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Science 24 August 1990:
Vol. 249. no. 4971, pp. 912 - 915
DOI: 10.1126/science.2144057
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Articles

Science, Vol 249, Issue 4971, 912-915
Copyright © 1990 by American Association for the Advancement of Science

articles

Suppression of human colorectal carcinoma cell growth by wild-type p53

SJ Baker, S Markowitz, ER Fearon, JK Willson, and B Vogelstein

Oncology Center, Johns Hopkins University School of Medicine, Baltimore, MD 21231.

Mutations of the p53 gene occur commonly in colorectal carcinomas and the wild-type p53 allele is often concomitantly deleted. These findings suggest that the wild-type gene may act as a suppressor of colorectal carcinoma cell growth. To test this hypothesis, wild-type or mutant human p53 genes were transfected into human colorectal carcinoma cell lines. Cells transfected with the wild-type gene formed colonies five- to tenfold less efficiently than those transfected with a mutant p53 gene. In those colonies that did form after wild-type gene transfection, the p53 sequences were found to be deleted or rearranged, or both, and no exogenous p53 messenger RNA expression was observed. In contrast, transfection with the wild-type gene had no apparent effect on the growth of epithelial cells derived from a benign colorectal tumor that had only wild-type p53 alleles. Immunocytochemical techniques demonstrated that carcinoma cells expressing the wild-type gene did not progress through the cell cycle, as evidenced by their failure to incorporate thymidine into DNA. These studies show that the wild-type gene can specifically suppress the growth of human colorectal carcinoma cells in vitro and that an in vivo-derived mutation resulting in a single conservative amino acid substitution in the p53 gene product abrogates this suppressive ability.


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J. Virol. 75, 7774-7777
   Abstract »    Full Text »    PDF »
After portal branch ligation in the rat, cellular proliferation in associated with selective induction of c-Ha-ras, p53, cyclin E, and Cdk2.
P Starkel, L Lambotte, C Sempoux, C De Saeger, A Saliez, D Maiter, and Y Horsmans (2001)
Gut 49, 119-130
   Abstract »    Full Text »    PDF »
Controlling Tumor-Derived and Vascular Endothelial Cell Growth : Role of the 4F2 Cell Surface Antigen.
M. Papetti and I. M. Herman (2001)
Am. J. Pathol. 159, 165-178
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Mutations and Allelic Loss of p53 in Primary Tumor DNA From Potentially Cured Patients With Colorectal Carcinoma.
A. Forslund, C. Lonnroth, M. Andersson, H. Brevinge, and K. Lundholm (2001)
J. Clin. Oncol. 19, 2829-2836
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Tetraploid State Induces p53-dependent Arrest of Nontransformed Mammalian Cells in G1.
P. R. Andreassen, O. D. Lohez, F. B. Lacroix, and R. L. Margolis (2001)
Mol. Biol. Cell 12, 1315-1328
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The Retinoblastoma Gene Regulates Somatic Growth during Mouse Development.
A. Yu. Nikitin, B. Shan, A. Flesken-Nikitin, K.-H. Chang, and W.-H. Lee (2001)
Cancer Res. 61, 3110-3118
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Change of the Death Pathway in Senescent Human Fibroblasts in Response to DNA Damage Is Caused by an Inability To Stabilize p53.
A. Seluanov, V. Gorbunova, A. Falcovitz, A. Sigal, M. Milyavsky, I. Zurer, G. Shohat, N. Goldfinger, and V. Rotter (2001)
Mol. Cell. Biol. 21, 1552-1564
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A TSG101/MDM2 regulatory loop modulates MDM2 degradation and MDM2/p53 feedback control.
L. Li, J. Liao, J. Ruland, T. W. Mak, and S. N. Cohen (2001)
PNAS 98, 1619-1624
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Effects of the (-)-anti-11R,12S-dihydrodiol 13S,14R-epoxide of dibenzo[a,l]pyrene on DNA adduct formation and cell cycle arrest in human diploid fibroblasts.
B. Mahadevan, A. Luch, A. Seidel, J. C. Pelling, and W. M. Baird (2001)
Carcinogenesis 22, 161-169
   Abstract »    Full Text »    PDF »
Hairless is translocated to the nucleus via a novel bipartite nuclear localization signal and is associated with the nuclear matrix.
K Djabali, V. Aita, and A. Christiano (2001)
J. Cell Sci. 114, 367-376
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Cells Degrade a Novel Inhibitor of Differentiation with E1A-Like Properties upon Exiting the Cell Cycle.
S. Miyake, W. R. Sellers, M. Safran, X. Li, W. Zhao, S. R. Grossman, J. Gan, J. A. DeCaprio, P. D. Adams, and W. G. Kaelin Jr. (2000)
Mol. Cell. Biol. 20, 8889-8902
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RB18A, Whose Gene Is Localized on Chromosome 17q12-q21.1, Regulates in Vivo p53 Transactivating Activity.
R. Frade, M. Balbo, and M. Barel (2000)
Cancer Res. 60, 6585-6589
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Dendritic Cells Break Tolerance and Induce Protective Immunity against a Melanocyte Differentiation Antigen in an Autologous Melanoma Model.
M. W. J. Schreurs, A. A. O. Eggert, A. J. de Boer, J. L. M. Vissers, T. van Hall, R. Offringa, C. G. Figdor, and G. J. Adema (2000)
Cancer Res. 60, 6995-7001
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The tumour suppressor protein p53 can repress transcription of cyclin B.
K. Krause, M. Wasner, W. Reinhard, U. Haugwitz, C. Lange-zu Dohna, J. Mossner, and K. Engeland (2000)
Nucleic Acids Res. 28, 4410-4418
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Defective nuclear localization of p53 protein in a Chinese hamster cell line is associated with the formation of stable cytoplasmic protein multimers in cells with gene amplification.
L. Ottaggio, S. Bozzo, F. Moro, A. Sparks, P. Campomenosi, M. Miele, S. Bonatti, G. Fronza, D. P. Lane, and A. Abbondandolo (2000)
Carcinogenesis 21, 1631-1638
   Abstract »    Full Text »    PDF »
Repression of RNA Polymerase I Transcription by the Tumor Suppressor p53.
W. Zhai and L. Comai (2000)
Mol. Cell. Biol. 20, 5930-5938
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Selection of a Dominant Negative Retinoblastoma Protein (RB) Inhibiting Satellite Myoblast Differentiation Implies an Indirect Interaction between MyoD and RB.
F.-Q. Li, A. Coonrod, and M. Horwitz (2000)
Mol. Cell. Biol. 20, 5129-5139
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A Pentamer Transcriptional Complex Including tal-1 and Retinoblastoma Protein Downmodulates c-kit Expression in Normal Erythroblasts.
L. Vitelli, G. Condorelli, V. Lulli, T. Hoang, L. Luchetti, C. M. Croce, and C. Peschle (2000)
Mol. Cell. Biol. 20, 5330-5342
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p53 Recruitment of CREB Binding Protein Mediated through Phosphorylated CREB: a Novel Pathway of Tumor Suppressor Regulation.
H. A. Giebler, I. Lemasson, and J. K. Nyborg (2000)
Mol. Cell. Biol. 20, 4849-4858
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Multiple Ras Downstream Pathways Mediate Functional Repression of the Homeobox Gene Product TTF-1.
C. Missero, M. T. Pirro, and R. Di Lauro (2000)
Mol. Cell. Biol. 20, 2783-2793
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