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• Broad utility of ultrasensitive analysis of ctDNA dynamics across solid tumors treated with immunotherapy

  Prior studies have suggested the biomarker potential of plasma circulating tumor DNA (ctDNA) in cancer patients treated with immune checkpoint inhibitors (ICIs). In order to characterize the potential role of ultrasensitive ctDNA detection in the management of these patients we have performed tumor whole-genome-informed, ultrasensitive ctDNA analysis—tracking approximately 1,800 tumor-specific mutations per patient—in a retrospective cohort (n=136) and a prospective validation cohort (n=66) across 24 cancer types treated with ICIs alone or in combination with bispecific antibodies or immune cell engagers. Analyzing 1,455 longitudinal samples, we found that ctDNA molecular response measured as early as 3 weeks after treatment initiation correlated with improved progression-free and overall survival, while ctDNA clearance at any time strongly correlated with radiological response and prolonged survival. Additionally, ctDNA dynamics distinguished true progression from pseudoprogression and predicted outcomes in patients receiving continued immunotherapy beyond initial progression. This study highlights the broader applicability of ultrasensitive ctDNA as a biomarker across cancer types and immunotherapy modalities.

  Study EGAS50000001333

• Djerroudi et al., E-cadherin inactivation shapes tumor microenvironment specificities in invasive lobular carcinoma

  Invasive lobular breast carcinoma (ILC) shows specific stromal features, T lymphocyte infiltration (TIL) being associated with poor prognosis. Here, we reveal the involved mechanism by performing single cell RNA sequencing, combined immunohistochemistry, deconvolution of bulk RNA sequencing from large retrospective ILC series, and functional assays using primary cells. We show that ILC accumulate FAP+ inflammatory cancer-associated fibroblasts (iCAF) through a previously undescribed mechanism mediated by E-cadherin/CDH1 on CAF plasticity. Indeed, CDH1 inactivation in ILC cancer cells prevents differentiation of iCAF into myofibroblastic CAF (myCAF), leading to iCAF accumulation. In turn, iCAF increase TIL infiltration and shape their spatial organization in ILC. Subsequently, CDH1-inactivated ILC cancer cells promote immune escape by lack of retention and activation of ITGAE-expressing resident memory CD8+ T lymphocytes (TRM). Hence, our study uncovers reciprocal interactions between CDH1-inactivated cancer cells, iCAF and CD8+ TRM, revealing why and how TILs have a poor prognosis in ILC patients, a mechanism extrapolated to other CDH1-mutated cancer types.

  Study EGAS50000000761

• Mitochondrial-Nuclear Mutational Cross-Talk Drives Recurrence of Localized Prostate Cancer

  Prostate cancer remains the most prevalent non-skin cancer in men, but has a remarkably quiet mutational profile. Exome sequencing studies have revealed few recurrent somatic single nucleotide variants (SNVs). Whole-genome sequencing studies have not yet identified highly recurrent driver non-coding SNVs (ncSNVs) or genomic rearrangements (Grs). As a result, the underlying events that drive this frequent disease remain unknown. While mitochondrial mutations have been linked to several tumour types, including prostate cancer, their global frequency and impact has remained unknown. To determine if mitochondrial mutations might drive some prostate cancers, we analyzed the mitochondrial genomes of 216 tumours from patients with the most commonly diagnosed form of prostate cancer. We developed a pipeline that conservatively identified only mitochondrial SNVs (mitoSNVs) that differed in the heteroplasmy fraction as compared to their paired-normal by at least 20%. We identified several features of the mitochondrial genome that were correlated with nuclear genomic mutations, as well as features that were significantly associated with biochemical recurrence.

  Study EGAS00001001782

• Integrated single cell analysis in transformed follicular lymphoma

  Histological transformation of follicular lymphoma to aggressive form occurs 2-3% per year with poor outcome. Divergent evolution and an altered tumour-microenvironment (TME) have been implicated during transformation. However, phenotypic consequences of this evolution and its implication in TME remain unknown. To address this, we performed single cell whole genome and whole transcriptome sequencing of paired pre/post transformation patient samples. We further performed scWTS of additional samples from patients without transformation. Our analysis revealed evolutionary dynamics of transformation at unprecedented resolution. Integration of scWGS and scWTS identified pathways upregulated during evolution. scWTS analysis revealed a shifting TME landscape, with an exhausted signature emerging during transformation. Using multi-color immunofluorescence we transferred these findings to a TME-based transformation biomarker, subsequently validated in independent pretreatment cohorts. Taken together, our results provide a comprehensive view of the combined genomic and phenotypic evolution of malignant cells during transformation, and shifting cross-talk between malignant cells and TME.

  Study EGAS00001007023

• DATA FILES FOR SJOS

  DATA FILES FOR SJOS

  Dataset EGAD00001000159

• DATA FILES FOR SJLGG

  DATA FILES FOR SJLGG

  Dataset EGAD00001000161

• Screening for abnormal CGI methylation in primary colorectal tumours

  Screening for abnormal CGI methylation in primary colorectal tumours

  Dataset EGAD00001000213

• DATA FILES FOR SJLGG

  DATA FILES FOR SJLGG

  Dataset EGAD00001000352

• DATA FILES FOR SJLGG

  DATA FILES FOR SJLGG

  Dataset EGAD00001000353

• Saliba Lab Data Access Committee

  DAC for data generated by Saliba Lab at Helmholtz institute for RNA-based Infection Research, Würzburg, Germany

  Dac EGAC50000000152

• WGS and WXS files for Dyer ATRX study

  WGS and WXS files for Dyer ATRX study

  Dataset EGAD00001003389

• RNA-Seq data for Juvenile Pilocytic Astrocytomas

  RNA-Seq data for 9 JPA samples.

  Dataset EGAD00001009043

• IFN-γ and TNF-α drive a CXCL10+ CCL2+ Macrophage Phenotype Expanded in Severe COVID-19 Lungs and Inflammatory Diseases with Tissue Inflammation

  We explored how the human macrophages response to different inflammatory factors, focusing particularly on the effects of antiviral interferons (IFN-β and IFN-γ), pro-inflammatory cytokines such as TNF-α, and other mediators like IL-4. Co-cultured fibroblasts were a component in some conditions to generate factors produced by resident stroma. We used a single-cell antibody-based hashing strategy to multiplex samples from different stimulatory conditions in one sequencing run. This macrophage transcriptomic data reveals distinct macrophage activation states and polarizations shaped by different tissue-related inflammatory conditions at single-cell resolution. We further performed an unbiased integration between tissue-level macrophages and this stimulated human blood-derived macrophages, which pinpoint an IFN-γ and TNF-α synergistically driven inflammatory macrophage phenotype expanded in severe COVID-19 lungs and other inflamed disease tissues.

  Study phs002780

• Translational analyses from a phase II study of pembrolizumab and epigenetic modification with azacitidine in platinum-resistant epithelial ovarian cancer

  Epigenetic modulators may sensitize platinum-resistant ovarian cancer (PROC) to immune checkpoint inhibition by reprogramming the tumor microenvironment. We report clinical and translational findings from a phase II non-randomized study of pembrolizumab and oral azacytidine in 34 women with PROC (NCT02900560). The effect of combined epigenetic and immunotherapy was evaluated by transcriptomic analyses of serially biopsied tumors. Differential gene expression analyses revealed an upregulation of inflammatory and cytolytic genes and co-inhibitory checkpoints 6 weeks on-therapy. Upregulation of interferon signaling, antigen presentation and immune cell adhesion and migration gene sets was prominent on-therapy, together with an increased density of CD8+ T -cells. Patients with a CA-125 and/or clinical response showed an enrichment of adaptive and conserved immune response gene sets on-therapy.

  Study EGAS50000001165

• WTCCC case-control study for Rheumatoid Arthritis

  WTCCC genome-wide case-control association study for Rheumatoid Arthritis (RA) using the 1958 British Birth Cohort and the UK National Blood Service collections as controls.

  Study EGAS00000000011

• WTCCC case-control study for Type 1 Diabetes

  WTCCC genome-wide case-control association study for Type 1 Diabetes (T1D) using the 1958 British Birth Cohort and the UK National Blood Service collections as controls.

  Study EGAS00000000014

• WTCCC case-control study for Type 2 Diabetes

  WTCCC genome-wide case-control association study for Type 2 Diabetes (T2D) using the 1958 British Birth Cohort and the UK National Blood Service collections as controls.

  Study EGAS00000000016

• WTCCC case-control study for Coronary Artery Disease

  WTCCC genome-wide case-control association study for Bipolar disorder (CAD) using the 1958 British Birth Cohort and the UK National Blood Service collections as controls.

  Study EGAS00000000003

• Genome-wide analysis for non alcoholic fatty liver disease

  Genome-wide association study for the 902 patients of non alcoholic fatty liver disease (NAFLD) including non alcoholic steato hepatitis (NASH) and hepatocellurar carcinoma and 7672 controls.

  Study JGAS000126

• BLUEPRINT September 2016, ATAC-seq for monocyte RPMI_LPS_T=24hrs_RPMI_T=5days from venous blood, on Genome GRCh38

  ATAC-seq data for 2 sample(s) for monocyte RPMI_LPS_T=24hrs_RPMI_T=5days from venous blood, on Genome GRCh38. 2 run(s), 2 experiment(s), 2 alignment(s). Part of BLUEPRINT (September 2016).

  Dataset EGAD00001002901

• ChIP-seq fastq and alignment files

  ChIP-seq experiments: fastq files; both ChIP and Input for each sample. Illumina HiSeq 2500. ChIP-seq alignment files for trimmed, mapping q20 and nonredundant reads; both ChIP and Input for each sample. Software: Trim Galore v0.3.7; Bowtie 2 v2.1.0; samtools v1.7

  Dataset EGAD00001006279

• BLUEPRINT September 2016, ATAC-seq for monocyte RPMI_BG_T=1hr from venous blood, on Genome GRCh38

  ATAC-seq data for 1 sample(s) for monocyte RPMI_BG_T=1hr from venous blood, on Genome GRCh38. 1 run(s), 1 experiment(s), 1 alignment(s). Part of BLUEPRINT (September 2016).

  Dataset EGAD00001002906

• BLUEPRINT September 2016, ATAC-seq for monocyte RPMI_BG_T=24hrs_RPMI_T=5days from venous blood, on Genome GRCh38

  ATAC-seq data for 1 sample(s) for monocyte RPMI_BG_T=24hrs_RPMI_T=5days from venous blood, on Genome GRCh38. 1 run(s), 1 experiment(s), 1 alignment(s). Part of BLUEPRINT (September 2016).

  Dataset EGAD00001002904

• BLUEPRINT September 2016, ATAC-seq for unswitched memory B cell from venous blood, on Genome GRCh38

  ATAC-seq data for 3 sample(s) for unswitched memory B cell from venous blood, on Genome GRCh38. 3 run(s), 3 experiment(s), 3 alignment(s). Part of BLUEPRINT (September 2016).

  Dataset EGAD00001002905

• BLUEPRINT September 2016, ATAC-seq for monocyte RPMI_BG_T=4hrs from venous blood, on Genome GRCh38

  ATAC-seq data for 1 sample(s) for monocyte RPMI_BG_T=4hrs from venous blood, on Genome GRCh38. 1 run(s), 1 experiment(s), 1 alignment(s). Part of BLUEPRINT (September 2016).

  Dataset EGAD00001002910