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• Clonal somatic copy number altered driver events inform drug sensitivity in high-grade serous ovarian cancer.

  This dataset consists of shallow whole genome sequencing data and amplicon sequencing data for 26 ovarian cancer patients (21 high-grade serous ovarian cancer, 4 low-grade serous ovarian cancer and 1 clear cell ovarian cancer). The data are provided as single end FASTQ files for the shallow whole genome sequencing data (31 libraries) and paired end FASTQ files for the amplicon sequencing data (98 libraries).

  Dataset EGAD00001008716

• Sequencing data for oesophageal and related samples - ICGC DCC release 26 (WGS)

  WGS sequencing for 303 cases (620 samples) from the ICGC ESAD-UK project Tumours 50x Normals 30x HiSeq X BAM files These samples are all available in ICGC release 26

  Dataset EGAD00001003580

• Comparison of 3 protocols for deriving pancreatic progenitors from hPSCs (RNA-seq)

  This dataset contains 26 mapped bam files. The samples were generated with 3 different protocols for deriving pancreatic progenitors from hPSC. Three parallel differentiations were performed, all done in a hPSC NKX6.1-GFP reporter line. For each protocol there are three cellular populations: total (presort), GFP+ and GFP- . In summary: 3 differentiations x 3 protocols x 3 cellular populations. We prepared Smart-Seq2 RNA-seq libraries for the 27 samples, 1 sample failed library preparation and is not therefore included in this dataset.

  Dataset EGAD00001004823

• Assessment of Complex Chromosomal Changes in De-Identified Cell Lines

  In this study, we obtained DNA from the Coriell Repository from individuals with complex chromosomal changes. The database ("Chromosome Abnormalities") of these de-identified samples contains 1,366 individuals as per https://www.coriell.org/1/NIGMS. We started with 16 individuals in this pilot study that we will hopefully expand out in a potential large NIH grant using information derived in this pilot study. De-identified samples were sequenced using internal funding from Washington University in St. Louis. A description of the sequencing we did on these individuals is provided in our medRxiv preprint at https://www.medrxiv.org/content/10.1101/2025.03.28.25324850v1.

  Study phs004000

• Biallelic tumor suppressor loss and DNA repair defects in de novo small cell prostate cancer

  Small cell prostatic carcinoma (SCPC) is an aggressive pathology that is managed similar to small cell lung cancer. SCPC can evolve from prostatic adenocarcinoma in response to androgen deprivation therapy but in rare cases is present at initial cancer diagnosis. The molecular etiology of de novo SCPC is incompletely understood due to the scarcity of tumor tissue and the brief life expectancy of patients. Through a retrospective search of our regional oncology pharmacy database, we identified 18 patients diagnosed with de novo SCPC between 2004 and 2017. Ten patients had pure SCPC pathology and the remainder had some admixed adenocarcinoma foci, but all were treated with first line platinum-based chemotherapy. Median overall survival was 28 months. We performed targeted DNA sequencing, whole exome sequencing and mRNA profiling on formalin-fixed paraffin embedded archival tumor tissue. We observed frequent biallelic deletion and/or mutation of tumor suppressors TP53, RB1 and PTEN, similar to treatment related SCPC. Indeed, at the RNA level pure de novo SCPC closely resembled treatment-related SCPC. However, five patients had biallelic loss of DNA repair genes including BRCA1, BRCA2, ATM and MSH2/6: potentially underlying the high genomic instability of this rare disease variant. Two patients with pure de novo SCPC harbored ETS gene rearrangements to androgen-driven promoters, consistent with evolution of de novo SCPC from an androgen-driven ancestor. Overall, our results reveal a highly aggressive molecular landscape underlies this unusual pathologic variant, and propose opportunities for targeted therapy strategies in a disease with few treatment options.

  Study EGAS00001003007

• Possible DNA damage after paternal exposure to ionizing radiation in radar technicians

  Effects of accidental and prolonged radiation exposure on the human germline remain a topic of medical interest. Transgenerational signatures of ionizing radiation exposure are primarily implicated to be clustered de-novo mutations (cDNMs, multiple de-novo mutations within 20bp). We sequenced the whole genome of 110 children from 70 families (Radar cohort). The father in this cohort were exposed to 0-353mSv of ionizing radiation and serve as exposed samples.

  Study EGAS00001007321

• Anaplastic meingioma methylation

  Methylation of anaplastic meningiona samples

  Dataset EGAD00010001629

• Error-corrected sequencing of 26 driver genes

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

  Dataset EGAD50000000079

• WGS in insulinomas

  Whole-Genome Sequencing datasets of insulinoma samples and paired blood controls

  Dataset EGAD50000000464

• The clinicopathologic spectrum and genomic landscape of de-/trans-differentiated melanoma

  De- and trans-differentiation is a rare and only poorly understood phenomenon in cutaneous melanoma. To study this disease more comprehensively we have retrieved 11 primary cutaneous melanomas from our pathology archives showing biphasic features characterized by a conventional melanoma and additional areas of de-/trans-differentiation as defined by a lack of immunohistochemical expression of all conventional melanocytic markers (S-100 protein, SOX10, Melan-A and HMB-45). The clinical, histologic and immunohistochemical findings were recorded and follow-up was obtained. The patients were mostly elderly (median: 81 years; range: 42-86 years) without significant gender predilection, and the sun-exposed skin of the head and neck area was most commonly affected. The tumors were deeply invasive with a mean tumor thickness of 7 mm (range: 4-80 mm). The dedifferentiated component showed atypical fibroxanthoma-like features in the majority (7), while additional rhabdomyosarcomatous and epithelial transdifferentiation was noted histologically and/or immunohistochemically in two tumors each. The background conventional melanoma component was of desmoplastic (4), superficial spreading (3), nodular (2), lentigo maligna (1) or spindle cell (1) types. For the 7 patients with available follow-up data (median follow-up period of 25 months; range: 8-36 months), 2 died from their disease and 3 developed metastases. Next-generation sequencing of the cohort revealed somatic mutation of established melanoma drivers including mainly NF1 mutations in the conventional component (5 cases), which were also detected in the corresponding de-/trans-differentiated components. In summary, the diagnosis of de-/trans-differentiated melanoma is challenging and depends on the morphologic identification of the conventional melanoma component. Molecular analysis is diagnostically helpful as the mutated gene profile is shared between the conventional and de-/trans-differentiated components. Importantly, de-/trans-differentiation does not appear to confer a more aggressive behavior.

  Dataset EGAD00001007033

• The clinicopathologic spectrum and genomic landscape of de-/trans-differentiated melanoma

  De- and trans-differentiation is a rare and only poorly understood phenomenon in cutaneous melanoma. To study this disease more comprehensively we have retrieved 11 primary cutaneous melanomas from our pathology archives showing biphasic features characterized by a conventional melanoma and additional areas of de-/trans-differentiation as defined by a lack of immunohistochemical expression of all conventional melanocytic markers (S-100 protein, SOX10, Melan-A and HMB-45). The clinical, histologic and immunohistochemical findings were recorded and follow-up was obtained. The patients were mostly elderly (median: 81 years; range: 42-86 years) without significant gender predilection, and the sun-exposed skin of the head and neck area was most commonly affected. The tumors were deeply invasive with a mean tumor thickness of 7 mm (range: 4-80 mm). The dedifferentiated component showed atypical fibroxanthoma-like features in the majority (7), while additional rhabdomyosarcomatous and epithelial transdifferentiation was noted histologically and/or immunohistochemically in two tumors each. The background conventional melanoma component was of desmoplastic (4), superficial spreading (3), nodular (2), lentigo maligna (1) or spindle cell (1) types. For the 7 patients with available follow-up data (median follow-up period of 25 months; range: 8-36 months), 2 died from their disease and 3 developed metastases. Next-generation sequencing of the cohort revealed somatic mutation of established melanoma drivers including mainly NF1 mutations in the conventional component (5 cases), which were also detected in the corresponding de-/trans-differentiated components. In summary, the diagnosis of de-/trans-differentiated melanoma is challenging and depends on the morphologic identification of the conventional melanoma component. Molecular analysis is diagnostically helpful as the mutated gene profile is shared between the conventional and de-/trans-differentiated components. Importantly, de-/trans-differentiation does not appear to confer a more aggressive behavior.

  Dataset EGAD00001007034

• HELIUS DAC The HELIUS data are owned by the Amsterdam University Medical Centers, location AMC in Amsterdam, The Netherlands. To allow sharing of microbiome data collected in HELIUS with (inter)national researchers, 16s rRNA sequence analysis has been stored at the European genome-phenome archive (EGA; accession code EGAD00001004106). This requires that access needs to be granted, also because the HELIUS data are stored with relevant phenotypical variables. Access is granted to all researchers affiliated with an internationally recognized research institution who request to use the HELIUS data within the EGA context, after having signed the data transfer agreement. Any researcher can request the data by submitting a proposal to the HELIUS Executive Board as outlined at http://www.heliusstudy.nl/en/researchers/collaboration, by email: heliuscoordinator at amsterdamumc dot nl. The HELIUS Executive Board will check proposals if they do not conflict with ethical approvals and informed consent forms of the HELIUS study.

  Dac EGAC00001000895

• Gut metagenomic data of 2,338 Pinggu adults

  Here we exploited a Han Chinese population-based cohort with extensive host metadata established in the Pinggu (PG) district of Beijing, and investigated gut microbiota from 2,338 adults (26-76 years) by metagenomic sequencing, revealing associations of the gut microbiota with sex, sex hormones, age, and a number of clinical and metabolic parameters.

  Study EGAS00001004820

• Pancreatic adenocarcinoma QCMG 20110901

  Pancreatic adenocarcinoma QCMG 20110901

  Dataset EGAD00001000049

• Error-corrected sequencing of 26 driver genes (additional cohort)

  An additional 320 swab samples were sequenced. The bam files contain consensus reads.

  Dataset EGAD50000000641

• RNAseq dataset

  RNAseq experiment after DIS3 ASO or Control ASO treatment on human cells under plasmablast differentiation.

  Dataset EGAD50000001243

• Whole Exome Sequencing

  Whole Exome Sequencing Data for 10 patients for treatment with the ICI Nivolumab

  Dataset EGAD00001011117

• Whole_genome_sequence_of__third_generation_family_member__SFHS_

  Previously we performed deep WGS on 6 parents and 13 children from 3 large families from the Scottish Family Health Study to identify de novo mutations. This prelim is cover the additional sequencing of one grandchild from one of these three families. The inclusion of a third generation individual will provide additional experimental validation for the de novo mutations found in the initial trio. As in the previous study, the DNA will be WGS to a depth of approximately 25X to achieve this purpose.

  Study EGAS00001000429

• Genetic landscape of relapsed DLBCL

  Diffuse large B-cell lymphoma is a heterogenous malignancy that can arise de novo or can result from histologic transformation from indolent lymphomas. Considerable sequencing effort has been placed on determining the mutations that are common at the time of diagnosis in DLBCL but little is known about the nature of relapsed disease. We have sequenced tumour and matched normal exomes of 38 rrDLBCL patients including 25 de novo DLBCLs and 13 transformed lymphomas to identify somatic mutations and copy number alterations associated with relapse.

  Study EGAS00001001553

• MeDALL epigenetics study

  MeDALL- (Mechanisms of the Development of ALLergy) is a collaborative project supported by the European Union under the Health Cooperation Work Programme of the 7th Framework programme (grant agreement number 261357).MeDALL epigenetics study includes illumina 450k methylation measurements from 4 cohorts: Infancia y Medio Ambiente (INMA), Etudes des Déterminants pré et postnatals précoces du développement et de la santé de l’ENfant (EDEN), Children’s Allergy Environment Stockholm Epidemiology study(BAMSE), and Prevention and Incidence of Asthma and Mite Allergy (PIAMA)

  Study EGAS00001002169

• Whole exome sequencing of 69 trios with bipolar disorder

  We performed whole exome sequencing to trios with bipolar disorder to elucidate genetic architecture of bipolar disorder including de novo mutations and transmitted variants.

  Study JGAS000273

• HV31 - De novo assembly of eight immune system regions

  De novo assembly of eight immune system regions for individual HV31, generated using a multi-platform pipeline. A full description of the generation of these assemblies can be found at https://doi.org/10.1101/2021.02.03.429586.

  Dataset EGAD00001007050

• Multi-focal genomic dissection of synchronous primary and metastatic tissue from de novo metastatic prostate cancer

  De novo metastatic prostate cancer is highly aggressive, but the paucity of routinely-collected tissue in this setting has hindered genomic stratification and jeopardizes precision oncology efforts. Here, we leveraged a rare study of surgical intervention in 43 de novo metastatic prostate cancers to assess somatic genotype across 607 synchronous primary and metastatic tissue foci plus circulating tumor DNA. Intra-prostate heterogeneity was pervasive and impacted clinically-relevant genes, resulting in frequent discordance between select primary-restricted foci and synchronous metastases. Additional complexity was driven in several instances by polyclonal metastatic seeding from the reservoir of phylogenetically-related primary populations. When simulating standard clinical practice relying on a single tissue focus, genomic heterogeneity plus highly variable per-sample tumor fraction caused false genotyping of dominant disease. However, in silico modeling demonstrated that analysis of multiple biopsy cores can rescue misassigned somatic genotypes. Our results define the relationship between synchronous treatment-naive primary and metastatic lesions in de novo metastatic prostate cancer and provide a framework for implementing genomics-guided patient management.

  Study EGAS00001006466

• WES of der(1;7)(q10;p10) myeloid neoplasms

  The study examined WES of der(1;7)(q10;p10) myeloid neoplasm cases. BAM files of WES of 26 myeloid neoplasm patients with der(1;7)(q10;p10) were used to identify key driver genes in patients with der(1;7)(q10;p10). This study is one of the largest WES for der(1;7)(q10;p10)(+) myeloid neoplasm cases.

  Study EGAS50000000704

• Long-read and short-read isoform sequencing in breast cancer

  The goal of this project was to perform long-read RNA sequencing (LR-seq, PacBio) in combination with short-read RNA-seq for systematic characterization of the isoform diversity in primary breast tumor samples. We sequenced the full-length transcriptomes of 26 breast tumors and 4 normal breast samples.

  Study EGAS00001004819