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Links from GEO DataSets

Items: 18

1.

Cancer-stromal cell interactions in breast cancer brain metastases induce glycocalyx-mediated resistance to HER2-targeting therapies [ATAC-seq]

(Submitter supplied) In a 3D coculture with stroma cells derived from breast cancer patients’ brain metastasis, HER2+ breast cancer cells were protected from HER2-targeted therapies, particularly the EGFR/HER2 small molecule inhibitor neratinib. To get insight into how this protection arises, ATAC-seq on coculture cells with or without neratinib as performed.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
24 Samples
Download data: BW
Series
Accession:
GSE249459
ID:
200249459
2.

Cancer-stromal cell interactions in breast cancer brain metastases induce glycocalyx-mediated resistance to HER2-targeting therapies

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platform:
GPL18573
64 Samples
Download data: BW
Series
Accession:
GSE249574
ID:
200249574
3.

Cancer-stromal cell interactions in breast cancer brain metastases induce glycocalyx-mediated resistance to HER2-targeting therapies [RNA-seq]

(Submitter supplied) In a 3D coculture with stroma cells derived from breast cancer patients’ brain metastasis, HER2+ breast cancer cells were protected from HER2-targeted therapies, particularly the EGFR/HER2 small molecule inhibitor neratinib. To get insight into how this protection arises, a Synthetic Notch (SynNotch) reporter model allowed to study the effect of direct contact between stroma and cancer cells.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
40 Samples
Download data: CSV
Series
Accession:
GSE249573
ID:
200249573
4.

A BRCA1 Deficient-Like Signature is Enriched in Breast Cancer Brain Metastases

(Submitter supplied) Purpose: There is an unmet clinical need for biomarkers to identify breast cancer patients who are at increased risk of developing brain metastases. The objective is to identify gene signatures and biological pathways associated with HER2+ brain metastasis. Experimental Design: Gene expression of 19 HER2+ breast cancer brain metastases was compared with HER2+ nonmetastatic primary tumors. Gene Set Enrichment Analysis was used to identify a signature, which was evaluated for correlation with BRCA1 mutation status and clinical outcome using published microarray datasets and for correlation with pharmacological inhibition by a PARP inhibitor and temozolomide using published microarray datasets of breast cancer cell lines. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS5306
Platform:
GPL1352
38 Samples
Download data: CEL
Series
Accession:
GSE43837
ID:
200043837
5.
Full record GDS5306

Human epidermal growth factor receptor 2-positive breast cancer brain metastases

Analysis of HER2+ breast cancer brain metastasis specimens and HER2+ nonmetastatic primary breast tumors. Samples were matched for patient age upon primary tumor detection and ER status of primary tumor. Results provide insight into the molecular basis of HER2+ breast cancer outgrowth in the brain.
Organism:
Homo sapiens
Type:
Expression profiling by array, count, 2 disease state, 38 other, 38 specimen, 2 tissue sets
Platform:
GPL1352
Series:
GSE43837
38 Samples
Download data: CEL
6.

RNAseq of parental and neratinib resistant 5637 and OVCAR8 cells with or withour neratinib treatment

(Submitter supplied) Pan-HER TKI neratinib has demonstrated clinical activity in patients with HER2-mutant cancers. However responses are heterogenoeus and not generally prolonged, suggesting de-novo and acquired resistance to neratinib. To study mechanisms of resistance to neratinib we generated neratinib resistant cells by gradual dose escalation until resistance was achieved and performed various analyses including RNAseq.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21290
24 Samples
Download data: TXT
7.

The 3D Genomic Landscape of Differential Response to EGFR/HER2 Inhibition in Endocrine-Resistant Breast Cancer

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Other; Expression profiling by high throughput sequencing
Platform:
GPL21290
24 Samples
Download data
Series
Accession:
GSE144380
ID:
200144380
8.

The 3D Genomic Landscape of Differential Response to EGFR/HER2 Inhibition in Endocrine-Resistant Breast Cancer [RNA-seq]

(Submitter supplied) Recent studies suggested that crosstalk between ERα and EGFR/HER2 pathways plays a critical role in mediating endocrine therapy resistance. Several targeting EGFR/HER2 signaling inhibitors including FDA-approved lapatinib and gefitinib as well as a novel dual tyrosine kinase inhibitor (TKI) sapitnib showed greater inhibitory efficacies. However, how a 3D chromatin landscape of the response to the inhibition to EGFR/HER2 pathway remains to be elucidated. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21290
18 Samples
Download data: TXT, XLSX
9.

The 3D Genomic Landscape of Differential Response to EGFR/HER2 Inhibition in Endocrine-Resistant Breast Cancer [HiC]

(Submitter supplied) Recent studies suggested that crosstalk between ERα and EGFR/HER2 pathways plays a critical role in mediating endocrine therapy resistance. Several targeting EGFR/HER2 signaling inhibitors including FDA-approved lapatinib and gefitinib as well as a novel dual tyrosine kinase inhibitor (TKI) sapitnib showed greater inhibitory efficacies. However, how a 3D chromatin landscape of the response to the inhibition to EGFR/HER2 pathway remains to be elucidated. more...
Organism:
Homo sapiens
Type:
Other
Platform:
GPL21290
6 Samples
Download data: XLSX
Series
Accession:
GSE144377
ID:
200144377
10.

Genome-wide chromatin interactions identify characteristic promoter-distal loops

(Submitter supplied) We developed a novel computational model, HiSIF (Hi-C Significant Interacting Fragments), which uses a Poisson Mixture Model (PMM) with a power-law decay background. We compared its performance to some existing programs with publicly available Hi-C data, and then applied it to in situ Hi-C data in breast cancer sensitive and resistant cells.
Organism:
Homo sapiens
Type:
Other
Platform:
GPL21290
4 Samples
Download data: TXT
Series
Accession:
GSE128676
ID:
200128676
11.

Breast cancer mutations HER2V777L and PIK3CAH1047R activate the p21-CDK4/6 –Cyclin D1 axis driving tumorigenesis and drug resistance.

(Submitter supplied) In metastatic breast cancer, HER2 activating mutations frequently co-occur with mutations in the PIK3CA, TP53, or E-cadherin genes. Of these co-occurring mutations, HER2 and PIK3CA mutations are the most prevalent gene pair, with approximately 40% of HER2 mutated breast cancers also having activating mutations in PIK3CA. To study the effects of co-occurring HER2 and PIK3CA mutations, we bred genetically engineered mice with the HER2V777L; PIK3CAH1047R transgenes (HP mice) and studied the resulting breast cancers both in vivo as well as ex vivo using cancer organoids.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
16 Samples
Download data: CSV, TSV
Series
Accession:
GSE216871
ID:
200216871
12.

Transcriptome analysis of patient-derived xenograft models of HER2+ breast cancer brain metastases

(Submitter supplied) To gain insights into tumor heterogeneity in anti-cancer drug responses of patient-derived xenograft models of HER2+ breast cancer brain metastases, we performed transcriptome gene expression profiling by Ion AmpliSeq™ Transcriptome sequencing that targets more than 20,000 human genes. Our data found that all anti-cancer drugs responders have significantly higher expression levels of AKT-mTOR-dependent signature genes as compared to the non-responders, suggesting that most HER2+ breast cancer brain metastases are depend on the AKT-mTOR pathway
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17303
10 Samples
Download data: XLS
13.

Divergent resistance mechanisms to HER2-targeted therapies in breast cancer

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome variation profiling by high throughput sequencing
Platforms:
GPL18573 GPL19415
64 Samples
Download data: CSV, TXT
Series
Accession:
GSE161423
ID:
200161423
14.

Divergent resistance mechanisms to HER2-targeted therapies in breast cancer (scRNA-Seq)

(Submitter supplied) Divergent resistance mechanisms to HER2-targeted therapies in breast cancer
Organism:
Mus musculus; Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19415
4 Samples
Download data: CSV, H5
Series
Accession:
GSE161422
ID:
200161422
15.

Divergent resistance mechanisms to HER2-targeted therapies in breast cancer (bulkRNA-Seq and Exome-Seq)

(Submitter supplied) Divergent resistance mechanisms to HER2-targeted therapies in breast cancer
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome variation profiling by high throughput sequencing
Platform:
GPL18573
60 Samples
Download data: TSV, TXT
16.

SNP arrays of BT474 Latpatinib and/or Trastuzumab resistant cell lines for copy number analysis.

(Submitter supplied) Targeting HER2 with lapatinib (L), trastuzumab (T), or the LT combination, is effective in HER2+ breast cancer (BC), but de novo and acquired resistance commonly occur. The purpose of this experiment was to investigate the somatic alterations found in Lapatinib and/or Trastuzumab resistant cells lines.
Organism:
Homo sapiens
Type:
Genome variation profiling by SNP array; SNP genotyping by SNP array
Platform:
GPL16104
4 Samples
Download data: TXT
Series
Accession:
GSE83608
ID:
200083608
17.

RNA-Seq analysis of estrogen-deprived MM134 HER2WT and HER2L755S cells

(Submitter supplied) We conducted RNA sequencing of MM134 lobular cell line expressing HER2 WT and L755S cells grown in low estrogen conditions followed by Gene Set Enrichment Analysis (GSEA) to identify altered gene expression pathways in L755S cells. mTOR (also called MTORC1) signaling was the top significantly up-regulated pathway in HER2 L755S cells as compared to HER2 WT cells
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
4 Samples
Download data: RESULTS
Series
Accession:
GSE197952
ID:
200197952
18.

MUC1 triggers lineage plasticity of Her2 positive mammary tumor

(Submitter supplied) The aberrant overexpression of mucin 1 (MUC1) and human epidermal growth factor receptor 2 (HER2) are often observed in breast cancer. However, the role of concomitant of MUC1/HERR2 in the development of breast cancer has not been fully illustrated. Following analysis public microarray datasets that revealed a correlation of double positive of MUC1 and HER2 to a worse clinical outcome, we generated a mouse model overexpressing both Her2 and MUC1 cytoplasmic domain (MUC1-CD) to investigate their interaction in mammary carcinogenesis. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL15887
12 Samples
Download data: PAIR
Series
Accession:
GSE198239
ID:
200198239
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