Project description:The goal of this Whole Genome Sequencing (WGS) analysis was to identify genes underlying TCS in C. elegans strain expressing the gut-specific hsp-90 hairpin RNAi construct compared to a control strain (strain AM994). To do this we performed a forward genetic screen using the mutagen EMS and screened progeny for reduced TCS-mediated expression of the hsp-70p::mCherry reporter in muscle cells.
Project description:Primary objectives: The primary objective is to investigate circulating tumor DNA (ctDNA) via deep sequencing for mutation detection and by whole genome sequencing for copy number analyses before start (baseline) with regorafenib and at defined time points during administration of regorafenib for treatment efficacy in colorectal cancer patients in terms of overall survival (OS).
Primary endpoints: circulating tumor DNA (ctDNA) via deep sequencing for mutation detection and by whole genome sequencing for copy number analyses before start (baseline) with regorafenib and at defined time points during administration of regorafenib for treatment efficacy in colorectal cancer patients in terms of overall survival (OS).
Project description:Whole-genome sequencing on PacBio of laboratory mouse strains. See http://www.sanger.ac.uk/resources/mouse/genomes/ for more details. This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/
Project description:We investigated how yeast cells deficient in performing homologous recombination-mediated DNA repair due to a deletion of the critical RAD52 gene respond to irreparable DNA damage inflicted by genotoxic treatment commonly applied in cancer therapy (camptothecin and irradiation). We found that upon persistence of irreparable DNA damage, yeast rad52 mutants readily undergo checkpoint adaptation accompanied by the acquisition of resistance to further genotoxic insults as well as the development of aneuploidy. Together, our findings can be used to elucidate how repair-defective cancer cells can become treatment-resistant thereby providing a way to target these resistant cell clones by tackling their aneuploidy-associated phenotypes. To investigate these characteristics commonly present in aneuploid cells in our experimental set-up, we treated yeast cells with genotoxic agents and performed whole genome sequencing. We could identify frequent whole chromosome loss events manifesting in a sensitivity of cells to aneuploidy-targeting agents.
Project description:Low coverage whole-genome sequencing have been performed on uterine leiomyosarcoma to uncovered novel potential driver genes and recurrently affected pathways.
