| [1] Lane DP, Crawford LV. T antigen is bound to a host protein in SV40-transformed cells. Nature, 1979, 278(5701): 261-263.[2] Linzer DI, Levine AJ. Characterization of a 54K dalton cellular SV40 tumor antigen present in SV40-transformed cells and uninfected embryonal carcinoma cells. Cell, 1979, 17(1): 43-52.[3] Rotter V, Witte ON, Coffman R, Baltimore D. Abelson murine leukemia virus-induced tumors elicit antibodies against a host cell protein, P50. J Virol, 1980, 36(2): 547-555.[4] Levine AJ, Finlay CA, Hinds PW. P53 is a tumor suppressor gene. Cell, 2004, 116(2 Suppl.): S67-S69.[5] Efeyan A, Serrano M. p53: guardian of the genome and policeman of the oncogenes. Cell Cycle, 2007, 6(9): 1006-1010.[6] Basse N, Kaar JL, Settanni G, Joerger AC, Rutherford TJ, Fersht AR. Toward the rational design of p53-stabilizing drugs: probing the surface of the oncogenic Y220C mutant. Chem Biol, 2010, 17(1): 46-56.[7] Joerger AC, Ang HC, Fersht AR. Structural basis for understanding oncogenic p53 mutations and designing rescue drugs. Proc Natl Acad Sci USA, 2006, 103(41): 15056-15061.[8] Joerger AC, Fersht AR. The tumor suppressor p53: from structures to drug discovery. Cold Spring Harb Perspect Biol, 2010, 2(6): a000919.[9] Kato S, Han SY, Liu W, Otsuka K, Shibata H, Kanamaru R, Ishioka C. Understanding the function-structure and function-mutation relationships of p53 tumor suppressor protein by high-resolution missense mutation analysis. Proc Natl Acad Sci USA, 2003, 100(14): 8424-8429.[10] Heinlein C, Krepulat F, Löhler J, Speidel D, Deppert W, Tolstonog GV. Mutant p53R270H gain of function phenotype in a mouse model for oncogene-induced mammary carcinogenesis. Int J Cancer, 2008, 122(8): 1701-1709.[11] Bossi G, Lapi E, Strano S, Rinaldo C, Blandino G, Sacchi A. Mutant p53 gain of function: reduction of tumor malignancy of human cancer cell lines through abrogation of mutant p53 expression. Oncogene, 2006, 25(2): 304-309.[12] Gadea G, de Toledo M, Anguille C, Roux P. Loss of p53 promotes RhoA-ROCK-dependent cell migration and invasion in 3D matrices. J Cell Biol, 2007, 178(1): 23-30.[13] Bougeard G, Brugières L, Chompret A, Gesta P, Charbonnier F, Valent A, Martin C, Raux G, Feunteun J, Bressacde Paillerets B, Frébourg T. Screening for TP53 rearrangements in families with the Li-Fraumeni syndrome reveals a complete deletion of the TP53 gene. Oncogene, 2003, 22(6): 840-846.[14] Scian MJ, Stagliano KER, Anderson MAE, Hassan S, Bowman M, Miles MF, Deb SP, Deb S. Tumor-derived p53 mutants induce NF-kappaB2 gene expression. Mol Cell Biol, 2005, 25(22): 10097-10110.[15] Strano S, Dell'Orso S, Di Agostino S, Fontemaggi G, Sacchi A, Blandino G. Mutant p53: An oncogenic transcription factor. Oncogene, 2007, 26(15): 2212-2219.[16] Fontemaggi G, Dell'Orso S, Trisciuoglio D, Shay T, Melucci E, Fazi F, Terrenato I, Mottolese M, Muti P, Domany E, Del Bufalo D, Strano S, Blandino G. The execution of the transcriptional axis mutant p53, E2F1 and ID4 promotes tumor neo-angiogenesis. Nat Struct Mol Biol, 2009, 16(10): 1086-1093.[17] Stambolsky P, Tabach Y, Fontemaggi G, Weisz L, Maor-Aloni R, Siegfried Z, Shiff I, Kogan I, Shay M, Kalo E, Blandino G, Simon I, Oren M, Rotter V. Modulation of the vitamin D3 response by cancer-associated mutant p53. Cancer Cell, 2010, 17(3): 273-285.[18] Caulin C, Nguyen T, Lang GA, Goepfert TM, Brinkley BR, Cai WW, Lozano G, Roop DR. An inducible mouse model for skin cancer reveals distinct roles for gain- and loss-of-function p53 mutations. J Clin Invest, 2007, 117(7): 1893-1901.[19] Lowe SW, Bodis S, McClatchey A, Remington L, Ruley HE, Fisher DE, Housman DE, Jacks T. p53 status and the efficacy of cancer therapy in vi |
