Project description:This dataset contains ChIP-seq data profiling genomic binding of H3K27ac and H3K4me3 in single cell-derived control, as well as CRISPR/Cas9 induced tRNA gene deletion clones and intergenic region deletion clones in human cancer cell lines HAP1. In this study, we found a large genomic deletion of 10q23 in Cas9 modified clones and further investigate the effect of H3K27ac binding.
Project description:Transcriptome analysis of 130 breast cancer samples (41 TNBCÂ ; 30 Her2Â ; 30 Luminal B and 29 Luminal A), 11 normal breast tissue samples and 14 TNBC cell lines. This dataset contains 178 arrays. 153 arrays were used to analyze 130 unique breast cancer samples from as many patients and 23 technical duplicates. In addition 11 âNormalâ samples from healthy breast tissue obtained from mammoplasty are included, as well as a collection of 14 breast cancer cell lines. Data production involved different array batches and hybridation series which were accounted for in the pre-processing of the data.
Project description:Transcriptome analysis of 130 breast cancer samples (41 TNBCM-BM- ; 30 Her2M-BM- ; 30 Luminal B and 29 Luminal A), 11 normal breast tissue samples and 14 TNBC cell lines. This dataset contains 178 arrays. 153 arrays were used to analyze 130 unique breast cancer samples from as many patients and 23 technical duplicates. In addition 11 M-bM-^@M-^\NormalM-bM-^@M-^] samples from healthy breast tissue obtained from mammoplasty are included, as well as a collection of 14 breast cancer cell lines. Data production involved different array batches and hybridation series which were accounted for in the pre-processing of the data.
Project description:To characterize genomic instability in breast cancer progression, we examined copy number loss and copy number gain in the MCF10A series of cell lines.
Project description:A variety of newly developed next-generation sequencing technologies are making their way rapidly into the research and clinical applications, for which accuracy and cross-lab reproducibility are critical, and reference standards are much needed. However, there is still a lack of well-characterized reference materials which include epigenomic and proteomic data. Our previous multicenter studies under the SEQC-2 umbrella using a breast cancer cell line with paired B-cell line have produced large amount different genomic data including whole genome sequencing (Illumina, PacBio, Nanopore), HiC, and scRNA-seq with detailed analyses on somatic mutations, single-nucleotide variations (SNVs), and structure variations (SVs). Here we further performed ATAC-seq, Methyl-seq, RNA-seq, and proteomic analyses and provided a comprehensive catalog of epigenomic landscape, which overlapped with the transcriptomes and proteomes for the two cell lines. We identified >7,700 peptide isoforms, where the majority (95%) of the genes had a single peptide isoform and found that the protein expression levels of the transcripts overlapping CGIs were much higher than the protein expression levels of the non-CGI transcripts in both cell lines. We observed that open chromatin regions had low methylation while closed chromatin regions had high methylation, which were largely regulated by CG density, where CG-rich regions had more accessible chromatin, low methylation, and higher gene and protein expressions. The CG-poor regions had higher repressive epigenetic regulations (less open chromatin and higher DNA methylation), resulting in a cell line specific methylation and gene expression patterns. Our studies provide well-defined reference materials consisting of two cell lines with genomic, epigenomic, transcriptomic, scRNA-seq and proteomic characterizations which can serve as standards for validating and benchmarking not only on various omics assays, but also on bioinformatics methods. It will be a valuable resource for both research and clinical communities.
Project description:Genomic hallmarks of homologous recombination deficiency in invasive breast carcinomas to appear in Internationa Journal of Cancer Transcriptome analysis of 243 (plus 12 duplicates) primary breast invasive carcinoma samples of various molecular subtypes. This dataset contains 255 arrays for 243 primary breast tumor samples obtained from 243 patient; 12 duplicated cases. Data production involved different array batches and hybridation series.