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• Polyclonal selection of immune checkpoint mutations in thyroid autoimmunity - LCMB_WES

  Our immune system contains multiple tolerance checkpoints to prevent the activation of self-reactive lymphocytes. How some lymphocytes escape these constraints to cause autoimmune disease remains poorly understood. A long-standing hypothesis in autoimmunity posits that somatic mutations in immune regulatory genes may enable self-reactive lymphocytes to bypass tolerance checkpoints. However, testing this hypothesis has proved challenging due to technical limitations in detecting somatic mutations in polyclonal cell populations. Here, we use deep whole-exome and targeted NanoSeq, a highly accurate single-molecule DNA sequencing protocol, to comprehensively search for driver mutations in autoimmune thyroid disease. This revealed a remarkably high number of B cell clones convergently acquiring loss-of-function somatic mutations in key immune checkpoint genes TNFRSF14 (also known as HVEM) and CD274 (encoding PD-L1), as well as less frequent driver mutations in a diversity of other immune genes. In highly inflamed biopsies, we detected tens to hundreds of independent immune-checkpoint mutant clones. Laser capture microdissection, methylation sequencing, spatial transcriptomics, immunohistochemistry and single-nucleus DNA sequencing localised these mutations to non-naive B cells and revealed frequent co-occurrence of drivers in single cells. We found widespread TNFRSF14 biallelic loss in mutant B cells, and several clones with as many as 4-6 driver mutations. Whilst each clone accounts for a small proportion of cells (typically <1%), the myriad mutant clones in each donor collectively amounted to a substantial fraction of B cells harbouring one or more driver mutations. Our results support the hypothesis that somatic mutations in autoimmune lymphocytes may allow them to escape tolerance constraints through a polyclonal cascade of somatic evolution. These findings provide new insights into the molecular basis of autoimmune disease and suggest novel diagnostic and therapeutic avenues.

  Dataset EGAD00001016065

• Using RNA-sequencing to characterize the resistance to lirafugratinib

  In addition to Exome-sequencing, we used RNA-sequencing to also characterize resistance to lirafugratinib with whole exome sequencing in patients with FGFR2-driven cancers, treated in the phase 1/2 ReFocus trial (NCT04526106) and enrolled in the UNLOCK program at Gustave Roussy

  Study EGAS50000001370

• 3D chromatin analysis of clear cell renal cell carcinoma using micro-C

  To investigate the 3D structure of chromatin in ccRCC, we performed micro-C on 3 ccRCC cell lines (786-O, A498, UMRC-2), and 1 normal kidney epithelium cell line (HK-2), cultured under normoxic (20% O2) and hypoxic (0.05% O2) conditions

  Study EGAS50000001323

• Single-cell RNA-seq of immune cell subsets isolated from human tumors (Kaptein et al., 2024)

  Single-cell RNA-seq profiling of effector (KLRG1+ PD1-), transitional (KLRG1+ PD1-intermediate), dysfunctional (CD39+ PD1+) and memory (IL7Rα+) CD8 T cells isolated from 4 human tumors (1 melanoma, 1 renal carcinoma and 2 ovarian carcinoma). Respective cell populations were identified and isolated using FACS. FASTQ files contain gene expression data, feature barcode antibody capture or TCR data on individual CD8 T cell subsets across the 4 different samples.

  Dataset EGAD50000000376

• Resistance_to_MAPK_inhibitor_induces_internal_duplication_in_BRAF

  2 BRAFV600E cell lines that have been made resistance to 1. the BRAF inhibitor PLX4720 and 2. the combination therapy of dabrafenib and trametinib seem to have a internal duplication in the kinase domain. We would like to know if this is caused by a translocation.

  Study EGAS00001001304

• Whole genome sequences and variant calls from human cells exposed to UV and CX5461

  Bulk whole genome sequencing data from 38 samples, including patient skin biopsies from 15 patients and RPE-1 cell line data. The targeted sequencing depth was 80X. The dataset also also includes somatic short variants from 15 patients treated with CX5461, and somatic short variants from 3 treatments of 2 genotypes of RPE-1 cells.

  Dataset EGAD50000001640

• Whole Genome sequencing of colorectal cancer patients (SG-BULK-1)

  Whole Genome sequencing of colorectal cancer patients (SG-BULK-1)

  Dataset EGAD00001008566

• ATAC-seq dataset of patient and healthy donors

  ATAC-seq dataset on a patient (P) presenting with defects of immunity and two (C5, C6) healthy donors. This dataset contains raw and processed files from ATAC-seq chromatin accessibility analysis. There are 3 single-read (50 bp) fastq files (1 per patient/ donor). Processed files consist of narrowPeak files (1 per patient/ donor) and one file that contains read counts in consensus peaks.

  Dataset EGAD00001008370

• Colorectal cancer samples WES

  The whole exome was sequenced in two cancer-affected members (II:1 and III:1) of the family. The family subject of this study showed an autosomal dominant mode of CRC inheritance, fulfilling the Amsterdam I clinical criteria with three CRCs in two consecutive generations. The exome capture was performed using SureSelectXT Human All Exon V3 (51Mb, Agilent Technologies), and the library was sequenced on an Illumina HiSeq 2000 platform with paired-end reads of 101bp and a 50x average coverage depth.

  Dataset EGAD00001009170

• Genomic Analysis of Anaplastic Thyroid Carcinoma

  This dataset includes WGS & WTS alignment data generated from 1 ATC tumor, its matched peripheral blood specimen and 3 authenticated ATC cell lines, THJ-16T, THJ-21T and THJ-29T. In addition, it includes WTS data from extra 4 unique anaplastic cell lines, ACT-1, C643, HTh7 and T238.

  Dataset EGAD00001001321