Fig. 6.

Genetic modifiers abrogate the response of p53^sh Myc to fluorouracil. (A) ptc>Myc,p53^sh Drosophila strains were cultured in medium containing screening-optimized doses of cancer drugs at 27°C. Viability was assessed and eclosion rate for each drug is shown in percent. DMSO was used as a control for drugs dissolved in DMSO and water was used as a control for drugs dissolved in water (black bars). Fluorouracil (red bar) significantly improved viability (Mann–Whitney U test versus DMSO: P=0.03). (B,C) Fluorouracil was tested on the ptc>Myc,p53^sh line at 27°C (B) and the ptc>Myc,p53^sh line plus six selected driver genes (Hey, Ppcs, aPKC, Dp110, Myb, Rop as indicated) at 27°C (C). In each case, addition of an additional driver led to loss of fluorouracil-mediated rescue. ns, not significant. (D) Fluorouracil was tested at two doses (10 or 50 µM) on control (ptc>w), ptc>Myc,p53^sh (Myc p53^sh), ptc>Myc,p53^sh,Myb (Myc,p53^sh Myb) and ptc>Myc,p53^sh,Dp110 (Myc,p53^sh Dp11) flies, and transgenic tissue overgrowth was quantified as described in Fig. 4B. Two-way ANOVA results were (C) genotype: P<0.0001, drug: ns, interaction: ns; (D) genotype: P<0.0001, drug: P=0.0054, interaction: P=0.0883. Displayed P-values reflect t-tests (see Materials and Methods). See also Table S8.