Distinct gene expression patterns of highly and poorly malignant melanocytic tumors from genetically engineered mouse models of mice carrying specific inactivating mutations in Ink4A or ARF respectively

Cutaneous malignant melanoma is among the most deadly human cancers, broadly resistant to most clinical therapies. A majority of patients with BRAFV600E melanomas respond well to inhibitors such as vemurafenib, but all ultimately relapse. Moreover, there are no viable treatment options available for other non-BRAF melanoma subtypes in the clinic. A key to improving treatment options lies in a better understanding of mechanisms underlying melanoma progression, which are complex and heterogeneous. In this study we perform gene expression profilling of highly and poorly malignant melanocytic tumors from genetically engineered mouse models to discover important drivers of cancer progression. Briefly, RNA (three biological replicates) was isolated using TRIzol reagent, according to the manufacturer's instructions (Invitrogen), and quantified fluorimetrically using an Agilent Bioanalyser (Agilent Technologies).vBiotinylated cRNA were prepared according to the standard Affymetrix protocol. Affymetrix GeneChip Mouse Genome 430 2.0 Array was scanned using Affymetrix standard scan protocol.