Autism spectrum disorder (ASD) is a neurodevelopmental disorder with many clinical manifestations and functional impacts. Though the causes of ASD are complex, it has a strong genetic basis, with copy number variations (CNVs) increasingly being implicated in its aetiology. To gain a further understanding of the mechanisms by which genes within CNVs affect the development of ASD, we developed an in-house bioinformatics pipeline to analyse the CNVs in a cohort of patients diagnosed with ASDs (n=232), to identify potentially novel causative genes and loci involved. 87 patients had no significant CNVs and a further 94 only had CNVs found in unaffected control individuals. For the 51 remaining, 44 had CNVs previously associated with ASD. For 7 patients we report 45 novel segments which have not previously reported as ASD CNV regions. This includes one novel CNV in an intergenic region of chromosome Y (ChrY:13870592-14048611), which is likely to be pathogenic for ASD. To identify likely candidate genes within these novel CNV regions we combined an integrative bioinformatics pipeline with functional genomic analysis using FANTOM5 data to prioritize those with enriched expression in brain and several other functional genomic databases. Using the pipeline, we analysed several novel candidate genes (including FOLH1B, FOLH1, SLC30A9, TBPL1, HMGA1P7, SGK1, MAP7, KIAA1244, NHSL1, REPS1, TXLNB, etc.) within our novel segments and find that alterations to the dosage levels of these genes could contribute to elevated ASD. Taken together, our findings broaden the association of genetic factors for Autism Spectrum Disorder, and identify new genomic loci for further investigation.