Gain or over-expression of MYCN has not previously been associated with serous ovarian cancer. Whilst a level of amplification is not as high as typically described in neuroblastoma, we find significant over-expression of N-myc target genes in C5 tumours supporting the view it is functionally active. Recent data shows that even low-level copy number gain of MYCN can significantly influence patient outcome in medulloblastoma. MYCN over-expression was highly C5-specific and mechanisms in addition to amplification are likely to contribute to this. Whilst elements of this pathway have been previously demonstrated to be de-regulated in ovarian cancer, our report is the first to show complete pathway disruption and its association with a specific subtype of HG-SOC. Our analysis indicates that the Let-7 pathway is uniquely prominent amongst signalling events disrupted in C5 tumours, and appears to sculpt their transcriptional profile. The identification of molecular subtypes of breast GYKI 52466 hydrochloride cancer and certain haematological cancers such as diffuse large B-cell lymphoma have provided powerful starting points to discover subtype-specific drivers of disease. Concomitant down regulation of Let-7 and augmented HMGA2 expression results in less differentiated tumours with stem cell-like characteristics. These observations are consistent with the low expression of differentiation markers in C5 tumours, including MUC16, the target of the CA125 antibody used 6β-Hydroxytestosterone clinically for ovarian cancer diagnosis and prognosis. Our work for the first time defines a pathway in HG-SOC that is associated with and appears to drive the biological and clinical behaviour of a distinct molecular subtype of ovarian cancer, suggesting a targeted therapeutic approach in this group of patients. The success of gene therapy to treat diseases in human patients was first demonstrated over a decade ago. Recent studies reporting significant improvement in vision with gene therapy in adult patients with Leber��s congenital amaurosis affirmed the promise of gene therapy to treat eye diseases and prevent blindness in humans. In spite of the progress in gene therapy research, many challenges including the severe side effects caused by the vector and untargeted gene transfer remain to be resolved. The success in the restoration of vision with gene therapy by curing retinal disorders has encouraged more research for defining gene therapy modalities for other ocular tissues.