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

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

PROVIDER: PRJNA678283 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13055107.fastq.gz	Fastqsanger.gz
	SRR13055108.fastq.gz	Fastqsanger.gz
	SRR13055109.fastq.gz	Fastqsanger.gz
	SRR13055110.fastq.gz	Fastqsanger.gz
	SRR13055111.fastq.gz	Fastqsanger.gz

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

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Project description:This SuperSeries is composed of the SubSeries listed below.

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

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Project description:Single cell RNA sequencing (scRNA-seq) is a powerful tool for defining cellular diversity in tumors, but its application towards dissecting mechanisms underlying immune-modulating therapies is scarce. We performed scRNA-seq analyses on immune and stromal populations from colorectal cancer patients, identifying specific macrophage and conventional dendritic cell (cDC) subsets as key mediators of cellular cross-talk in the tumor microenvironment. Defining comparable myeloid populations in mouse tumors enabled characterization of their response to myeloid-targeted immunotherapy. Treatment with anti-CSF1R preferentially depleted macrophages with an inflammatory signature but spared macrophage populations that in mouse and human expresses pro-angiogenic/tumorigenic genes. Treatment with a CD40 agonist antibody preferentially activated a conventional dendritic cell population and increased Bhlhe40+ Th1-like cells and CD8+ memory T cells. Our comprehensive analysis of key myeloid subsets in human and mouse identifies critical cellular interactions regulating tumor immunity and defines mechanisms underlying myeloid-targeted immunotherapies currently undergoing clinical testing.

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