Project description:Control and CDYL1-depleted U2OS-DIvA cells were treated with 4-hydroxy tamoxifen (4OHT) to induce multiple DNA double-strand breaks (DSBs) at defined loci in the genome via AsiSI restriction enzyme. This system was used to map the changes in lysine crotonylation (Kcr) and ENL at DSB sites in control and CDYL1-deficient cells.
Project description:We used Single-cell RNA-sequencing to analyze the composition of the tumor microenvironment of MC38mOVA tumors upon transcutaneous immunization with our immunization method DIVA.
Project description:We used the Differential Viral Integration (DIVA) technique to compare chromatin accessibility in wild-type versus MORC2 knockout HeLa cells.
Project description:IDH1 mutation impacts CTCF binding and function through methylating cytosine in the CTCF binding motif. We hypothesize that the impairment of CTCF-associated DNA repair process may be relevant to the loss of CTCF chromatin association and shifts in chromatin conformation. Chromatin immunoprecipitation-sequencing confirmed the loss of CTCF coverage in the proximity sites of AsisI sites in IDH1 mutant 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:Determining the role of DDX17 in the formation of DNA:RNA-hybrids around active DNA double-strand breaks (DSBs) using DRIP-seq in the damaged induced via AsiSI (DIvA) cell system that induced DSBs at known genomic loci in response to hydroxytamoxifen (OHT) treatment via and AsiSI enzyme fused to an oestrogen receptor. Sequencing was done using either control or DDX17 siRNA, and mock or 4 hours 300nM OHT treatment. Paired-end 150 cycles was completed on an Illumina NextSeq 500 and library prep was completed using the NEB NEBNext Ultra II library prep kit.
Project description:DNA Double Strands Breaks (DSBs) are highly detrimental since they can lead to mutations and chromosomes rearrangements (amplification, deletion, translocation and chromosome loss). Here, we used in a standardized system, where multiples DSBs are induced at defined positions across the human genome (U2OS-DIvA cells), to describe the distribution of eighteen histone modifications before and after damage using ChIP-Seq. This provides a comprehensive picture of the chromatin landscape induced at DSBs.
