Novel therapeutic interventions for p53-altered tumors through manipulation of its family members, p63 and p73

References

• Iwakuma T, Lozano G, Flores ER. Li-Fraumeni syndrome: a p53 family affair. Cell Cycle 2005; 4:865-7; PMID:15917654; http://dx.doi.org/10.4161/cc.4.7.1800
   PubMed Web of Science ®Google Scholar
• Muller PA, Vousden KH. p53 mutations in cancer. Nat Cell Biol 2013; 15:2-8; PMID:23263379; http://dx.doi.org/10.1038/ncb2641
   PubMed Web of Science ®Google Scholar
• Martins CP, Brown-Swigart L, Evan GI. Modeling the therapeutic efficacy of p53 restoration in tumors. Cell 2006; 127:1323-34; PMID:17182091; http://dx.doi.org/10.1016/j.cell.2006.12.007
   PubMed Web of Science ®Google Scholar
• Ventura A. Restoration of p53 function leads to tumour regression in vivo. Nature 2007; 445:661-5; PMID:17251932; http://dx.doi.org/10.1038/nature05541
   PubMed Web of Science ®Google Scholar
• Khoo KH, Verma CS, Lane DP. Drugging the p53 pathway: understanding the route to clinical efficacy. Nat Rev Drug Discov 2014; 13:217-36; PMID:24577402; http://dx.doi.org/10.1038/nrd4288
   PubMed Web of Science ®Google Scholar
• Brown CJ, Lain S, Verma CS, Fersht AR, Lane DP. Awakening guardian angels: drugging the p53 pathway. Nature Rev Cancer 2009; 9:862-73; http://dx.doi.org/10.1038/nrc2763
   PubMed Web of Science ®Google Scholar
• Lane DP. Cancer p53, guardian of the genome. Nature 1992; 358:15-6; PMID:1614522; http://dx.doi.org/10.1038/358015a0
   PubMed Web of Science ®Google Scholar
• Brady CA. Distinct p53 transcriptional programs dictate acute DNA-damage responses and tumor suppression. Cell 2011; 145:571-83; PMID:21565614; http://dx.doi.org/10.1016/j.cell.2011.03.035
   PubMed Web of Science ®Google Scholar
• Feldser DM, Kostova KK, Winslow MM, Taylor SE, Cashman C, Whittaker CA, Sanchez-Rivera FJ, Resnick R, Bronson R, Hemann MT, et al. Stage-specific sensitivity to p53 restoration during lung cancer progression. Nature 2010; 468:572-5; PMID:21107428; http://dx.doi.org/10.1038/nature09535
   PubMed Web of Science ®Google Scholar
• Xue W. Senescence and tumour clearance is triggered by p53 restoration in murine liver carcinomas. Nature 2007; 445:656-60; PMID:17251933; http://dx.doi.org/10.1038/nature05529
   PubMed Web of Science ®Google Scholar
• Wang Y, Suh YA, Fuller MY, Jackson JG, Xiong S, Terzian T, Quintás-Cardama A, Bankson JA, El-Naggar AK, Lozano G. Restoring expression of wild-type p53 suppresses tumor growth but does not cause tumor regression in mice with a p53 missense mutation. J Clin Invest 2011; 121:893-904; PMID:21285512; http://dx.doi.org/10.1172/JCI44504.
   PubMed Web of Science ®Google Scholar
• Lang GA, Iwakuma T, Suh YA, Liu G, Rao VA, Parant JM, Valentin-Vega YA, Terzian T, Caldwell LC, Strong LC, et al. Gain of function of a p53 hot spot mutation in a mouse model of Li-Fraumeni syndrome. Cell 2004; 119:861-72; PMID:15607981; http://dx.doi.org/10.1016/j.cell.2004.11.006
   PubMed Web of Science ®Google Scholar
• Flores ER. p63 and p73 are required for p53-dependent apoptosis in response to DNA damage. Nature 2002; 416:560-4; PMID:11932750; http://dx.doi.org/10.1038/416560a
   PubMed Web of Science ®Google Scholar
• Flores ER. Tumor predisposition in mice mutant for p63 and p73: evidence for broader tumor suppressor functions for the p53 family. Cancer Cell 2005; 7:363-73; PMID:15837625; http://dx.doi.org/10.1016/j.ccr.2005.02.019
   PubMed Web of Science ®Google Scholar
• Olive KP, Tuveson DA, Ruhe ZC, Yin B, Willis NA, Bronson RT, Crowley D, Jacks T. Mutant p53 gain of function in two mouse models of Li-Fraumeni syndrome. Cell 2004; 119:847-60; PMID:15607980; http://dx.doi.org/10.1016/j.cell.2004.11.004
   PubMed Web of Science ®Google Scholar
• Su X, Chakravarti D, Flores ER. p63 steps into the limelight: crucial roles in the suppression of tumorigenesis and metastasis. Nat Rev Cancer 2013; 13:136-43; http://dx.doi.org/10.1038/nrc3446
   PubMed Web of Science ®Google Scholar
• Yang A. p63 is essential for regenerative proliferation in limb, craniofacial and epithelial development. Nature 1999; 398:714-8; PMID:10227294; http://dx.doi.org/10.1038/19539
   PubMed Web of Science ®Google Scholar
• Yang A. p73-deficient mice have neurological, pheromonal and inflammatory defects but lack spontaneous tumours. Nature 2000; 404:99-103; PMID:10716451; http://dx.doi.org/10.1038/35003607
   PubMed Web of Science ®Google Scholar
• Comperat E. p63 gene expression study and early bladder carcinogenesis. Urology 2007; 70:459-62; PMID:17905096; http://dx.doi.org/10.1016/j.urology.2007.04.030
   PubMed Web of Science ®Google Scholar
• Di Como C. J. p63 expression profiles in human normal and tumor tissues. Clin Cancer Res 2002; 8:494-501; PMID:11839669
   PubMed Web of Science ®Google Scholar
• Nylander K. Differential expression of p63 isoforms in normal tissues and neoplastic cells. J Pathol 2002; 198:417-27; PMID:12434410; http://dx.doi.org/10.1002/path.1231
   PubMed Web of Science ®Google Scholar
• Zaika AI, Slade N, Erster SH, Sansome C, Joseph TW, Pearl M, Chalas E, Moll UM. Np73, A Dominant-Negative Inhibitor of Wild-type p53 and TAp73, Is Up-regulated in Human Tumors. J Exp Med 2002; 196:765-80; PMID:12235210; http://dx.doi.org/10.1084/jem.20020179
   PubMed Web of Science ®Google Scholar
• Venkatanarayan A, Raulji P, Norton W, Chakravarti D, Coarfa C, Su X, Sandur SK, Ramirez MS, Lee J, Kingsley CV, et al. IAPP-driven metabolic reprogramming induces regression of p53-deficient tumours in vivo. Nature 2015; 517:626-30; PMID:25409149; http://dx.doi.org/10.1038/nature13910
   PubMed Web of Science ®Google Scholar
• Yang A, p63, a p53 homolog at 3q27-29, encodes multiple products with transactivating, death-inducing, and dominant-negative activities. Mol Cell 1998; 2:305-16; PMID:9774969; http://dx.doi.org/10.1016/S1097-2765(00)80275-0
   PubMed Web of Science ®Google Scholar
• Su X. TAp63 suppresses metastasis through coordinate regulation of Dicer and miRNAs. Nature 2010; 467:986-90; PMID:20962848; http://dx.doi.org/10.1038/nature09459
   PubMed Web of Science ®Google Scholar
• Tomasini R. TAp73 knockout shows genomic instability with infertility and tumor suppressor functions. Genes Dev 2008; 22:2677-91; PMID:18805989; http://dx.doi.org/10.1101/gad.1695308
   PubMed Web of Science ®Google Scholar
• Suzuki S. Phosphate-activated glutaminase (GLS2), a p53-inducible regulator of glutamine metabolism and reactive oxygen species. Proc Natl Acad Sci USA 2010; 107:7461-6; http://dx.doi.org/10.1073/pnas.1002459107
   PubMed Web of Science ®Google Scholar
• Bensaad K. TIGAR, a p53-inducible regulator of glycolysis and apoptosis. Cell 2006; 126:107-20; PMID:16839880; http://dx.doi.org/10.1016/j.cell.2006.05.036
   PubMed Web of Science ®Google Scholar
• Pillay K, Govender P. Amylin uncovered: a review on the polypeptide responsible for type II diabetes. Bio Med Res Int 2013; 2013:826706; PMID:23607096; http://dx.doi.org/10.1155/2013/826706
   PubMed Web of Science ®Google Scholar
• Edelman S, Maier H, Wilhelm K. Pramlintide in the treatment of diabetes mellitus. Bio Drugs 2008; 22:375-86; PMID:18998755; http://dx.doi.org/10.2165/0063030-200822060-00004
   PubMed Web of Science ®Google Scholar
• Christopoulos G. Multiple amylin receptors arise from receptor activity-modifying protein interaction with the calcitonin receptor gene product. Mol Pharmacol 1999; 56:235-42; PMID:10385705
   PubMed Web of Science ®Google Scholar