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Ovarian cancer is the most malignant gynecologic cancer causing an estimated 140,000 deaths per year worldwide(Jemal et al 2011). In greater than 75% of incident cases, the disease is detected only after it has reached an advanced stage (stage III and IV) when standard therapy is unlikely to be curative. Even after maximal cytoreductive surgery followed by platinum-based chemotherapy, the survival rate at 5 years is only 15-30% (Kosary 1994). Epithelial ovarian cancer is a heterogeneous disease that can be subdivided into four histological categories: serous, clear cell, endometrial, and mucinous. The pathogenesis of the individual subtypes relies on different molecular and pathway aberrations and thus will likely respond with different sensitivities to systemic and targeted therapies(Kurman and Shih Ie 2008). The identification of critical molecular and pathway aberrations specific to each subtype could provide key insights into the mechanisms driving tumorigenesis and direct efforts in the development of targeted therapies. Tumors characteristically display alterations in gene expression that lead to the acquisition of the hallmark features of cancer: uncontrolled proliferation, evasion of growth suppression and of the immune system, resistance to death signals, unlimited replicative potential, development of a supportive microenvironment (including angiogenesis), and ability to invade and metastasize(Hanahan and Weinberg 2011). Aberrant gene expression is manifest through a number of different mechanisms including DNA copy number alterations (amplifications, deletions, gains and losses of whole chromosomes resulting in aneuploidy), epigenetic regulation via methylation or histone acetylation, fusion proteins and individual gene mutations. Amplifications that are critical to tumorigenesis likely are essential because they result in the overexpression of gene products on which the tumor is dependent. These are often referred to as “driver” genes, as dysregulated expression leads to the activation of oncogenic pathways, while other genes in the amplified region may or may not be overexpressed and instead are “passenger” genes. Analysis of individual amplifications have elucidated driver pathways of cancer and revealed potential targets for drug development. For example, amplification of the Her-2/neu gene occurs in 25-30% of breast cancers and is associated with a more aggressive phenotype(Slamon et al 1989). However, treatment with HER-2 targeted therapy, in particular trastuzumab, has dramatically improved the natural history of HER2-positive breast cancer(Ferretti et al 2007). Similarly,

Gene Amplification in Ovarian Carcinomas: Lessons from Selected Amplified Gene Families