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
9.

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
10.

Effect of tamoxifen on early gene expression in T47D and MDA-MB-231 cells

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
6 Samples
Download data: CEL
Series
Accession:
GSE60882
ID:
200060882
11.

Effect of tamoxifen on early gene expression in MDA-MB-231 cells

(Submitter supplied) Tamoxifen is the treatment of choice in estrogen receptor alpha breast cancer patients. However, ~50% of ERα-positive tumors exhibit intrinsic or rapidly acquire resistance to endocrine treatment, requiring chemotherapy. Ιt has been difficult to predict de novo resistance to endocrine therapy and/or assess the likelihood of early relapse, while no concrete mechanism regulating the acquisition and the maintenance of endocrine resistance has been identified. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
3 Samples
Download data: CEL
Series
Accession:
GSE60879
ID:
200060879
12.

Effect of tamoxifen on early gene expression in T47D cells

(Submitter supplied) Tamoxifen is the treatment of choice in estrogen receptor alpha breast cancer patients. However, ~50% of ERα-positive tumors exhibit intrinsic or rapidly acquire resistance to endocrine treatment, requiring chemotherapy. Ιt has been difficult to predict de novo resistance to endocrine therapy and/or assess the likelihood of early relapse, while no concrete mechanism regulating the acquisition and the maintenance of endocrine resistance has been identified. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
3 Samples
Download data: CEL
Series
Accession:
GSE60878
ID:
200060878
13.

Heat Shock Factor 1 (HSF1) regulates ESR1 action in breast cancer

(Submitter supplied) Heat shock factor 1 (HSF1) is a key regulator of transcriptional responses to proteotoxic stress. It has been recently linked to signaling of estrogen via ESR1. To study the cooperation of HSF1 and ESR1 in the transcriptional response to estrogen, we established estrogen receptor (ER)-positive breast cancer cell lines with reduced HSF1 levels using specific shRNA or CRISPR/Cas9 approach. HSF1 deficiency led to the inhibition of the mitogenic effect of estrogen in MCF7 and T47D cells. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18460
12 Samples
Download data: TXT
14.

Heat Shock Factor 1 (HSF1) supports the ESR1 action in breast cancer

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18460
28 Samples
Download data: BED, TXT
Series
Accession:
GSE159803
ID:
200159803
15.

Heat Shock Factor 1 (HSF1) supports the ESR1 action in breast cancer (RNA-seq)

(Submitter supplied) Heat shock factor 1 (HSF1) is a key regulator of transcriptional responses to proteotoxic stress. It has been recently linked to signaling of estrogen via ESR1. To study the cooperation of HSF1 and ESR1 in the transcriptional response to estrogen, we established estrogen receptor (ER)-positive breast cancer cell lines with reduced HSF1 levels using specific shRNA or CRISPR/Cas9 approach. HSF1 deficiency led to the inhibition of the mitogenic effect of estrogen in MCF7 and T47D cells. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18460
18 Samples
Download data: TXT
16.

Heat Shock Factor 1 (HSF1) supports the ESR1 action in breast cancer (ChIP-seq)

(Submitter supplied) Heat shock factor 1 (HSF1) is a key regulator of transcriptional responses to proteotoxic stress. It has been recently linked to signaling of estrogen via ESR1. To study the cooperation of HSF1 and ESR1 in the transcriptional response to estrogen, we established estrogen receptor (ER)-positive breast cancer cell lines with reduced HSF1 levels using specific shRNA or CRISPR/Cas9 approach. HSF1 deficiency led to the inhibition of the mitogenic effect of estrogen in MCF7 and T47D cells. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18460
10 Samples
Download data: BED, TXT
Series
Accession:
GSE159724
ID:
200159724
17.

Expression data from age-dichotomized ER+, N0 breast tumors

(Submitter supplied) Signaling pathways that converge on two different transcription factor complexes, NFκB and AP-1, have been identified in estrogen receptor (ER)-positive breast cancers resistant to the antiestrogen, tamoxifen. In this study, biomarkers co-ordinately up-regulated by NFKB and AP-1 with prognositic significance are identified in a largely TAM-treated set of ER+ node negative breast cancers. The prognostic value with respect to age is also investigated. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL4685
54 Samples
Download data: CEL
Series
Accession:
GSE7378
ID:
200007378
18.

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
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