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Science 5 July 1991:
Vol. 253. no. 5015, pp. 49 - 53
DOI: 10.1126/science.1905840

Articles

Science, Vol 253, Issue 5015, 49-53
Copyright © 1991 by American Association for the Advancement of Science


articles

p53 mutations in human cancers

M Hollstein, D Sidransky, B Vogelstein, and CC Harris

Laboratory of Human Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.

Mutations in the evolutionarily conserved codons of the p53 tumor suppressor gene are common in diverse types of human cancer. The p53 mutational spectrum differs among cancers of the colon, lung, esophagus, breast, liver, brain, reticuloendothelial tissues, and hemopoietic tissues. Analysis of these mutations can provide clues to the etiology of these diverse tumors and to the function of specific regions of p53. Transitions predominate in colon, brain, and lymphoid malignancies, whereas G:C to T:A transversions are the most frequent substitutions observed in cancers of the lung and liver. Mutations at A:T base pairs are seen more frequently in esophageal carcinomas than in other solid tumors. Most transitions in colorectal carcinomas, brain tumors, leukemias, and lymphomas are at CpG dinucleotide mutational hot spots. G to T transversions in lung, breast, and esophageal carcinomas are dispersed among numerous codons. In liver tumors in persons from geographic areas in which both aflatoxin B1 and hepatitis B virus are cancer risk factors, most mutations are at one nucleotide pair of codon 249. These differences may reflect the etiological contributions of both exogenous and endogenous factors to human carcinogenesis.


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   Abstract »    Full Text »    PDF »
In vitro analysis of DNA-protein interactions by proximity ligation.
S. M. Gustafsdottir, J. Schlingemann, A. Rada-Iglesias, E. Schallmeiner, M. Kamali-Moghaddam, C. Wadelius, and U. Landegren (2007)
PNAS 104, 3067-3072
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Common Genetic Variation in TP53 Is Associated with Lung Cancer Risk and Prognosis in African Americans and Somatic Mutations in Lung Tumors.
L. E. Mechanic, E. D. Bowman, J. A. Welsh, M. A. Khan, N. Hagiwara, L. Enewold, P. G. Shields, L. Burdette, S. Chanock, and C. C. Harris (2007)
Cancer Epidemiol. Biomarkers Prev. 16, 214-222
   Abstract »    Full Text »    PDF »
p53 Enhances Gefitinib-Induced Growth Inhibition and Apoptosis by Regulation of Fas in Non-Small Cell Lung Cancer.
J. K. Rho, Y. J. Choi, B.-Y. Ryoo, I. I. Na, S. H. Yang, C. H. Kim, and J. C. Lee (2007)
Cancer Res. 67, 1163-1169
   Abstract »    Full Text »    PDF »
Sensitizing Effect of Galectin-7 in Urothelial Cancer to Cisplatin through the Accumulation of Intracellular Reactive Oxygen Species.
Y. Matsui, S. Ueda, J. Watanabe, I. Kuwabara, O. Ogawa, and H. Nishiyama (2007)
Cancer Res. 67, 1212-1220
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Inactive full-length p53 mutants lacking dominant wild-type p53 inhibition highlight loss of heterozygosity as an important aspect of p53 status in human cancers.
L. R. Dearth, H. Qian, T. Wang, T. E. Baroni, J. Zeng, S. W. Chen, S. Y. Yi, and R. K. Brachmann (2007)
Carcinogenesis 28, 289-298
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Protoporphyrin IX Interacts with Wild-type p53 Protein in Vitro and Induces Cell Death of Human Colon Cancer Cells in a p53-dependent and -independent Manner.
J. Zawacka-Pankau, N. Issaeva, S. Hossain, A. Pramanik, G. Selivanova, and A. J. Podhajska (2007)
J. Biol. Chem. 282, 2466-2472
   Abstract »    Full Text »    PDF »
Dissecting the Senescence-like Program in Tumor Cells Activated by Ras Signaling.
T. Bihani, A. Chicas, C. P.-K. Lo, and A. W. Lin (2007)
J. Biol. Chem. 282, 2666-2675
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Abrogation of the Transactivation Activity of p53 by BCCIP Down-regulation.
X. Meng, J. Yue, Z. Liu, and Z. Shen (2007)
J. Biol. Chem. 282, 1570-1576
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Synergistic Tumor Suppression by Coexpression of FUS1 and p53 Is Associated with Down-regulation of Murine Double Minute-2 and Activation of the Apoptotic Protease-Activating Factor 1-Dependent Apoptotic Pathway in Human Non-Small Cell Lung Cancer Cells.
W.-G. Deng, H. Kawashima, G. Wu, G. Jayachandran, K. Xu, J. D. Minna, J. A. Roth, and L. Ji (2007)
Cancer Res. 67, 709-717
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A Novel Application for Murine Double Minute 2 Antagonists: The p53 Tumor Suppressor Network Also Controls Angiogenesis.
B. R. Binder (2007)
Circ. Res. 100, 13-14
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Is there a role for PCR-SSCP among the methods for missense mutation detection of TP53 gene?.
J Peltonen, J A Welsh, and K H Vahakangas (2007)
Human and Experimental Toxicology 26, 9-18
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Development of a novel site-specific mutagenesis assay using MALDI-ToF MS (SSMA-MS).
K. I. E. McLuckie, J. H. Lamb, J. K. Sandhu, H. L. Pearson, K. Brown, P. B. Farmer, and D. J. L. Jones (2006)
Nucleic Acids Res.
   Abstract »    Full Text »    PDF »
Reprimo Methylation Is a Potential Biomarker of Barrett's-Associated Esophageal Neoplastic Progression..
J. P. Hamilton, F. Sato, Z. Jin, B. D. Greenwald, T. Ito, Y. Mori, B. C. Paun, T. Kan, Y. Cheng, S. Wang, et al. (2006)
Clin. Cancer Res. 12, 6637-6642
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BM88 Is a Dual Function Molecule Inducing Cell Cycle Exit and Neuronal Differentiation of Neuroblastoma Cells via Cyclin D1 Down-regulation and Retinoblastoma Protein Hypophosphorylation.
N. Georgopoulou, C. Hurel, P. K. Politis, M. Gaitanou, R. Matsas, and D. Thomaidou (2006)
J. Biol. Chem. 281, 33606-33620
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Retinoblastoma Pathway Defects Show Differential Ability to Activate the Constitutive DNA Damage Response in Human Tumorigenesis.
F. Tort, J. Bartkova, M. Sehested, T. Orntoft, J. Lukas, and J. Bartek (2006)
Cancer Res. 66, 10258-10263
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Schedule-Dependent Synergy between the Heat Shock Protein 90 Inhibitor 17-(Dimethylaminoethylamino)-17-Demethoxygeldanamycin and Doxorubicin Restores Apoptosis to p53-Mutant Lymphoma Cell Lines..
A. I. Robles, M. H. Wright, B. Gandhi, S. S. Feis, C. L. Hanigan, A. Wiestner, and L. Varticovski (2006)
Clin. Cancer Res. 12, 6547-6556
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The Consensus Coding Sequences of Human Breast and Colorectal Cancers.
T. Sjoblom, S. Jones, L. D. Wood, D. W. Parsons, J. Lin, T. D. Barber, D. Mandelker, R. J. Leary, J. Ptak, N. Silliman, et al. (2006)
Science 314, 268-274
   Abstract »    Full Text »    PDF »



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