ENAapplication/xmlftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR306/029/SRR30648829/SRR30648829.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR306/025/SRR30648825/SRR30648825.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR306/021/SRR30648821/SRR30648821.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR306/028/SRR30648828/SRR30648828.fastq.gzftp://primaryOK200GenomicsCancer, Hospital del Mar Medical Research Institutehttps://www.ebi.ac.uk/ena/browser/view/PRJNA1160298Mus musculusPancreatic cancer represents one of the most lethal tumours, characterised by an immunosuppressive microenvironment and a lack of cytotoxic immune cell infiltrates, which confers resistance to immunotherapy. Here, we demonstrate that the deletion of Poly(ADP-ribose)polymerase 2 (PARP2) delays tumour progression in c-Myc-driven and KRas-driven mouse models of pancreatic cancer. Transcriptomic analysis revealed that the absence of PARP2 induces an enrichment of pathways associated with anti-tumor immune responses and genomic instability. Analysis of tumour-infiltrating immune cells within the tumor microenvironment showed that PARP2 deletion leads to an increase in effector CD4 and CD8 T cells as well as natural killer (NK) cells, accompanied by a significant reduction in pro-tumor regulatory T (Treg) cells and M2 macrophages. Collectively, our data support that selective PARP2 inhibition is a promising therapeutic strategy for pancreatic cancer by boosting anti-tumor immune response, thereby opening new avenues for combating this recalcitrant neoplasia. Overall design: To investigate the role of PARP2 in pancreatic tumor development, we isolated pancreatic tissue from 3-month old Ela-myc wildy type and PARP2 knocked-out animals. We then performed gene expression profiling analysis using data obtained from RNA-seq of 3 different animals of each genotype (WT or PARP2 KO).ENAfalseEffect of depletion of PARP2 on gene expression in 3 month-old pancreas from Ela-myc miceEffect of depletion of PARP2 on gene expression in 3 month-old pancreas from Ela-myc mice2025-09-242025-06-07PRJNA1160298GSE27705510090