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Cell-type-specific epigenomic variations associated with BRCA1 mutation in pre-cancer human breast tissues

ABSTRACT: Cell-type-specific epigenomic variations associated with BRCA1 mutation in pre-cancer human breast tissues

PROVIDER: PRJNA626688 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11576900.fastq.gz	Fastqsanger.gz
	SRR11576901.fastq.gz	Fastqsanger.gz
	SRR11576902.fastq.gz	Fastqsanger.gz
	SRR11576903.fastq.gz	Fastqsanger.gz
	SRR11576904.fastq.gz	Fastqsanger.gz

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Cell-type-specific epigenomic variations associated with BRCA1 mutation in pre-cancer human breast tissues

Project description:BRCA1 germline mutation carriers are predisposed to breast cancers. Epigenomic regulations have been known to strongly interact with genetic variations and potentially mediate biochemical cascades involved in tumorigenesis. Due to the cell-type specificity of epigenomic features, profiling of individual cell types is critical for understanding the molecular events in various cellular compartments within complex breast tissue. Here we report cell-type specific profiling of genome-wide histone modifications, including H3K27ac and H3K4me3 in basal, luminal progenitor, mature luminal, and stromal cells, extracted from pre-cancer BRCA1 mutation carriers and non-carriers, using a low-input technology. We discover that basal and stromal cells present the most substantial epigenomic differences between mutation carriers and non-carriers while luminal progenitor and mature luminal cells are relatively unchanged with the mutation. Furthermore, the epigenomic changes in basal cells due to BRCA1 mutation appear to facilitate their transformation into luminal progenitor cells. Our findings shed light on the pre-cancer epigenomic dynamics due to BRCA1 mutation and how they may contribute to eventual development of basal-like breast cancer.

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Cell-type-specific epigenomic variations associated with <i>BRCA1</i> mutation in pre-cancer human breast tissues.

Project description:BRCA1 germline mutation carriers are predisposed to breast cancers. Epigenomic regulations have been known to strongly interact with genetic variations and potentially mediate biochemical cascades involved in tumorigenesis. Due to the cell-type specificity of epigenomic features, profiling of individual cell types is critical for understanding the molecular events in various cellular compartments within complex breast tissue. Here, we produced cell-type-specific profiles of genome-wide histone modifications including H3K27ac and H3K4me3 in basal, luminal progenitor, mature luminal and stromal cells extracted from a small pilot cohort of pre-cancer BRCA1 mutation carriers (BRCA1mut/+ ) and non-carriers (BRCA1+/+ ), using a low-input ChIP-seq technology that we developed. We discovered that basal and stromal cells present the most extensive epigenomic differences between mutation carriers (BRCA1mut/+ ) and non-carriers (BRCA1+/+ ), while luminal progenitor and mature luminal cells are relatively unchanged with the mutation. Furthermore, the epigenomic changes in basal cells due to BRCA1 mutation appear to facilitate their transformation into luminal progenitor cells. Taken together, epigenomic regulation plays an important role in the case of BRCA1 mutation for shaping the molecular landscape that facilitates tumorigenesis.

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Normal human mammary tissues from BRCA1 mutation carriers, non-BRCA1/2 mutation carriers and normal women

Project description:Gene expression profiles of normal human mammary tissue from BRCA1 mutation carriers, non-BRCA1/2 mutation carriers and normal women. RNA was prepared from normal breast tissue (confirmed by pathology) from reduction mammoplasties (n=5) and prophylactic mastectomies of known BRCA1 (n=7) and non-BRCA1/2 mutation carriers (n=8). non-BRCA1/2 carriers were individuals with a strong family history of breast cancer (kConFab Category 1 (http://www.kconfab.org/Collection/Eligibility.shtml) where no mutation in BRCA1 or BRCA2 has been identified in the family by high sensitivity testing (http://www.kconfab.org/Progress/Sensitivity.shtml) of any individual affected by breast or ovarian cancer. Normal breast samples refer to reduction mammoplasty specimens, where family history is generally not known. Microarray expression profiles were obtained from whole pre-neoplastic breast tissue from three categories of patient, as described in the summary. Samples were checked for keratin gene expression levels as a marker for epithelium tissue, and a number of samples were removed because two or more keratin genes lacked detectable expression (BeadStudio detection p-value 0.01). One other sample was removed because its expression profile appeared abnormal. Out of 36 samples initially profiled, 20 passed the quality filters and were used for the final analysis.

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Project description:In order to investigate whether carriers of BRCA1 heterozygous mutation show altered gene expression profiles, we used a whole genome microarray expression profiling of a panel of lymphoblastoid cell lines (LCLs) harboring either mutated or WT BRCA1 (control). We were especially interested whether we find differences in gene expression between carriers of missense versus truncating mutation in BRCA1 gene. We evaluated gene expression of a panel of 21 non-treated lymphoblastoid cell lines (LCLs). Among them, 6 LCLs with WT BRCA1, 5 LCLs carrying missense mutation in BRCA1, and 10 LCLs harboring truncating mutation in BRCA1 were included in this study.

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