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• WGS of 50 Intellectual Disability (ID) trios with Complete Genomics Sequencing. Dataset of sample: MW52_C

  50 trios were whole genome sequenced with Complete Genomics to a depth of 80x. For each trio the child was affected with severe ID, and the parents were unaffected. All trios were negative for array, targeted gene and whole exome screening. Dataset consists of sample: MW52_C

  Dataset EGAD00001001841

• WGS of 50 Intellectual Disability (ID) trios with Complete Genomics Sequencing. Dataset of sample: MW51_M

  50 trios were whole genome sequenced with Complete Genomics to a depth of 80x. For each trio the child was affected with severe ID, and the parents were unaffected. All trios were negative for array, targeted gene and whole exome screening. Dataset consists of sample: MW51_M

  Dataset EGAD00001001840

• WGS of 50 Intellectual Disability (ID) trios with Complete Genomics Sequencing. Dataset of sample: MW51_F

  50 trios were whole genome sequenced with Complete Genomics to a depth of 80x. For each trio the child was affected with severe ID, and the parents were unaffected. All trios were negative for array, targeted gene and whole exome screening. Dataset consists of sample: MW51_F

  Dataset EGAD00001001839

• WGS of 50 Intellectual Disability (ID) trios with Complete Genomics Sequencing. Dataset of sample: MW51_C

  50 trios were whole genome sequenced with Complete Genomics to a depth of 80x. For each trio the child was affected with severe ID, and the parents were unaffected. All trios were negative for array, targeted gene and whole exome screening. Dataset consists of sample: MW51_C

  Dataset EGAD00001001838

• WGS of 50 Intellectual Disability (ID) trios with Complete Genomics Sequencing. Dataset of sample: MW50_M

  50 trios were whole genome sequenced with Complete Genomics to a depth of 80x. For each trio the child was affected with severe ID, and the parents were unaffected. All trios were negative for array, targeted gene and whole exome screening. Dataset consists of sample: MW50_M

  Dataset EGAD00001001837

• WGS of 50 Intellectual Disability (ID) trios with Complete Genomics Sequencing. Dataset of sample: MW50_F

  50 trios were whole genome sequenced with Complete Genomics to a depth of 80x. For each trio the child was affected with severe ID, and the parents were unaffected. All trios were negative for array, targeted gene and whole exome screening. Dataset consists of sample: MW50_F

  Dataset EGAD00001001836

• WGS of 50 Intellectual Disability (ID) trios with Complete Genomics Sequencing. Dataset of sample: MW50_C

  50 trios were whole genome sequenced with Complete Genomics to a depth of 80x. For each trio the child was affected with severe ID, and the parents were unaffected. All trios were negative for array, targeted gene and whole exome screening. Dataset consists of sample: MW50_C

  Dataset EGAD00001001835

• WGS of 50 Intellectual Disability (ID) trios with Complete Genomics Sequencing. Dataset of sample: MW4_F

  50 trios were whole genome sequenced with Complete Genomics to a depth of 80x. For each trio the child was affected with severe ID, and the parents were unaffected. All trios were negative for array, targeted gene and whole exome screening. Dataset consists of sample: MW4_F

  Dataset EGAD00001001833

• WGS of 50 Intellectual Disability (ID) trios with Complete Genomics Sequencing. Dataset of sample: MW49_F

  50 trios were whole genome sequenced with Complete Genomics to a depth of 80x. For each trio the child was affected with severe ID, and the parents were unaffected. All trios were negative for array, targeted gene and whole exome screening. Dataset consists of sample: MW49_F

  Dataset EGAD00001001830

• WGS of 50 Intellectual Disability (ID) trios with Complete Genomics Sequencing. Dataset of sample: MW32_F

  50 trios were whole genome sequenced with Complete Genomics to a depth of 80x. For each trio the child was affected with severe ID, and the parents were unaffected. All trios were negative for array, targeted gene and whole exome screening. Dataset consists of sample: MW32_F

  Dataset EGAD00001001815

• Molecular analysis of diffuse cerebellar gliomas

  Among diffuse gliomas, oligodendrogliomas show relatively better prognosis, respond well to radiotherapy and chemotherapy, and seldom progress to very aggressive tumors. To elucidate the genetic and epigenetic background for such behavior and tumor evolution during tumor relapse, we comparatively analyzed 12 pairs of primary and recurrent oligodendrogliomas with 1p/19q-codeletion. Initial treatment for these patients was mostly chemotherapy alone. Temozolomide was used for 3, and procarbazine, nimustine and vincristine (PAV chemotherapy) were used for 7 patients. World Health Organization histological grade at recurrence was mostly stable; it was increased in 2, the same in 9, and decreased in 1 cases. Whole-exome sequencing demonstrated that the rate of shared mutation between the primary and recurrent tumors was relatively low, ranging from 3.2-57.9% (average, 33.3%), indicating a branched evolutionary pattern. The trunk alterations that existed throughout the course were restricted to IDH1 mutation, 1p/19q-codeletion, and TERT promoter mutation, and mutation of the known candidate tumor suppressor genes CIC and FUBP1 were not consistently observed between primary and recurrent tumors. Multiple sampling from different regions within a tumor showed marked intratumoral heterogeneity. Notably, in general, the number of mutations was not significantly different after recurrence, remaining under 100, and no hypermutator phenotype was observed. FUBP1 mutation, loss of chr. 9p21, and TCF12 mutation were among a few recurrent de novo alterations that were found at recurrence, indicating that these events were clonally selected at recurrence but were not enough to enhance malignancy. Genome-wide methylation status, measured by Illumina 450 K arrays, was stable between recurrence and the primary tumor. In summary, although oligodendroglioma displays marked mutational heterogeneity, histological malignant transformation accompanying events such as considerable increase in mutation number and epigenetic profile change were not observed at recurrence, indicating that noticeable temporal and spatial genetic heterogeneity in oligodendrogliomas does not result in rapid tumor progression.

  Study JGAS000106

• Breast Cancer Risk Pathways

  We sought to identify genomic variants that differed between individuals who developed familial breast cancer and individuals who had a family history of breast cancer but who had not developed breast cancer. We aggregated these data at the pathway level to identify pathways that play a role in familial breast cancer development. We profiled peripheral blood cells, extracted DNA, and sequenced the DNA using exome-capture sequencing to identify genomic variants in these samples. For 34 of the 35 samples, we also profiled peripheral blood using Affymetrix Human Exon 1.0 ST Array microarrays. Those data can be found in Gene Expression Omnibus under accession identifier GSE47862.

  Study phs001044

• Phase I Study of the Oral PI3kinase Inhibitor BKM120 or BYL719 and the Oral PARP Inhibitor Olaparib in Patients with Recurrent Triple Negative Breast Cancer or High Grade Serous Ovarian Cancer

  We analyzed massive parallel sequence data from patients with breast and ovarian cancer and identified single base substitution mutational signature 3 (Sig3) - extracted using SigMA - as a biomarker of homologous recombination deficiency (HRD) and predictive for response to PARP inhibitors. Participants were patients enrolled in clinical trials as 2 independent datasets: (1) high-grade serous ovarian cancer and triple-negative breast cancer (TNBC) from a Phase 1b trial of the PARP inhibitor olaparib in combination with the PI3K inhibitor buparlisib (BKM120) (NCT01623349), and (2) TNBC patients who received neoadjuvant olaparib in the Phase II PETREMAC trial (NCT02624973).

  Study phs003019

• Assessing Individual Head and Neck Squamous Cell Carcinoma Patient Response to Therapy Through Integration of Functional and Genomic Data

  This study combines RNA sequencing (RNASeq), whole exome sequencing (WES), reverse phase protein array (RPPA) and copy number variation (CNV) data, along with a custom high throughput inhibitor assay to characterize tumor cells from patients with head and neck squamous cell carcinoma (HNSCC), in order to identify potential therapy targets on an individual patient basis. The data that will be available through dbGaP include the RNASeq, WES, RPPA and array CNV data for the tumor and matched normal samples. This study represents a proof-of-concept. No treatments were administered to patients as part of this study.

  Study phs003456

• GOSH_Paediatric_Tumour_23P108_WSSS_WGS_Managed_Access

  We have a case of two siblings (twins) who were born with nodular blue rashes over their body. The first twin had a large periorbital subcutaneous mass which was diagnosed as infantile undifferentiated sarcoma. This baby was too systematically unwell for chemotherapy and died at 12 days of age. The second sibling received two cycles of emergency chemotherapy however died due to disease progression and secondary haemorrhage at 2 months of age. Post-mortem normal and tumour samples have been taken. In addition to placental tissue and parental germline DNA, the goal will be to investigate intra-uterine transfer of sarcoma and the phylogenetic relationship of tumours in both twins.

  Study EGAS00001007536

• NICOLA Epigenetic Data Wave 1 - Beta values

  Beta values generated from Illumina EPIC methylation array data for a subset of NICOLA Wave 1 samples.

  Dataset EGAD50000001965

• GSA reference

  reference whole exome sequence serving as a reference of individuals. Includes the raw GSa files and the called variants in vcf format merge for all individuals (S1-S5).

  Dataset EGAD50000000481

• Reconstruction oral cavity tumor evolution through brush biopsy

  A dataset of samples analyzed for the publication "Reconstructing oral cavity tumor evolution through brush biopsy", Springer Nature, DOI: 10.1038/s41598-024-72946-3

  Dataset EGAD50000000856

• WTCCC2 bacteraemia susceptibility replication samples

  A WTCCC2 project - replication study for bacteraemia susceptibility in 2518 individuals from Kenya, genotyped on the Illumina Immunochip chip.

  Dataset EGAD00010001509

• DNA sequencing for gastric cancer ascites

  Whole-exome sequencing (WES) was performed on a total of 34 PC specimens, with 15 cases having matched gDNAs extracted from blood.

  Dataset EGAD00001004364

• ICGC Benchmark 2 (Medulloblastoma)

  Raw fastq files for sequence data generated at 5 sequencing centers from a Medulloblastoma sample and matching blood normal control.

  Dataset EGAD00001001859

• NextGen Consortium: Globin Gene Expression in Sickle Cell Genotype-Specific iPS Cells

  Implement an efficient, highly reproducible and 'scalable' system for the production of large numbers of sickle cell anemia-specific iPS cells (iPSC). Derive and characterize a novel, in vitro system for the production of an unlimited supply of erythroid lineage cells from the directed differentiation of 'clinical grade' transgene-free iPS cells; use this system to recapitulate erythroid-lineage ontogeny in vitro with the sequential development of primitive and definitive erythropoiesis, accompanied by the appropriate expression of stage-specific globin genes. Identify developmental gene expression profile differences between erythroid precursors that produce primarily HbF and those that produce primarily HbA or HbS. Determine the effects of the three known HbF major quantitative trait loci (QTL) on globin gene expression in disease-specific iPS cells during in vitro erythropoiesis. Search for novel HbF genetic modifiers associated with markedly elevated HbF levels found in sickle cell anemia patients naturally, or in response to hydroxyurea treatment, by examining gene expression profiles and mRNA sequence of their iPSC-derived erythroid cells. Develop and use a CRISPR-based gene editing platform to study the effect of novel HbF genetic modifiers, explore globin switching, and correct the HbS mutation in sickle iPSC lines.

  Study phs001212

• FASTQ files of total RNA-Seq data from the POPS PET (pre-eclamptic) samples

  All the samples were obtained from the Pregnancy Outcome Prediction–a prospective cohort study of nulliparous women attending the Rosie Hospital, Cambridge (UK) for their dating ultrasound scan between January 14, 2008, and July 31, 2012. Ethical approval for the study was given by the Cambridgeshire 2 Research Ethics Committee (reference number 07/H0308/163) and all participants provided written informed consent. Cases of preeclampsia (PET) were defined on the basis of the 2013 ACOG criteria and cases of small for gestational age (SGA)infants were confined to severe SGA, i.e. a customized birth weight <5th percentile. Chorionic villi from the corresponding placentas (free from decidua, visible infarction, calcification, hematoma, or damage) were collected and processed within 30 minutes of separation from the uterus. After repeated washes in chilled phosphate buffered saline, the samples were placed in RNA later (Applied Biosystems) and stored at -80°C. Total placental RNA was extracted using mirVana Isolation Kit (Ambion). For each placenta, approximately 5 mg of tissue were homogenized in the Lysis/Binding solution for 20 sec at 6 m/s using a bead beater (FastPrep24) and Lysing Matrix D Tubes (MP Biomedicals). The samples were then spun at 13,000 rpm for 5 min at 4°C and the supernatants recovered. Afterwards, the manufacturer's instructions were followed. Immediately after the RNA extraction, placental RNA samples were DNase-treated using DNA-free DNA Removal Kit (Ambion), aliquoted, and stored in -80°C. Quantity and quality of the RNA samples were assessed using the Agilent 2100 Bioanalyzer, the Agilent RNA 6000 Nano Kit (Agilent Technologies), and Qubit fluorometer. Libraries were prepared starting with 300-500 ng of good quality total RNA (RIN ≥7.5) using the TruSeq Stranded Total RNA Library Prep Kit with Ribo-Zero Human/Mouse/Rat (Illumina), according to the manufacturer's instructions. The kit contains 96 uniquely indexed adapter combinations in order to allow pooling of multiple samples prior to sequencing. After determining their size (with the Agilent 2100 Bioanalyzer and the Agilent High Sensitivity DNA Kit by Agilent Technologies) and concentration (by qPCR with the KAPA Illumina ABI Prism Library Quantification Kit, Kapa Biosystems), libraries have been pooled and sequenced (single-end, 125 bp) using a Single End V4 Cluster Kit and an Illumina HiSeq2500 or HiSeq4000 instrument.

  Dataset EGAD00001003508

• Distinct evolutionary trajectories of primary high grade serous ovarian cancers revealed through spatial mutational profiling

  High-grade serous ovarian cancer (HGSC) is characterized by poor outcome, often attributed to the emergence of treatment-resistant subclones. We sought to measure the degree of genomic diversity within primary, untreated HGSCs to examine the natural state of tumour evolution prior to therapy. We performed exome sequencing, copy number analysis, targeted amplicon deep sequencing and gene expression profiling on 31 spatially and temporally separated HGSC tumour specimens (six patients), including ovarian masses, distant metastases and fallopian tube lesions. We found widespread intratumoural variation in mutation, copy number and gene expression profiles, with key driver alterations in genes present in only a subset of samples (eg PIK3CA, CTNNB1, NF1). On average, only 51.5% of mutations were present in every sample of a given case (range 10.2 to 91.4%), with TP53 as the only somatic mutation consistently present in all samples. Complex segmental aneuploidies, such as whole-genome doubling, were present in a subset of samples from the same individual, with divergent copy number changes segregating independently of point mutation acquisition. Reconstruction of evolutionary histories showed one patient with mixed HGSC and endometrioid histology, with common aetiologic origin in the fallopian tube and subsequent selection of different driver mutations in the histologically distinct samples. In this patient, we observed mixed cell populations in the early fallopian tube lesion, indicating that diversity arises at early stages of tumourigenesis. Our results revealed that HGSCs exhibit highly individual evolutionary trajectories and diverse genomic tapestries prior to therapy, exposing an essential biological characteristic to inform future design of personalized therapeutic solutions and investigation of drug-resistance mechanisms

  Dataset EGAD00001000669

• Distinct evolutionary trajectories of primary high grade serous ovarian cancers revealed through spatial mutational profiling

  High-grade serous ovarian cancer (HGSC) is characterized by poor outcome, often attributed to emergence of treatment-resistant sub-clones. We sought to measure the degree of genomic diversity within primary, untreated HGSC to examine the natural state of tumor evolution prior to therapy. We performed exome sequencing, copy number analysis, targeted amplicon deep sequencing and gene expression profiling on thirty-one spatially and temporally separated HGSC tumor specimens (six patients) including ovarian masses, distant metastases, and fallopian tube lesions. We found widespread intra-tumoral variation in mutation, copy number, and gene expression profiles, with key driver alterations in genes present in only a subset of samples (e.g. PIK3CA, CTNNB1, NF1). On average, only 51.5% of mutations were present in every sample of a given case (range: 10.2% to 91.4%), with TP53 as the only somatic mutation consistently present in all samples. Complex segmental aneuploidies, such as whole genome doubling, were present in a subset of samples from the same individual, with divergent copy number changes segregating independently of point mutation acquisition. Reconstruction of evolutionary histories showed one patient with mixed HGSC and endometrioid histology with common etiologic origin in the fallopian tube and subsequent selection of different driver mutations in the histologically distinct samples. In this patient, we observed mixed cell populations in the early fallopian tube lesion, indicating diversity arises at early stages of tumorigenesis. Our results reveal that HGSC exhibit highly individual evolutionary trajectories and diverse genomic tapestries prior to therapy, exposing an essential biological characteristic to inform future design of personalized therapeutic solutions and investigation of drug resistance mechanisms.

  Dataset EGAD00001000974