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• Identification of fusion transcripts by RNA-sequencing and Whole genome sequencing of a METABRIC patient sample

  Fusion transcripts and their exact breakpoints were identified in RNA-seq data (30X) of an ER-,HER2+ breast cancer. DNA-level breakpoints associated with the fusion events were determined by analyzing whole genome sequencing (WGS) data (30X) from the same donor. The RNA-seq and WGS data for this case were generated on the Illumina platform using standard protocols. The patient (MB-0152) derives from the METABRIC cohort for which array based copy number and gene expression data were previously described (EGAS00000000083).

  Study EGAS00001002475

• RUNX1 mutated families show phenotype heterogeneity and a somatic mutation profile unique to germline predisposed AML

  We present the clinical phenotypes and genetic mutations detected in 10 novel RUNX1 mutated FPD-MM families. Genomic analyses on these families detected two partial gene deletions, three novel mutations and five recurrent mutations as the germline RUNX1 alterations leading to FPD-MM. On 15 individuals, across the 10 families, we performed additional whole exome or myeloid panel sequencing on blood or bone marrow to determine somatic mutations that co-exist with the germline RUNX1 mutation in tumour and pre-leukaemic states.

  Study EGAS00001004273

• FASTQ files of the polyA+ (oligo-dT) RNA-Seq dataset from the POPS SGA (Small for Gestational Age) samples and their matched controls.

  FASTQ files of the polyA+ (oligo-dT) RNA-Seq dataset from the POPS SGA (Small for Gestational Age) samples and their matched controls. The POP study placental biopsies were collected within 30 minutes of birth and flash frozen in RNAlater (ThermoFisher). For each biopsy, total placental RNA was extracted from approximately 5 mg of tissue using the “mirVana miRNA Isolation Kit” (Ambion) followed by DNase treatment (“DNA-free DNA Removal Kit”, Ambion). RNA quality was assessed with the Agilent Bioanalyzer and all the samples with RIN values ≥ 7.0 were used in the downstream experiments. RNA-libraries were prepared from 1g of total placental RNA with the TruSeq Stranded mRNA Library Prep Kit (Illumina) which captures polyA-tailed transcripts by oligo-dT beads, then pooled and sequenced (single-end, 50bp) using a Single End V4 cluster kit and Illumina HiSeq2500

  Dataset EGAD00001006304

• Lenalidomide Resistance in del(5q) Myelodysplastic Syndrome Follows Loss of RUNX1/TP53-mediated Megakaryocytic Differentiation

  Interstitial deletion of the long arm of chromosome 5 (del(5q)) is the commonest structural genomic variant in myelodysplastic syndromes (MDS). Lenalidomide (LEN) is the treatment of choice for patients with del(5q) MDS, but half of the responding patients become resistant within two years. TP53 mutations are detected in ~20% of patients who become resistant to LEN. Our data show that patients who become resistant to LEN harbor either TP53 or RUNX1 mutations or loss of RUNX1 expression. Here we show that LEN-induced degradation of IKZF1 permits a RUNX1/GATA2 complex to drive megakaryocytic differentiation and consequent del(5q) MDS progenitor cell death via CRBN-mediated CSNK1A1 degradation. Overexpression of GATA2 is able to restore LEN sensitivity in the context of RUNX1 or TP53 mutations by enhancing LEN-induced megakaryocytic differentiation. Screening for TP53 and RUNX1 mutations or downregulation should identify patients resistant to LEN, and strategies to activate GATA2 may resensitize del(5q) MDS cells to LEN.

  Dataset EGAD00001005769

• WGS dataset of Characterization of UV DNA damage in B-cell precursor acute lymphoblastic leukemia

  We characterized B-cell precursor acute lymphoblastic leukemia (BCP-ALL) patients that present with the mutational signature SBS7a. We found clear subtype specificity, but presence of SBS7a did not seem linked to heterogeneity within subtypes. To further distinguish the incidence of SBS7a in pediatric cancer we analyzed a pan-cancer WGS cohort and identified frequent SBS7a in anaplastic large cell lymphomas. As SBS7a is commonly found in skin cancers and has been linked to UV-light induced DNA damage, we compared the features of UV-light induced DNA damage in skin cancer and SBS7a in ALL, and found high similarity. We found no defects in UV damage response pathways in SBS7a-positive samples, indicating no additional UV vulnerability. Additionally, transcriptomic data showed no differences between samples with and without SBS7a. Finally we looked into the moment of exposure to the source of SBS7a by deep sequencing of diagnosis-relapse pairs and single cell whole genome sequencing of diagnosis samples with high SBS7a.

  Dataset EGAD00001015600

• WES data

  WES FASTq files of 76 bulk pre-treatment tumors and 76 matched peripheral blood mononuclear cells from GO30140 group A

  Dataset EGAD00001008129

• Whole exome sequencing of non-small cell lung cancer patient-derived xenografts

  Non-small cell lung cancer (NSCLC) is the leading cause of cancer deaths worldwide. Only a fraction of NSCLC harbour actionable driver mutations and there is an urgent need for patient-derived model systems that will enable the development of new targeted therapies. We generated NSCLC patient-derived xenografts (PDXs) that recapitulate the histology and molecular features of primary NSCLC. Here, we completed whole exome sequencing on 122 NSCLC PDXs.

  Dataset EGAD00001008601

• Tagged-amplicon deep sequencing

  This dataset contains a collection of tumour samples from high grade serous ovarian carcinoma patients with recurrent disease collected near the point of diagnosis as well as tumour samples collected after patient relapse upon or some time after study entry. Whole blood samples were also collected from patients at study entry for the purpose of germline variant detection. The majority of diagnosis samples were preserved in neutral buffered formalin whereas the majority of post-relapse samples were preserved in universal molecular fixative (UMFIX, Sakura Finetek USA, Inc). DNA was extracted and the tagged-amplicon deep sequencing assay was applied (TAm-Seq, Forshew et al. 2002, Sci Transl Med) with the aid of fluidigm access array technology. Targeted loci were sequenced at very high depths (typically >100X) for the detection of both somatic and germline variants. Sequenced reads were aligned to the GRCh37 reference genome (release hs37d5).

  Dataset EGAD00001011058

• Genomics of acral lentiginous melanoma

  Melanoma is the most aggressive type of skin cancer, causing about 75% of dermatological cancer deaths. Acral lentiginous melanoma (ALM) is the most common subtype of melanoma in admixed Latin American populations, but very few tumour genomes and exomes, all from European-descent individuals, have been analysed across several studies. Because of this, the genomic landscape of ALM is mostly unknown. Our aim in this project is to define this landscape and identify driver somatic alterations by whole-exome sequencing a collection of ALM germline/tumour paired FFPE samples from the National Cancer Institute of Mexico. . This dataset contains all the data available for this study on 2023-03-09.

  Dataset EGAD00001010126

• The ALT pathway generates telomere fusions that can be detected in the blood of cancer patients

  Telomere fusions (TFs) can trigger the accumulation of oncogenic alterations leading to malignant transformation and drug resistance. Despite their relevance in tumour evolution, our understanding of the patterns and consequences of TFs in human cancers remains limited. Here, we characterize the rates and spectrum of somatic TFs across >30 cancer types using whole-genome sequencing data. TFs are pervasive in human tumours with rates varying markedly across and within cancer types. In addition to end-to-end fusions, we find novel patterns of TFs that we mechanistically link to the activity of the alternative lengthening of telomeres (ALT) pathway. We show that TFs can be detected in the blood of cancer patients, which enables cancer detection with high specificity and sensitivity even for early-stage tumours and cancers of high unmet clinical need. Overall, we report a novel genomic footprint that enables characterization of the telomere maintenance mechanism of tumours and liquid biopsy analysis.

  Dataset EGAD00001012101