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Science 27 October 1989:
Vol. 246. no. 4929, pp. 491 - 494
DOI: 10.1126/science.2554494
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Articles

Science, Vol 246, Issue 4929, 491-494
Copyright © 1989 by American Association for the Advancement of Science

articles

p53: a frequent target for genetic abnormalities in lung cancer

T Takahashi, MM Nau, I Chiba, MJ Birrer, RK Rosenberg, M Vinocour, M Levitt, H Pass, AF Gazdar, and JD Minna

National Cancer Institute-Navy Medical Oncology Branch, Bethesda, MD 20814.

Allele loss is a hallmark of chromosome regions harboring recessive oncogenes. Lung cancer frequently demonstrates loss of heterozygosity on 17p. Recent evidence suggests that the p53 gene located on 17p13 has many features of such an antioncogene. The p53 gene was frequently mutated or inactivated in all types of human lung cancer. The genetic abnormalities of p53 include gross changes such as homozygous deletions and abnormally sized messenger RNAs along with a variety of point or small mutations, which map to the p53 open reading frame and change amino acid sequence in a region highly conserved between mouse and man. In addition, very low or absent expression of p53 messenger RNA in lung cancer cell lines compared to normal lung was seen. These findings, coupled with the previous demonstration of 17p allele loss in lung cancer, strongly implicate p53 as an anti-oncogene whose disruption is involved in the pathogenesis of human lung cancer.


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Multistep carcinogenesis: a 1992 perspective.
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Wild-type p53 mediates positive regulation of gene expression through a specific DNA sequence element..
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Oncogenic forms of p53 inhibit p53-regulated gene expression.
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P. Chen, Y. Chen, R Bookstein, and W. Lee (1990)
Science 250, 1576-1580
   Abstract »    PDF »
Germ line p53 mutations in a familial syndrome of breast cancer, sarcomas, and other neoplasms.
D Malkin, F. Li, L. Strong, J. Fraumeni Jr, C. Nelson, D. Kim, J Kassel, M. Gryka, F. Bischoff, M. Tainsky, et al. (1990)
Science 250, 1233-1238
   Abstract »    PDF »
Different tumor-derived p53 mutants exhibit distinct biological activities.
O Halevy, D Michalovitz, and M Oren (1990)
Science 250, 113-116
   Abstract »    PDF »
Transcriptional activation by wild-type but not transforming mutants of the p53 anti-oncogene.
L Raycroft, H. Wu, and G Lozano (1990)
Science 249, 1049-1051
   Abstract »    PDF »
Suppression of human colorectal carcinoma cell growth by wild-type p53.
S. Baker, S Markowitz, E. Fearon, J. Willson, and B Vogelstein (1990)
Science 249, 912-915
   Abstract »    PDF »
Association of human papillomavirus types 16 and 18 E6 proteins with p53.
B. Werness, A. Levine, and P. Howley (1990)
Science 248, 76-79
   Abstract »    PDF »
Tumorigenicity in human melanoma cell lines controlled by introduction of human chromosome 6.
J. Trent, E.