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

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

PROVIDER: PRJNA1049733 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27128838_1.fastq.gz	Fastqsanger.gz
	SRR27128838_2.fastq.gz	Fastqsanger.gz
	SRR27128839_1.fastq.gz	Fastqsanger.gz
	SRR27128839_2.fastq.gz	Fastqsanger.gz
	SRR27128840_1.fastq.gz	Fastqsanger.gz

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

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

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

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

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

Project description: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.

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

Project description: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.

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Project description:Divergent resistance mechanisms to HER2-targeted therapies in breast cancer

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Project description: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

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Divergent resistance mechanisms to HER2-targeted therapies in breast cancer

Project description:Divergent resistance mechanisms to HER2-targeted therapies in breast cancer

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Project description:Divergent resistance mechanisms to HER2-targeted therapies in breast cancer

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

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

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

Project description: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. Results: A BRCA1 Deficient-Like (BD-L) gene signature is significantly correlated with HER2+ metastases in both our and an independent cohort. BD-L signature is enriched in BRCA1 mutation carrier primary tumors and HER2-/ER- sporadic tumors, but high values are found in a subset of ER+ and HER2+ tumors. Elevated BD-L signature in primary tumors is associated with increased risk of overall relapse, brain relapse, and decreased survival. The BD-L signature correlates with pharmacologic response to PARP inhibitor and temozolomide in two independent microarray datasets, and the signature outperformed four published gene signatures of BRCA1/2 deficiency. Conclusions: The BD-L signature is enriched in breast cancer brain metastases and identifies a subset of primary tumors with increased propensity for brain metastasis. Furthermore, this signature may serve as a biomarker to identify sporadic breast cancer patients who could benefit from a therapeutic combination of PARP inhibitor and temozolomide. Gene expression of 19 HER2+ human breast cancer brain metastases was compared with gene expression of 19 HER2+ nonmetastatic primary human breast tumors.

2014-04-24 | E-GEOD-43837 | biostudies-arrayexpress

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