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• Melanoma_multi_site_metastases

  Despite multiple large-scale sequencing studies offering substantial insight into the genomic landscape of cutaneous melanoma, the molecular events surrounding disease progression and the resulting molecular heterogeneity between metastases have not been fully elucidated. We have been applying whole genome and transcriptome sequencing across metastases collected during post mortem as well as to multi-site metastases during treatment

  Study EGAS00001001348

• Searching for variants associated with endometriosis

  We explored regulatory mechanism of a SNP on chromosome 9p21 associated with endometriosis by leveraging “allele-specific” functional genomic approaches. By re-sequencing 1.29 Mb of 9p21 region and scrutinizing DNase-seq data from the ENCODE project, we prioritized rs17761446 as a candidate functional variant that was in perfect linkage disequilibrium with the original GWAS SNP (rs10965235) and located on DNase I hypersensitive site. Chromosome conformation capture followed by high-throughput sequencing revealed that the protective G allele of rs17761446 exerted stronger chromatin interaction with ANRIL promoter. We demonstrated that the protective allele exhibited preferential binding affinities to TCF7L2 and EP300 by bioinformatics and chromatin immunoprecipitation (ChIP) analyses. ChIP assays for histone H3 lysine 27 acetylation and RNA polymerase II reinforced the enhancer activity of the SNP site. The allele specific expression analysis for eutopic endometrial tissues and endometrial carcinoma cell lines showed that rs17761446 was a cis-regulatory variant where G allele was associated with increased ANRIL expression.

  Study EGAS00001001741

• CTCF-dependent enhancer hijacking by the EVI1 oncogene in leukemia

  Chromosomal rearrangements are a frequent cause of oncogene deregulation in human malignancies. Overexpression of EVI1 is found in a subgroup of acute myeloid leukemia (AML) with 3q26 chromosomal rearrangements which are often therapy resistant. In a cohort of primary t(3;8)(q26;q24) AML samples we observed the translocation of a MYC super-enhancer to EVI1. We generated a patient-based t(3;8)(q26;q24) model in vitro using CRISPR-Cas9 technology and demonstrated hyper-activation of EVI1 by the hijacked MYC super-enhancer. One MYC super-enhancer element in particular, which recruits early hematopoietic regulators, is critical for EVI1 expression and enhancer-promoter interaction. This interaction is facilitated by a CTCF-bound motif upstream of the EVI1 promoter that acts as an enhancer-docking site in t(3;8) AML. Genomic analyses of 3q26-rearranged AML samples point to a common mechanism by which EVI1 uses this CTCF-bound enhancer-docking site to hijack early hematopoietic enhancers.

  Study EGAS00001004808

• Inferring tumor genomes from peripheral blood i.e. CTCs and plasma-DNA using deep sequencing and targeted enrichment

  In this study we tested whether complex tumor genomes can be inferred from the peripheral blood (plasma DNA /CTCs) of 32 patients with stage IV colorectal carcinoma (CRC). To establish the percentage of mutated plasma DNA fragments we used 8 patient samples with different plasma DNA size distributions and KRAS mutations in their corresponding primary tumors and employed ultra-deep pyrosequencing with 3 different sequencing reaction sizes (i.e., 119 bp, 168 bp, and 323 bp). Furthermore, we used massive parallel sequencing of a panel of 68 CRC-associated genes to establish the mutation spectrum of cancer driver genes in the primary tumors, metastases, and CTCs of two colorectal cancer patients. To investigate, whether mutations found in only one CTC (“private CTC mutations”) are true mutations occurring with allele frequencies below the resolution limits of current detection methods, or whether they are amplification or sequencing artifacts, we performed ultra-deep sequencing of the primary tumors, metastases, plasma DNAs and normal tissues.

  Study EGAS00001000337

• Error-corrected sequencing of 26 driver genes

  387 swab samples were sequenced. The bam files contain consensus reads.

  Dataset EGAD50000000079

• Development of Precision Neoadjuvant-Adjuvant Therapies

  In clinical trials assessing neoadjuvant androgen deprivation therapy plus next-generation androgen receptor axis inhibitors, a subset of patients fail to demonstrate a complete pathologic response following treatment and radical prostatectomy. We performed exome and transcriptome analyses on laser capture microdissected foci of residual tumor from these patients.

  Study phs001399

• Tetralogy of Fallot Exome Trios

  Exome sequencing of 30 parent-offspring trios to >50X mean depth, where the offspring has sporadic TOF, to identify potential causal de novo mutations. We will use the exome plus design for pulldown that incorporates ~6.8Mb of additional regulatory sequences in addition to the ~50Mb GENCODE exome.

  Study EGAS00001000071

• WGS data of pediatric T-ALL acute lymphoblastic leukemia (set3)

  The dataset includes FASTQ and CRAM files from diagnostic and matched remission (control) samples of two T-ALL patient (ALLK-126, ALLT-503). ALLT-503 sample has two diagnostic samples one extracted from the BM (ALLT-503D) and from the lymph node (ALLT-503lympD). Sequencing library was made using PCR free-based WGS library preparation (PCR-), using Novogene NGS DNA Library Prep Set (Cat No. PT004). Both diagnostic/relapse (90x) and remission (30x) samples were sequenced using Illumina NovaseqX Plus.

  Dataset EGAD50000002015

• RNA sequencing data of pediatric T-cell acute lymphoblastic leukemia (set 3)

  The dataset includes RNA sequencing FASTQ files from diagnostic tumor samples of two T-ALL patients (ALLK-126, ALLT-503). Two diagnostic samples of ALLT-503 were sequenced: one extracted from the bone marrow (ALLT-503D-RNA) and one from the lymph node (ALLT-503lympD-RNA). Novogene's internal method was used in directional library preparation including rRNA removal. The diagnostic tumor samples were sequenced using Illumina Novaseq X Plus, and the target sequencing depth was 21 Gb per sample.

  Dataset EGAD50000002586

• Circulating tumor DNA, pathological and immunologic responses to neoadjuvant nivolumab or nivolumab plus relatlimab and chemoradiotherapy in resectable esophageal/gastroesophageal junction cancer

  The dataset for the study “Circulating tumor DNA, pathological and immunologic responses to neoadjuvant nivolumab or nivolumab plus relatlimab and chemoradiotherapy in resectable esophageal/gastroesophageal junction cancer” includes 173 bam files from hybrid capture targeted error-correction next-generation sequencing (TEC-Seq) from plasma cell-free DNA and matched white blood cell DNA from 32 individuals with esophageal/gastroesophageal junction cancer, who received immunotherapy-containing regimens.

  Dataset EGAD00001011822