This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Shirasawa, S. Articles by Sasazuki, T. Search for Related Content PubMed PubMed Citation Articles by Shirasawa, S. Articles by Sasazuki, T.

p53 Gene Mutations in Colorectal Tumors from Patients with Familial Polyposis Coli¹

Department of Genetics, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812 [S. S., K. U., Y. Y., K. T., T. S.], and The Research Center for Polyposis and Intestinal Disease, Tokyo Medical and Dental University, Yushima, Bunkyo-ku, Tokyo 113 [T. I.], Japan

The p53 gene has been elucidated as a tumor suppressor gene, and inactivation of this gene caused by deletion or point mutations may play a crucial role in the development of human malignancies. In colorectal carcinomas with an allelic deletion of the p53 gene, the remaining p53 gene was mutated with considerable frequency. It is most difficult to detect point mutations or small deletions of the gene because the mutations occur in diverse regions, although four hot spots have been observed [J. M. Nigro et al., Nature (Lond.), 342: 705–708, 1989]. The polymerase chain reaction and denaturing gradient gel electrophoresis facilitate detection of mutations in the hot spots of the p53 gene. Using these methods, we detected mutations in three adenomatous polyps and one carcinoma from familial polyposis coli patients and three carcinomas of sporadic cases. The DNA sequence analysis confirmed mutations of the p53 gene in 2 adenomas (13 base-pair deletions in one and a point mutation in the other) and 1 carcinoma (point mutation) from familial polyposis coli patients. These results suggest that the p53 gene mutations may be involved in the formation not only of carcinomas but also of adenomas which occur in familial polyposis coli patients.

¹ This work was supported by Cancer Research Grant-in-Aid 01015079 from the Ministry of Education, Science and Culture, Japan, and by a grant-in-aid from the Fukuoka Cancer Society.

² To whom requests for reprints should be addressed.

Received 9/25/90. Accepted 3/14/91.

This article has been cited by other articles:

				C. J. Piyathilake, A. R. Frost, U. Manne, H. Weiss, D. C. Heimburger, and W. E. Grizzle Nuclear Accumulation of p53 Is a Potential Marker for the Development of Squamous Cell Lung Cancer in Smokers Chest, January 1, 2003; 123(1): 181 - 186. [Abstract] [Full Text] [PDF]

				S Shirasawa, M Furuse, N Yokoyama, and T Sasazuki Altered growth of human colon cancer cell lines disrupted at activated Ki-ras Science, April 2, 1993; 260(5104): 85 - 88. [Abstract] [PDF]

				J E Hulla The rat genome contains a p53 pseudogene: detection of a processed pseudogene using PCR. Genome Res., May 1, 1992; 1(4): 251 - 254. [Abstract] [PDF]