The CCA Genome Core is responsible for archiving the sequencing data generated by the Cancer Centre Amsterdam (CCA).

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This DAC controls 19 datasets

Dataset ID	Description	Technology	Samples
EGAD00001000779	None	AB SOLiD 4 System	2
EGAD00001000780	None	Illumina HiSeq 2000	18
EGAD00001001000	Background: The disease course of patients with diffuse low-grade glioma is notoriously unpredictable. Temporal and spatially distinct samples may provide insight into the evolution of clinically relevant copy number aberrations (CNAs). The purpose of this study is to identify CNAs that are indicative of aggressive tumor behaviour and can thereby complement the prognostically favorable 1p/19q co-deletion. Results: Genome-wide, 50 base pair single-end, sequencing was performed to detect CNAs in a clinically well-characterized cohort of 98 formalin-fixed paraffin-embedded low-grade gliomas. CNAs are correlated with overall survival as an endpoint. Seventy-five additional samples from spatially distinct regions and paired recurrent tumors of the discovery cohort were analysed to interrogate the intratumoral heterogeneity and spatial evolution. Loss of 10q25.2-qter is a frequent subclonal event and significantly correlates with an unfavorable prognosis. A significant correlation is furthermore observed in a validation set of 126 and confirmation set of 184 patients. Loss of 10q25.2-qter arises in a longitudinal manner in paired recurrent tumor specimens, whereas the prognostically favorable 1p/ 19q co-deletion is the only CNA that is stable across spatial regions and recurrent tumors. Conclusions: CNAs in low-grade gliomas display extensive intratumoral heterogeneity. Distal loss of 10q is a late onset event and a marker for reduced overall survival in low-grade glioma patients. Intratumoral heterogeneity and higher frequencies of distal 10q loss in recurrences suggest this event is involved in outgrowth to the recurrent tumor.	Illumina HiSeq 2000	175
EGAD00001001644	MicroRNAs (miRs) have been recognized as promising biomarkers. It is unknown to what extent tumor-derived miRs are differentially expressed between primary colorectal cancers (pCRCs) and metastatic lesions, and to what extent the expression profiles of tumor tissue differ from the surrounding normal tissue. Next-generation sequencing (NGS) of 220 fresh-frozen samples, including paired primary and metastatic tumor tissue and non-tumorous tissue from 38 patients, revealed expression of 2245 known unique mature miRs and 515 novel candidate miRs. Unsupervised clustering of miR expression profiles of pCRC tissue with paired metastases did not separate the two entities, whereas unsupervised clustering of miR expression profiles of pCRC with normal colorectal mucosa demonstrated complete separation of the tumor samples from their paired normal mucosa. Two hundred and twenty-two miRs differentiated both pCRC and metastases from normal tissue samples (false discovery rate (FDR) <0.05). The highest expressed tumor-specific miRs were miR-21 and miR-92a, both previously described to be involved in CRC with potential as circulating biomarker for early detection. Only eight miRs, 0.5% of the analysed miR transcriptome, were differentially expressed between pCRC and the corresponding metastases (FDR <0.1), consisting of five known miRs (miR-320b, miR-320d, miR-3117, miR-1246 and miR-663b) and three novel candidate miRs (chr 1-2552-5p, chr 8-20656-5p and chr 10-25333-3p). These results indicate that previously unrecognized candidate miRs expressed in advanced CRC were identified using NGS. In addition, miR expression profiles of pCRC and metastatic lesions are highly comparable and may be of similar predictive value for prognosis or response to treatment in patients with advanced CRC.	Illumina HiSeq 2000	125
EGAD00001002738	Background: In follicular lymphoma (FL), studies addressing the prognostic value of microenvironment-related immunohistochemical (IHC) markers and tumor cell-related genetic markers have yielded conflicting results, precluding implementation in practice. Therefore, the Lunenburg Lymphoma Biomarker Consortium (LLBC) performed a validation study for published markers. Methods: To maximize sensitivity, an end-of-spectrum design was applied for 122 uniformly immunochemotherapy-treated FL patients retrieved from international trials and registries; early failure (EF): progression or lymphoma-related death <2 years versus long remission: response duration of >5 years. IHC staining for T-cells and macrophages was performed on tissue microarrays from initial biopsy and scored with a validated computer-assisted protocol. Shallow whole-genome and deep targeted sequencing was performed on the same samples. Results: 96/122 cases with complete molecular and immunohistochemical data were included in the analysis. EZH2 wild-type (p=0.006), gain of chromosome 18 (p=0.002), low percentages of CD8+ cells (p=0.011) and CD163+ areas (p=0.038) were associated with EF. No significant differences in other markers were observed, thereby refuting previous claims on their prognostic significance. Conclusion: Using an optimized study design, this LLBC study validates wild-type EZH2 status, gain of chromosome 18, low percentages of CD8+ cells and CD163+ area as predictors of EF to immunochemotherapy in FL.	Illumina HiSeq 2000	96
EGAD00001003990	Shallow sequencing of metastatic colorectal cancer samples for the Angiopredict and Nobev cohorts described in: van Dijk et al., JCO, in revision	Illumina HiSeq 2000 Illumina HiSeq 2500	186
EGAD00001006433	Shallow whole genome sequencing of 29 BIA-ALCL patients for copy number analysis and 24 Alk-negative ALCL samples as control cohort. 7 Whole exome sequencing BIA-ALCL samples.	Illumina HiSeq 4000	66
EGAD00001006438	Contains data for all cells sequenced for this study. Data is organized as one bam-file per sample. Individual cells can be identified through the CB tag in the bam-files.	NextSeq 500	7
EGAD00001007711	Control cohort of lymphoma samples sequenced with a hybrid capture panel designed to be able to detect translocations and mutations in lymphoma samples. used in the paper "Robust detection of translocations in lymphoma FFPE samples using Targeted Locus Capture-based sequencing"	Illumina HiSeq 2500 Illumina HiSeq 4000	19
EGAD00001007758	Shallow WGS of neuroblastoma cell lines with large-scale deletions induced through CRISPR-Cas9 and matching controls. Deletion of 11q was induced in the cell line SKNSH and loss of 6q was induced in the cell line NMB.	Illumina HiSeq 2000	13
EGAD00001008280	None	Illumina HiSeq 4000	287
EGAD00001008364	Genomic profiling of effusion-based fluid samples from 8 HHV8-negative effusion-based lymphoma patients.	Illumina HiSeq 2500	8
EGAD00001008385	Stage I and stage III/IV Follicular lymphoma samples, shallow whole genome sequencing for copy number analysis and targeted capture sequencing for mutation and translocation analysis.	Illumina HiSeq 4000	269
EGAD00001008386	Shallow whole genome sequencing and targeted sequencing of DLBCL patients treated in the PETAL trial	Illumina HiSeq 4000 Illumina NovaSeq 6000	216
EGAD00001008387	Shallow whole genome sequencing for copy number analysis and targeted capture sequencing data for translocation and mutation anslysis of paired primary and relapse PCNSL and PTL samples	Illumina HiSeq 4000	335
EGAD00001008389	Shallow whole genome sequencing and targeted sequencing of DLBCL patients treated in the HOVON84 trial	Illumina HiSeq 4000	220
EGAD00001008402	small RNA next generation sequencing in head and neck cancer	Illumina HiSeq 2000	51
EGAD00001011994	Shallow-whole genome sequencing for copy numbers in resectable gastric cancer treated with surgery alone	Illumina HiSeq 4000	269
EGAD00010002002	4 oesophageal cancer derived organoid lines and 2 ovarian cancer derived organoid lines	GSA-MD V3	6