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• Allogeneic induced pluripotent stem (iPS) cell-derived cartilage transplantation for articular cartilage damage in knee joints: a phase I, first-in-human study

  Damaged articular cartilage seldom heals due to a limited capacity for self-repair, frequently leading to osteoarthritis. Regenerative interventions are expected to heal the damage. We have recently established a method to produce cartilage from induced pluripotent stem cells (iPSCs) in a clinically applicable process. The primary aim of this study was to evaluate the safety including tumorigenesis and the subsequence efficacy of allogeneic iPSC-derived cartilage transplantation into damaged areas of knee articular cartilage.

  Study EGAS50000001167

• BE_screens_of_WRN_gene_in_MSI_models

  We will take advantage of a base-editing screening strategy to engineer mutations in the WRN gene by deep mutagenesis. Two MSI-H cell lines sensitive to WRNi will be genetically modified to express doxycycline-inducible ABE and CBE base editors through a knock-in strategy. Moreover, we will design a pooled library of ~4000 gRNAs targeting the WRN gene plus appropriate controls gRNAs. Library-transduced cells will be selected with WRNi to identify WRN mutations able to interfere with the activity of WRNi.

  Study EGAS00001006872

• Exploring_the_landscape_of_somatic_mutations_in_normal_tissue___UGI___WGS

  The aim of this project is to investiagte somatic mutations, including rates of mutations and signatures, and clonal dynamics in normal (non-cancerous) human tissues from the gastrointestinal tract. The project will involve the studyof normal tissues from healthy individuals and those with specific candidate diseases. We are utilising laser capture microscopy to idnetifiy and isolate specific cell populations which are then subjected to whole genome sequencing to estimate mutational burdens and begin to understand clonal structures across the normal tissues.

  Study EGAS00001003541

• Barcelona_kids_with_melanoma

  This set of samples is composed of eight young people (7-16 years old) that have developed melanoma with first-degree relatives that have also developed cancer, which suggests a genetic component to their disease. Here we want to sequence these samples in order to find the causative mutations. As these samples do not carry any of the high-penetrance mutations known to date, finding the genes(s) responsible will offer new insights into the genetic mechanisms underlying predisposition to melanoma.

  Study EGAS00001000733

• Chromosomal instability shapes the tumor microenvironment of oesophageal adenocarcinoma via a cGAS–chemokine–myeloid axis

  This study employed whole-genome sequencing (WGS) to investigate genomic alterations in oesophagogastric adenocarcinoma, with a focus on mechanisms of chromosomal instability. Twelve tumour samples were analysed, including specimens obtained prior to neoadjuvant chemotherapy and at surgical resection. WGS was used to identify structural variants, quantify tumour mutational burden, and detect potential driver mutations across samples. The study aimed to correlate genomic measures of chromosomal instability with clinicopathological features to improve understanding of tumour biology.

  Study EGAS50000001561

• Exploring_the_landscape_of_somatic_mutations_in_normal_tissue___GI___WGS

  The aim of this project is to investiagte somatic mutations, including rates of mutations and signatures, and clonal dynamics in normal (non-cancerous) human tissues from the gastrointestinal tract. The project will involve the studyof normal tissues from healthy individuals and those with specific candidate diseases. We are utilising laser capture microscopy to idnetifiy and isolate specific cell populations which are then subjected to whole genome sequencing to estimate mutational burdens and begin to understand clonal structures across the normal tissues.

  Study EGAS00001003012

• Melanoma_TIL_Study_Exomes

  In this study, mutations present in a series of human melanomas (stage IV disease) will be determined, using autologous blood cells to obtain a reference genome. From each of teh samples that are analyzed, tumour-infiltrating T lymphocytes have also been isolated. This offers a unique opportunity to determine which (fraction of) mutations in human cancer leads to epitopes that are recognized by T cells. The resulting information is likely to be of value to understand how T cell activating drugs exert their action.

  Study EGAS00001000216

• Melanoma_Til_Study_RNAseq

  In this study, mutations present in a series of human melanomas (stage IV disease) will be determined, using autologous blood cells to obtain a reference genome. From each of the samples that are analyzed, tumour-infiltrating T lymphocytes have also been isolated. This offers a unique opportunity to determine which (fraction of) mutations in human cancer leads to epitopes that are recognized by T cells. The resulting information is likely to be of value to understand how T cell activating drugs exert their action.

  Study EGAS00001000251

• Blood RNA-seq from Mexican DMD patients and healthy controls

  These data are part of a study that aimed to assess the potential of blood RNA-seq to track non-invasively disease progression for DMD. In particular, here we focus on a study designed to compare gene expression in blood from DMD patients to that of healthy controls. These data are analysed in the following manuscript: Signorelli, M., Ebrahimpoor, M. et al. (accepted). Peripheral blood transcriptome profiling enables monitoring disease progression in dystrophic mice and patients. To appear in EMBO Molecular Medicine.

  Study EGAS00001004907

• PELICAN33 longitudinal clinical and autopsy phenomic assessment in lethal metastatic prostate cancer

  Objective: To identify novel phenotypes and features associated with metastatic prostate cancer (mPC) outcome, and to identify biomarker and data requirements to be tested in future precision oncology trials. Design, Setting, and Participants: We analyzed deep longitudinal clinical, neuroendocrine expression, and autopsy data of 33 men who died from mPC between 1995 and 2004 (PELICAN33), and related findings to mPC biomarkers reported in the literature. Intervention: 33 men prospectively consented to participate in an integrated clinical-molecular rapid autopsy study of mPC.

  Study EGAS00001005399