Figure 5. Reduced p16^INK4A levels in an atypical HPV+ PDX are shared by recurrent HPV+ cases.

A. Tumor suppressors mutated or deleted in LNT20 relative to the other HPV+ PDXs and TCGA cases. B. CDKN2A DNA levels in the LNT20 PDX and its tumor of origin, relative to control PDXs with WT or deleted CDKN2A. C. p16^INK4A protein by western blot (top) with band densities normalized to actin (bottom) in HPV+ PDXs. D. HPV16 E7 mRNA levels normalized to actin in HPV+ PDXs. E RB protein (top) with corresponding band densities normalized to HSP90 (bottom) in HPV+ PDXs. F. phospho-RB protein (Ser780) (top) and phospho-RB to total RB ratios (bottom). G. E7 vs. p16^INK4A mRNA in all TCGA HPV+ HNSCCs (left) and those with a normalized p16^INK4A mRNA level of <3000 (right inset). Recurrences within 2 years (early recurrence) are highlighted in orange. Pearson correlation coefficients and p-values based on two-tailed Student t-distribution are shown for each plot. H. p16^INK4A mRNA expression in TCGA HPV+ HNSCCs that recurred within 2 years (early recurrence) or were disease-free at the time of last early recurrence. Bars represent mean ± SEM. p-values were determined by randomization test (n = 100,000 permutations) with Welch’s t-statistic. I. p16^INK4A expression in recurrent vs. non-recurrent HPV+ cases with matched follow-up duration in the JHU cohort. Bars represent mean ± SEM. p-values were determined by randomization test (n = 100,000 permutations) with Welch’s t-statistic.