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Melanoma, a cancer derived from pigment-producing melanocytes of the skin, is a disease of major public health significance. Although it is the least common form of skin cancer, melanoma is by far the most lethal due to its propensity to metastasize to a number of vital organs, including the brain, lungs, liver, and other visceral organs (1). According to the American Cancer Society’s 2015 Cancer Facts & Figures statistics, melanoma accounts for <2% of all skin cancer cases but is responsible for nearly 75% of skin cancer-related deaths, and it is predicted that melanoma will cause 9,940 deaths in the U.S. this year (2). Worldwide estimates of mortality for melanoma are that this disease is responsible for over 65,000 deaths annually (3). Moreover, recent data collected by the Surveillance, Epidemiology, and End Results (SEER) Program show that melanoma incidence rates have continued to increase over the previous 40 years (4). In the U.S. alone, the current annual costs for treatment and productivity losses associated with melanoma are near $3.3 billion (5). These numbers are even more staggering when considering a recent study by the International Agency for Research on Cancer, which ranked North America only fourth in melanoma incidence worldwide (6), thus highlighting the need to address melanoma as a global public health concern. With these statistics in mind, it is vital that we increase our understanding of the progression of melanoma so that we may improve current – and develop new – therapies for the treatment of this cancer.  The B16 murine melanoma cell line is one of the most widely used models for studying the progression and treatment of melanoma in pre-clinical settings (7, 8). Characterized by its rapid outgrowth as both primary tumors and metastatic lesions, the B16-F1 subline has also been shown to elicit dysfunctional CD8+ T cell responses (9) that mimic those frequently observed in many melanoma patients (10–12), and soluble factors derived from this tumor have been shown to alter the function of dendritic cells (DC) as well (13–15). We have recently described a chemically mutated variant of B16 melanoma, D5.1G4, that is significantly less tumorigenic and immunosuppressive than its wild-type counterpart (13, 15), though the basis for these differences between B16-F1 and D5.1G4 are poorly understood. Therefore, we sought to gain insights into factors that regulate melanoma tumorigenicity by comparing whole genome expression profiles of these murine melanomas. The microarray dataset obtained from these experiments and described herein offers a great resource for investigators wishing to study melanoma growth and progression and will likely drive the design of future experiments aimed at understanding the role of both individual gene products and entire pathways in melanoma tumorigenesis.

frontiers in immunology

Whole Genome Expression Microarray Analysis of Highly Versus Poorly Tumorigenic Murine Melanoma Cell Lines Provides Insights into Factors That Regulate Tumor Growth, Metastasis, and Immunogenicity