Comparison of transcriptomic profile of the murine B16F1-GFP-M melanoma cells with the derived dormant B16F1-GFP-D, B16F1-GFP-DB#1, B16F1-GFP-DB#2, B16F1-GFP-DB#3 melanoma cells

Cancer patients after successful therapy contain nested in their organs and/or circulating in the systemic fluids tumor cells that remain asymptomatic for an extended period of time. They stay dormant with no apparent immediate potential to develop into a clinically manifested tumor until activated by yet not well defined mechanisms. We previously developed tumor dormancy model of murine melanoma, a cancer with a high potential of phenotype plasticity to adapt to micro-environmental changes, in which to investigate cellular quiescence and related factors as a potential mechanism of tumour dormancy. In this study, to explore molecular mechanism responsible for cellular dormancy, we performed a comparative transcriptome analysis of dormant B16F1-GFP-D and derived dormant brain metastasis (DB) with maternal B16F1-GFP-M cells. Transcriptomic profiling of myeloid and melanoma cell lines in the context of dormancy.