DAC

DKFZ-HIPO Data Access Committee of Heidelberg Center for Personalized Oncology

Dac ID Contact Person Email Access Information
EGAC00001000452 Katja Beck hipo_daco [at] dkfz-heidelberg [dot] de No additional information is available

This DAC controls 84 datasets:

Dataset ID Description Technology Samples
EGAD00001000366 WGBS data of whole blood samples from smoking and non-smoking mothers and their children at gestation/birth and follow-up years. Illumina HiSeq 2000 52
EGAD00001000884 In order to elucidate whether newly acquired genetic alterations during serial transplantation of patient derived primary pancreatic cancer cultures contribute to the observed clonal dynamics in vivo, all coding genes of two patient derived primary cultures and derived genetically marked serial xenografts (1°/2°/3°) were sequenced. Illumina HiSeq 2000 10
EGAD00001000992 HIPO blastemal Wilms (nephroblastoma) characterisation of tumor driving events caused by differential SIX1 binding of the SIX1 Q177R mutatns Illumina HiSeq 2500 3
EGAD00001000993 HIPO blastemal Wilms (nephroblastoma) characterisation of tumor driving gene expression events Illumina HiSeq 2000 40
EGAD00001000994 HIPO blastemal Wilms (nephroblastoma) characterisation of tumor driving chromosomal aberrations Illumina HiSeq 2000,Illumina HiSeq 2500 56
EGAD00001000995 HIPO blastemal Wilms (nephroblastoma) characterisation of tumor driving DNA alterations Illumina HiSeq 2000 112
EGAD00001000997 Whole-exome sequencing of a chronic lymphocytic leukemia (CLL) developed during vemurafenib treatment of a patient with malignant melanoma. Peripheral blood mononuclear cells were separated by Ficoll gradient centrifugation. DNA was extracted from highly purified (>97%) CD19+CD5+ cells obtained from the patient while being under BRAF inhibition versus CD14+ germline control cells (>90% purity). No alterations that could be linked to aberrant RAS activity or paradoxical RAF/MEK/ERK signaling could be identified in the CLL, which shows characteristic copy number alterations. Illumina HiSeq 2500 2
EGAD00001001384 Mutations that activate the RAF-MEK-ERK signaling pathway, in particular BRAFV600E, occur in many cancers, and mutant BRAF-selective inhibitors have clinical activity in these diseases. Activating BRAF alleles are usually considered to be mutually exclusive with mutant RAS, whereas inactivating mutations in the D594F595G596 motif of the BRAF activation segment can coexist with oncogenic RAS and cooperate via paradoxical MEK/ERK activation. We determined the functional consequences of a largely uncharacterized BRAF mutation, F595L, which was detected along with an HRASQ61R allele by clinical exome sequencing in a patient with histiocytic sarcoma and also occurs in epithelial cancers, melanoma, and neuroblastoma, and investigated its interaction with mutant RAS. We demonstrate that, unlike previously described DFG motif mutants, BRAFF595L is a gain-of-function variant with intermediate activity towards MEK that does not act paradoxically, but nevertheless cooperates with mutant RAS to promote oncogenic signaling. Of immediate clinical relevance, BRAFF595L shows divergent responses to different mutant BRAF-selective inhibitors, whereas signaling driven by BRAFF595L with and without mutant RAS is efficiently blocked by pan-RAF and MEK inhibitors. Mutation data from primary patient samples and cell lines show that BRAFF595L, as well as other BRAF mutations with intermediate activity, frequently coincide with mutant RAS in a broad spectrum of cancers. These data define a novel class of activating BRAF mutations that cooperate with oncogenic RAS in a non-paradoxical fashion to achieve an optimal level of MEK-ERK signaling, extend the spectrum of patients with systemic histiocytic disorders and other malignancies who are candidates for therapeutic blockade of the RAF-MEK-ERK pathway, and underscore the value of comprehensive genetic profiling for understanding the signaling requirements of individual cancers. Illumina HiSeq 2500 2
EGAD00001001444 Atypical teratoid/rhabdoid tumor (ATRT) is one of the most common brain tumors in infants and young children. Although the prognosis of ATRT patients is poor, some patients respond very well to current treatments, suggesting inter-tumor molecular heterogeneity. To investigate this further, we genetically and epigenetically analyzed a large cohort of ATRTs (n = 170). Three distinct molecular subgroups of ATRTs, associated with differences in demographics, tumor location and type of SMARCB1 alterations, were identified using DNA-methylation or gene expression analyses. Whole genome DNA- and RNA-sequencing found no other recurrent mutations explaining the differences between subgroups. However, whole genome bisulfite-sequencing and H3K27Ac ChIP-sequencing of primary tumors revealed clear differences in methylation patterns and enhancer landscapes, leading to the identification of subgroup-specific regulatory networks. Illumina HiSeq 2000,Illumina HiSeq 2500 55
EGAD00001002011 RNA sequencing data of whole blood samples from smoking and non-smoking mothers and their children at gestation/birth and follow-up years. 64
EGAD00001002012 ChIPseq data of whole blood samples from smoking and non-smoking mothers and their children at gestation/birth and follow-up years. 16
EGAD00001002055 Whole exome sequencing from matched tumor-control samples of 121 primary lymphoma samples. Sequencing was performed on Illumina HiSeq2000. The dataset contains FASTQ files. Illumina HiSeq 2000 242
EGAD00001002056 Paired-end RNA sequencing using total RNA from 136 primary lymphoma samples. Sequencing was performed on the Illumina HiSeq2000 with 300bp insert size. The dataset contains FASTQ files. Illumina HiSeq 2000 136
EGAD00001002135 ChIPseq data of Atypical teratoid/rhabdoid tumors (ATRT) Illumina HiSeq 2000,Illumina HiSeq 2500 15
EGAD00001002136 RNA sequencing data of Atypical teratoid/rhabdoid tumors (ATRT) Illumina HiSeq 2000 25
EGAD00001002137 WGBS data of Atypical teratoid/rhabdoid tumors (ATRT) Illumina HiSeq 2000,Illumina HiSeq 2500 15
EGAD00001002138 WGS data of Atypical teratoid/rhabdoid tumors (ATRT) Illumina HiSeq 2000 36
EGAD00001002159 Exome Seq for Study EGAS00001001844 Illumina HiSeq 2000 2
EGAD00001002160 Exome Seq for EGAS00001001845 Illumina HiSeq 2500 2
EGAD00001002161 Transcriptome from EGAS00001001845 Illumina HiSeq 2500 1
EGAD00001002162 Exome Seq from EGAS00001001846 Illumina HiSeq 2500 2
EGAD00001002163 Transcriptome from EGAS00001001846 Illumina HiSeq 2500 1
EGAD00001002164 Exome from EGA00001001848 Illumina HiSeq 2000 2
EGAD00001002166 Exome from EGAS00001001861 Illumina HiSeq 2000 17
EGAD00001002528 WGS from EGAS00001001857 Illumina HiSeq 2000 18
EGAD00001003325 Exome from EGAS00001002441 Illumina HiSeq 2500 2
EGAD00001003408 Chip-Seq sequencing data of Atypical teratoid/rhabdoid tumors (ATRT) Illumina HiSeq 2000 19
EGAD00001003421 Sequence data of 28 Samples (19 chronic lymphocytic leukemia, 9 control) Including RNA-Seq and ChIP-Seq of following histone modifications: H3, H3K4me1, H3K4me3, H3K9ac, H3K9me3, H3K27ac, H3K27me3, H3K36me3 Project see: http://www.cancerepisys.org/ 28
EGAD00001003827 The data set contains bam files aligned using bwa-0.7.8 mem -t 8 -R. HiSeq X Ten 4
EGAD00001003828 This dataset contains paired fastq files for LMS tumor samples Illumina HiSeq 2000,Illumina HiSeq 2500 37
EGAD00001003829 The data set contains paired end fastq files for whole exome sequencing data for Leiomyosarcoma tumor and control samples Illumina HiSeq 2000,Illumina HiSeq 2500 96
EGAD00001003965 Whole genome sequencing of Control (blood), Tumor and metastasis triplets for 12 samples. Illumina HiSeq 2000 36
EGAD00001004068 Whole-genome, whole-exome and transcriptome sequencing of pancreatic ductal adenocarcinomas from young adults reveals recurrent NRG1-fusions in KRAS wild-type tumors. HiSeq X Ten,Illumina HiSeq 2500,Illumina HiSeq 4000 36
EGAD00001004563 This dataset contains whole genome sequencing data from 21 primary and relapsed IDH-wt glioblastomas and matched blood controls. Tumors were sequenced at a target coverage of 150x, blood controls at 80x. HiSeq X Ten 63
EGAD00001004564 This dataset contains strand-specific RNA sequencing data from 16 primary/relapsed sample pairs of IDH-wt glioblastomas Illumina HiSeq 2000 32
EGAD00001004565 This dataset contains gene panel sequencing data from 43 sample pairs of primary and relapsed IDH-wt glioblastomas. The gene panel covers 50 glioma-associated genes. 14 of the sequenced sample pairs were sequenced with whole genome sequencing also and are accessible under EGAD00001004563. Ion Torrent Proton 86
EGAD00001004825 Case series of the rare tumor entity chordoma. 9 cases sequenced with Whole Exome Sequencing (WES) and 2 cases sequenced with Whole Genome Sequencing (WGS) were recruited from the personalized oncology program NCT-MASTER/DKTK-MASTER at the German Cancer Research Center. One of the WES patients was re-sequenced at a later time point when he relapsed, this resequencing was done by WGS. Therefore there are 11 patients, one of which with two samples, all of which were sequenced with matched normal controls, amounting to a total number of 24 NGS samples. HiSeq X Ten,Illumina HiSeq 2500,Illumina HiSeq 4000 24
EGAD00001005061 Bam files for 124 samples (62 tumor vs blood pairs); Whole Genome Sequencing performed on Illumina HiSeq X Ten HiSeq X Ten 124
EGAD00001005069 Whole genome and transcriptome sequencing of a pancreatic tumor harboring a RASGRP1 gene fusion HiSeq X Ten,Illumina HiSeq 4000 2
EGAD00001005113 50 samples of 16 individuals with Gastrointestinal Tumor. Patients were sequenced in various combinations of WGS, Exome and RNA sequencing. HiSeq X Ten,Illumina HiSeq 2500,Illumina HiSeq 4000 50
EGAD00001005249 Exome and RNA sequencing data for EGAS00001003776 - one female patient with neurofibroma/schwannoma hybrid nerve sheath tumor (N/S HNST) Illumina HiSeq 2500 2
EGAD00001005492 Content: 60 GB patient tumours and 4 normal brain samples combined in pairs by region (x2=8 total input samples). RNAseq: 1 lane per sample, total strand-specific rRNA-depleted (normal samples were combined = 2 lanes/samples per brain region). WGBS: 2 lanes per sample (normal samples were combined = 2 lanes/samples per brain region). ChIPseq (histone mark): a subset of 20 GB samples were profiled. For the same modification were multiplexed and sequenced on 4 lanes each (H3K27ac, H3K4me1) or a single lane (all others). WGS: used as matching input control for the 20 ChIPseq samples. Data type and technology: RNA-seq: PE 100bp sequenced on HiSeq2000. WGBS: PE 100bp sequenced on HiSeq2000/4000. ChIPseq: SE 50bp sequenced on HiSeq2000/4000. WGS: PE 150bp sequenced on HiSeq X. 172
EGAD00001005493 Content: 2 GB RTK I cell lines (LN229, ZH487) in two conditions (NT control and shSOX10). RNAseq: single replicates per condition, polyA+ RNA sequencing, SE. ATACseq: biological replicates per condition, SE. ChIPseq (histone H3 modifications, LN229 only): all marks for each condition were pooled and sequenced on two lanes for each pool. ChIPseq (BRD4 and SOX10): SOX10 libraries were sequenced on single lanes. BRD4 samples were multiplexed and sequenced in two lanes. ChIPseq input samples are also included. Data type and technology: RNAseq: SE 50bp sequenced on HiSeq2000/4000. ATACseq: SE 50bp sequenced on HiSeq2000/4000. ChIPseq: SE 50bp sequenced on HiSeq2000/4000. 6
EGAD00001005938 This dataset contains 3 pairs of exomes, germline (from whole blood) and patient-derived xenograft (PDX), from human pancreatic durctal adenocarcinoma patients. The data is referred to in the publication: "Pro-immunogenic impact of MEK inhibition synergizes with agonist anti-CD40 immunostimulatory antibodies in tumor therapy" (Nature Communications, 2020) Abstract: Cancer types with lower mutational load and a non-permissive tumor microenvironment are intrinsically resistant to immune checkpoint blockade. While the combination of cytostatic drugs and immunostimulatory antibodies constitutes an attractive concept for overcoming this refractoriness, suppression of immune cell function by cytostatic drugs may limit therapeutic efficacy. Here we show that targeted inhibition of mitogen-activated protein kinase (MAPK) kinase (MEK) does not impair dendritic cell-mediated T-cell priming and activation. Accordingly, combining MEK inhibitors (MEKi) with agonist antibodies (Abs) targeting the immunostimulatory CD40 receptor resulted in potent synergistic anti-tumor efficacy. Detailed analysis of the mechanism of action of MEKi GDC-0623 by means of flow cytometric analysis of the tumor immune infiltrate and whole tumor transcriptomics showed that, in addition to its cytostatic impact on tumor cells, this drug exerts multiple pro-immunogenic effects, including the suppression of M2-type macrophages, myeloid derived suppressor cells and CD4+ T-regulatory cells. In addition, MEKi was found to induce tumor-cell intrinsic interferon signaling, which contributed to antigen presentation by tumor cells. Finally, the tumoridical impact of MEKi involves the activation of multiple pro-inflammatory pathways involved in immune cell effector function in the tumor microenvironment. Our data therefore indicate that the combination of MEK inhibition with agonist anti-CD40 Ab is a promising therapeutic concept, especially for the treatment of mutant Kras-driven tumors such as pancreatic ductal adenocarcinoma. Illumina HiSeq 2500 6
EGAD00001005965 Single-cell ATAC-seq data for 5 CLL samples (2 controls, 3 tumor) of the CancerEpiSys-PRECiSe project. Illumina HiSeq 2000 5
EGAD00001005966 Tagged-WGBS for 3 Naive B Cell samples of the CancerEpiSys-PRECiSe project. Illumina HiSeq 2000 3
EGAD00001005967 ATAC-seq data for 26 CLL samples (7 controls, 19 tumor) of the CancerEpiSys-PRECiSe project. Illumina HiSeq 2000,Illumina HiSeq 4000 26
EGAD00001005968 long RNA data for 27 CLL samples (8 controls, 19 tumor) of the CancerEpiSys-PRECiSe project. Illumina HiSeq 2000 27
EGAD00001005969 ChIPseq data for 31 CLL samples (12 controls, 19 tumor) of the CancerEpiSys-PRECiSe project; containing histone H3, histone modifications and transcription factor binding sites (CTCF, EBF1). Illumina HiSeq 2000,NextSeq 550 31
EGAD00001005970 WGBS data for 75 paired fastq, spread over 31 samples (4 healthy T-cell, 7 healthy B-cell, 20 B-cell CLL tumors) of the CancerEpiSys-PRECiSe project. Illumina HiSeq 2000 31
EGAD00001006005 liver cancer paired with normal controls, viral and non-viral origin 108
EGAD00001006014 NA HiSeq X Ten,Illumina HiSeq 4000 2
EGAD00001006016 NA HiSeq X Ten,Illumina HiSeq 2000 12
EGAD00001006023 NA HiSeq X Ten,Illumina HiSeq 4000 2
EGAD00001006057 paired WGS sequencing of nodal B-cell lymphoma, one tumor and one control, one patient (H021). Sequencing on Hiseq XTen with TruSeq Nano library preparation kit. HiSeq X Ten 2
EGAD00001006058 paired WGS data of one tumor of one patient with nodal B-cell lymphoma. Tumor cells were sorted according to CD48 expression in a high and low fraction. Library preparation with TruSeq Nano and sequencing on Hiseq XTen. HiSeq X Ten 2
EGAD00001006059 Tumors and control of nodal B-cell lymphoma of one patient. WES sequencing on Illumina HiSeq 4000 with Agilent SureSelect V5+UTRs. Bam files were aligned with bwa mem to hg19. Illumina HiSeq 4000 5
EGAD00001006060 paired EXOME sequencing on Illumina HiSeq 4000 using Agilent SureSelect V6 of one tumor sample of one patient with B-cell lymphoma. The bam-file was mapped to the hg19 genome. Illumina HiSeq 4000 1
EGAD00001006184 linking MASTER H021-Cohort to EGAS0001004157 HiSeq X Ten,Illumina HiSeq 2500,Illumina HiSeq 4000 10
EGAD00001006263 linking 3 samples out of EGAD00001002528 to EGAS0001004517 Illumina HiSeq 2000 3
EGAD00001006264 18 samples of RNA-Seq of serially passaged TIC-enriched spheres of colorectal cancer (CRC), sequenced on HiSeq2000 and HiSeq2500 Illumina HiSeq 2500 8
EGAD00001006265 WGS data of serially passaged TIC-enriched spheres of colorectal cancer HiSeq X Ten 6
EGAD00001006266 WES data of serially passaged TIC-enriched spheres of colorectal cancer (CRC) Illumina HiSeq 2000,Illumina HiSeq 2500 15
EGAD00001006297 270 samples with ALK-positiv non-small cell lung cancer, targeted sequencing (198 kb panel size) 270
EGAD00001006298 268 samples with ALK-positiv non-small cell lung cancer, ultra-low coverage whole genome sequencing 268
EGAD00001006336 Paired whole exome sequencing data of the HIPO head and neck cancer (HNC) (n=83), using Agilent SureSelect V4+UTRs and V6+UTRs with the sequencing platforms HiSeq2000 and HiSeq2500. The reads were aligned to hg19. This is part of project H019. 166
EGAD00001006538 WGBS data for EGAS00001004660, "Aggressive PDACs show hypomethylation of repetitive elements and the execution of an intrinsic IFN program linked to a ductal cell-of-origin" 13
EGAD00001006539 RNA data for EGAS00001004660, "Aggressive PDACs show hypomethylation of repetitive elements and the execution of an intrinsic IFN program linked to a ductal cell-of-origin" 23
EGAD00001006544 ATAC-seq data for 2 glioblastoma cell lines (LN229, ZH487), NT and SOX10KD. 2
EGAD00001006545 Whole genome sequencing data for 20 human glioblastoma patients. 20
EGAD00001006546 Whole Genome Bisulfite data for human glioblastoma patients, EGAS00001003953. 68 human samples 68
EGAD00001006547 RNA data for human glioblastoma patients, EGAS00001003953. 64 human samples, 2 cell lines (LN229, ZH487). 66
EGAD00001006548 ChIPseq data for human glioblastoma patients, EGAS00001003953. Mix of input, H3K27ac, H3K27me1, H3K27me3, H3K36me3, H3K4me1, H3K4me3, H3K9me3 and BRD, 20 human samples, 2 cell lines (LN229, ZH487). 22
EGAD00001006739 NA HiSeq X Ten 17
EGAD00001006785 NA Illumina HiSeq 4000 9
EGAD00010000947 Lymphoma samples using CytoSNP Illumina CytoSNP 35
EGAD00010000948 Lymphoma samples using 450k Illumina 450k 95
EGAD00010000949 Lymphoma samples using HumanOmni Illumina HumanOmni2.5 104
EGAD00010001642 Illumina EPIC methylation bead array 25
EGAD00010001643 Illumina 450k methylation bead array 73
EGAD00010001797 Methylation microarray profiling (Illumina Human Methylation 450k and EPIC platforms) of 60 adult glioblastomas. Tumours were subtyped using the approach from Sturm et al. (https://doi.org/10.1016/j.ccr.2012.08.024): 12 IDH, 18 MES, 12 RTK I, 18 RTK II. DNA was prepared, assayed on the microarrays, and raw data computationally processed as described in Capper et al., "DNA methylation-based classification of central nervous system tumours": https://www.nature.com/articles/nature26000 60
EGAD00010001936 Gene expression of 12 colon cancer TSCs (sensitive or resistant) after 12h treatment with 3µM NCT02 or DMSO (control) was analyzed using Illumina microarrays (HumanHT-12 v4 BeadChip). oligonucleotide beads of HumanHT-12 V4 R2 Expression BeadChips (Illumina) 24
EGAD00010002004 PDAC primary cell lines methylation 7
EGAD00010002005 PDAC PDX methylation 18