a Protein analysis of GTML2 and GTML2/ + MYC cell lines. MYCN expression and apoptotic activity decreases following dox treatment when replaced by MYC expression in this system. b GTML2/ + MYC cells treated with dox in vitro see a partial decrease in cell survival and viability when MYCN expression is suppressed, but cells are selected and proliferate when MYC likely becomes the new oncogenic driver. n = 3 for each treatment variable. Mean ± SD. c GTML2/ + MYC cells treated with dox in vitro over a period of 7 days show an increase in MYC levels and reduction of MYCN levels during the dox/TetOFF switch. This switch leads to reduction of ARF levels from de novo suppression of ARF. d Protein analysis of GMYC1, GMYC/ + MYCVD, GTML2, and GTML2/ + MYC cell lines. e Protein analysis of GMYC1 and GTML2 cell lines. Demethylation agent, 5-Azacytidine, shows a concentration gradient of ARF upregulation in response over 12 h of treatment in GMYC1 cells. Such as response is not elicited in GTML2 cells. f Dose response curve showing a similar, non-significant difference of 5-Azacytidine treatment on GMYC and GTML cells. g GMYC and GTML cells treated with the calculated EC50 value (for GMYC cells) for 5-Azacytidine concentration. ANOVA analysis shows there is no difference in treatment response to this agent for MYC- or MYCN-driven cell lines. h GMYC1 cells were treated in vitro with 5-Azacytidine over 3 days. The highest concentration (1 μmol/L) caused a reduction in cell viability and proliferation. n = 3 for each treatment variable. Mean ± SD. i GMYC1 cells were then treated in vitro with 5-Azacytidine (demethylation), cisplatin (alkylation), or combination treatment over 3 days. Independent treatments saw a reduction in cell viability and proliferation. n = 3 for each treatment variable. Mean ± SD. All experimental data from immunostainings (a, c, d, e) and treatments (b, f, h, i) was verified from at least two independent biological replicates.