Verifying the the safety of any viral vector is an important precursor to clinical applications of gene therapy. Recent evidence links integrations of AAV genomes within or near oncogenes within the liver to hepatocellular carcinoma1, with a potential cause being a liver-specific promoter-enhancer element in the 3’ UTR of the wild-type AAV2 genome2. Indeed, viruses are estimated to cause 10-15% of all human cancer cases with well-characterised examples including the association between human papillomavirus (HPV) and cervical cancers, as well as hepatitis B virus (HBV) and cancers of the liver (hepatocellular carcinoma, HCC)3. We sought to explore the pattern of viral integration in cells treated with AAV vectors. Furthermore, with a large amount of genomic data available from consortia such as The Cancer Genome Atlas (TCGA)2 and the International Cancer Genome Consortium (ICGC)3, we investigated whether viruses without previously established roles in cancer might be associated with particular cancer types. We therefore aimed to investigate insertional mutagenesis in next-generation sequencing (NGS) data from AAV-treated cells and publicly available data from cancer tissue and matched healthy control tissue. To analyse these data, we developed a pipeline for the identification of viral integration sites. In this approach, we aligned reads first to the human and viral genomes, and then identified potential chimeric reads as evidence for integration. We then used this pipeline to search publicly available cancer sequence data for evidence of viral insertional mutagenesis. Preliminary results identify a large number of viral integrations in vector-treated cells, and confirm the role of known cancer-associated viruses in particular cancer types. Our findings may have implications for the safety of gene therapy vectors, and for prevention of cancers caused by novel cancer-associated viruses.