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. 2018 Sep 6;9(9):912. doi: 10.1038/s41419-018-0919-9

Fig. 2. Apoptosis induction in p53/p16 mutant malignancy remains toxic to normal cells while simultaneous linked to refractory disease.

Fig. 2

a Data was downloaded from TCGA and ICGC and analyzed in cBioPortal for mutations in TP53 and CDKN2A genes. b Top 10 malignancies with high TP53/CDKN2A alterations (TP53/CDKN2A high). *Cases where these alterations were linked to poor disease-free or overall survival with a p-value < 0.05 (Table S1). c Bottom 10 cases with least frequency of alterations in TP53/CDKN2A (TP53/CDKN2A low). *Cases where these alterations were linked to poor disease-free or overall survival with a p-value ≤ 0.05 d Disease-free survival of testicular cancer, cases with minor alterations (gains, and heterozygous loss of one allele in TP53 and CDKN2A) vs. cases with wild type TP53 and CDKN2A (p-value = 0.211, LogRank test). e Disease-free survival of pancreatic cancer with mutant TP53 and CDKN2A cases was significantly lower vs. cases with wild-type TP53 and CDKN2A (p-value = 0.0078, LogRank test). f Disease-free survival of liver cancer was also significantly lower in mutant TP53 and CDKN2A cases vs. wild-type (p-value = 0.0068, LogRank test). g Quantitative analysis of TP53 and CDKN2A mutations demonstrated less frequency of alteration of these genes in curable vs. high refractory/treatment resistant human malignancies. h During physiologic maturation, unhealthy cells with WT p53/p16 undergo irreversible apoptosis. Alterations in these proteins sustain oncogenic evolution leading to aberrant proliferation without apoptosis