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• Small RNA sequencing of endometrial cancer patients with samples collected prior to diagnosis and controls

  This dataset contains unpaired FASTQ files of 316 endometrial cancer cases and 316 matched controls representing circulating RNAs. RNA count files are provided as the output of sncRNA pipeline and represent 12 RNA types (isomiR, lncRNA, precursor miRNA, miRNA, miscRNA, mRNA, piRNA, scaRNA, snoRNA, snRNA, tRF, and tRNA). We also provide metadata of the samples.

  Dataset EGAD50000000391

• Pharmacological improvement of CFTR function rescues airway epithelial homeostasis and host defense in cystic fibrosis children

  Rationale: Recent clinical trials have shown that elexacaftor/tezacaftor/ivacaftor (ETI) provides significant benefit to patients with cystic fibrosis (CF) by improving CFTR function. Despite these promising clinical findings, the specific effects on the airway inflammatory status leading to structural damage and impaired lung function, remain elusive. Objectives: We investigated the transcriptional changes at the single cell level of airway epithelial and immune cells that underlie the clinical improvement by ETI therapy in children with CF. Methods: Nasal swabs from thirteen children with CF and at least one F508del allele aged 6 to 12 years were collected at baseline and three months after initiation of ETI and subjected to scRNA-seq. In addition, we collected nasal swabs from 12 age- and sex-matched controls. Sweat chloride concentrations, spirometry and multiple breath washout were used for clinical evaluation of CF children. Measurements and main results: ETI significantly reduced sweat chloride concentrations (-52.2 ± 14.3 mmol/L, P < 0.001) and improved the lung clearance index (-1.3 ± 1.8, P < 0.05). Single cell transcriptomics revealed an impaired interferon signalling in epithelial cells of CF children at baseline, which was partially restored by ETI in conjunction with an ETI-induced increase in expression of MHC I and II encoding genes similar to control levels. Additionally, ETI markedly reduced the inflammatory phenotype of immune cells, particularly of neutrophils and macrophages. Conclusions: Improvement of CFTR function by ETI restores epithelial homeostasis and reduces immune cell inflammatory responses in the upper airways of children with CF, highlighting the potential of early initiation of ETI therapy.

  Study EGAS50000000128

• Pilot study of adoptive cell therapy using cultured tumor infiltrating lymphocytes for Japanese melanoma patients refractory to immune-checkpoint inhibitors

  To evaluate feasibility of the adoptive cell therapy (ACT) using tumor infiltrating lymphocytes (TIL) in Japanese melanoma patients who failed the immune checkpoint inhibitors (ICIs) and investigate the immune components and immunologic milieu within the pretreatment tumor and expanded TILs from there.?Three patients whose clinical subtype were mucosal, superficial spreading, and acral melanoma were treated and the all completed the TIL-ACT. Clinical response were one short-partial response, one relatively long-stable disease, and one progression disease. Whole-exome and transcriptional analysis of pretreatment tumor revealed the various?immunophenotypes including tumor mutation burden with immunogenic neoantigens and upregulation of immunosuppressive gene signatures.

  Study JGAS000249

• Dataset for colorectal_cancer-RNA

  Rare cancer sequencing data of 97 runs in tumor/control pairs, which were uploaded to umbrella studies. The sequencing was always paired

  Dataset EGAD00001008855

• GCAT| WGS FASTQ V1

  This dataset include FASTQ files of 808 samples from GCAT cohort. Technology used HiSeq 4000, read length 150 bp, inner mate distance 300 bp. For each sample the paired -ends are generated in separated files. Each FASTQ is splitted in multiple LANEs and grouped by the Multiplex index.

  Dataset EGAD00001008201

• Integrated genomic analyses reveal molecular correlates of clinical response and resistance to atezolizumab in combination with bevacizumab in advanced hepatocellular carcinoma

  Atezolizumab (anti–programmed death-ligand 1 [anti-PD-L1]) and bevacizumab (anti-vascular endothelial growth factor [anti-VEGF]) combination therapy has become the new standard of care in patients with unresectable hepatocellular carcinoma. However, potential predictive biomarkers and mechanisms of response and resistance remain less understood. We report integrated molecular analyses of tumor samples from 358 patients enrolled in the GO30140 phase 1b or IMbrave150 phase 3 trials who were treated with atezolizumab combined with bevacizumab, atezolizumab alone, or sorafenib. Pre-existing immunity assessed by high expression of CD274 (PD-L1 mRNA), T-effector signature, and intratumoral CD8+ T cell density were associated with response and better clinical outcomes with the combination treatment. Less clinical benefit was associated with high regulatory T cell (Treg) to effector T-cell ratio and high expression of oncofetal genes such as GPC3 and AFP. Improved outcomes from the combination vs atezolizumab alone appeared to be associated with high expression of KDR (VEGFR2), Treg, and myeloid inflammation signatures, indicating anti-VEGF may contribute by targeting these axes. These findings were further validated by transcriptome analysis of paired pre- and post-treatment biopsies, in situ analysis by multiplex IHC and digital pathology, and in vivo study of an immunogenic hepatocellular carcinoma mouse model. Our findings highlight that anti-VEGF therapy might augment antitumor immunity and enhance anti–PD-L1 immunotherapy by targeting VEGF-mediated angiogenesis, Treg proliferation, and myeloid cell inflammation. Furthermore, our study identified candidate biomarkers for predicting response and resistance to anti–PD-L1 and anti-VEGF combination therapy.

  Study EGAS00001005503

• Oncogenic cooperation in a human de novo T-ALL model

  We previously modelled T-cell acute lymphoblastic leukemia (T-ALL) by over-expressing four oncogenes (activated NOTCH1, LMO2, TAL1, and BMI1) in healthy human umbilical cord blood cells through lentiviral transduction (Kusakabe et al, Nat Commun 10, 2913 (2019). https://doi.org/10.1038/s41467-019-10510-8). We have now tested individual effects of the four oncogenes by transducing human cells with all possible combinations of one, two, three, and four oncogenes. We also tested the effects of additional known T-ALL oncogenes including HOXA9, LYL1, MEF2C, NXK2.1, TLX1, and TLX3. In addition to culture in vitro on OP9-DL1 feeders, we also injected transduced cells into immunodeficient NSG mice. We observed differing abilities of the various oncogene combinations to support growth in vitro and frank leukemia in vivo. This study includes RNA-seq data from samples of transduced cells cultured in vitro as well as cells harvested from clinically moribund mice after development of leukemia in vivo.

  Study EGAS00001006055

• WGS BAM files fromxa0Genomic Features and Classification of Homologous Recombination Deficient Pancreatic Ductal Adenocarcinoma

  Background and Aims: Homologous recombination deficiency (HRD) in pancreatic ductal adenocarcinoma (PDAC), remains poorly defined beyond germline(g) alterations in BRCA1, BRCA2 and PALB2. Methods: We interrogated whole genome sequencing (WGS) data on 391 patients including 49 carriers of pathogenic variants (PVs) in g_BRCA_ and PALB2. HRD classifiers were applied to the dataset and included: 1) the genomic instability score (GIS) used by Myriad MyChoice HRD assay; 2) substitution base signature 3 (SBS3); 3) HRDetect; and, 4) Structural Variant (SV) burden. Clinical outcomes and responses to chemotherapy were correlated with HRD status. Results: Biallelic tumour inactivation of g_BRCA_ or PALB2 was evident in 43/49 germline carriers identifying HRD-PDAC. HRDetect (score ?0.7) predicted gBRCA1/PALB2 deficiency with highest sensitivity (98%) and specificity (100%). HRD genomic tumour classifiers suggested that 7-10% of PDAC that do not harbor g_BRCA/PALB2_ have features of HRD. Of the somatic HRDetect cases, 69% were attributed to alterations in BRCA1/2, PALB2, RAD51C/D and XRCC2, and a tandem duplicator phenotype. TP53 loss was more common in BRCA1- compared to BRCA2-associated HRD-PDAC. HRD status was not prognostic in resected PDAC. However in advanced disease the GIS (p=0.02), SBS3 (p=0.03) and HRDetect score (p=0.005) were predictive of platinum response and superior survival. PVs in g_ATM_ (n=6) or g_CHEK2_ (n=2) did not result in HRD-PDAC by any of the classifiers. In four patients, BRCA2 reversion mutations associated with platinum resistance. Conclusions: Germline and parallel somatic profiling of PDAC outperforms germline testing alone in identifying HRD-PDAC. An additional 7-10% of patients without gBRCA/PALB2 mutations may benefit from DNA damage response agents.

  Dataset EGAD00001007571

• Translating Gene-Calcium Interactions to Precision Medicine for Colorectal Cancer

  Identify functional and rare SNPs and their interactions with Ca intake levels in relation to risk of incident adenoma using whole-exome resequencing of 2468 colorectal adenoma cases and controls from PLCO. We will genotype promising rare and functional SNPs associated with incident adenoma in 570 incident cancer cases, 1,710 healthy controls, 710 adenoma recurrence cases and 966 recurrent adenoma controls from the intervention arm of PLCO to both confirm the associations with adenoma, and to identify when, in the natural history of CRC, chemoprevention by Ca-gene interactions occurs. We hypothesize that Ca-gene interactions prevent early-stage (incident adenoma) and mid-stage (adenoma recurrence) carcinogenesis as well as span the entire CRC carcinogenesis spectrum (i.e. incident CRC).

  Study phs002164

• Dataset for hepatopancreaticobiliary_malignancy-RNA

  Rare cancer sequencing data of 119 runs in tumor/control pairs, which were uploaded to umbrella studies. The sequencing was always paired

  Dataset EGAD00001008863