This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend 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 Mazars, R. Articles by Theillet, C. Search for Related Content PubMed PubMed Citation Articles by Mazars, R. Articles by Theillet, C.

p53 Mutations Occur in Aggressive Breast Cancer¹

CNRS URA 1191, Laboratoire de Biologie Moléculaire, Université Montpellier II, place Eugène Bataillon, 34095 Montpellier Cedex 2 [R. M., L. S., M. B., P. J., C. T.]; Laboratoire de Biochimie, CRLC Val d'Aurelle, 34094 Montpellier Cedex 5 [R. M., M. B., P. J., C. T.]; and Service d'Anatomo-Pathologie [J. S-L.], France

Using a polymerase chain reaction-single strand conformation polymorphism approach we analyzed 96 human primary breast tumors for the presence of mutations in exons 2, 5, 6, 7, 8, and 9 of the p53 gene. These exons have been shown to comprise highly conserved sequences and the portion including exons 5 through 9 is believed to be the target for over 90% of the acquired mutations in human cancer. Eighteen tumors of the 96 (18.7%) tested showed reproducibly a variant band indicative of a mutation. Most (15 tumors) of the mutations were single nucleotide substitutions and G:C to A:T transitions were prevalent (6 tumors), G:C to T:A transversions came next (4 tumors), and guanines were always on the nontranscribed strand. Concomitant loss of the wild type allele and mutation of the other copy was observed in only 3 of 18 mutated cases; this is consistent with the heterogeneous cellular composition of breast tumors. Furthermore p53 mutations were correlated to estrogen and/or progesterone receptor negative tumors, thus indicating their relationships to aggressive breast cancer. No association could be observed with DNA amplification events in these tumors.

¹ R. M. was supported by a predoctoral fellowship from the Association de la Recherche sur le Cancer; M. B. C. was supported by a predoctoral fellowship from the Comité Départemental de l'Hérault de la Ligue Nationale Contre le Cancer; L. S. was on exchange supported by a program from the EEC (Eureka). This work was in part funded by the Caisse Régionale d'Assurance Maladie, the Fédération Nationale des Centres de Lutte Contre le Cancer, and the Ligue Nationale de Lutte Contre le Cancer.

² Permanent address: Department of Biomedical Science, Medical School of the University of Torino, 10121 Torino, Italy.

³ To whom requests for reprints should be addressed.

Received 12/ 9/91. Accepted 5/ 7/92.

This article has been cited by other articles:

				M. Amari, T. Moriya, T. Ishida, Y. Harada, K. Ohnuki, M. Takeda, H. Sasano, A. Horii, and N. Ohuchi Loss of Heterozygosity Analyses of Asynchronous Lesions of Ductal Carcinoma in situ and Invasive Ductal Carcinoma of the Human Breast Jpn. J. Clin. Oncol., November 1, 2003; 33(11): 556 - 562. [Abstract] [Full Text] [PDF]

				C. D. Nicholls, K. G. McLure, M. A. Shields, and P. W. K. Lee Biogenesis of p53 Involves Cotranslational Dimerization of Monomers and Posttranslational Dimerization of Dimers. IMPLICATIONS ON THE DOMINANT NEGATIVE EFFECT J. Biol. Chem., April 5, 2002; 277(15): 12937 - 12945. [Abstract] [Full Text] [PDF]

				J. Lawler, W.-M. Miao, M. Duquette, N. Bouck, R. T. Bronson, and R. O. Hynes Thrombospondin-1 Gene Expression Affects Survival and Tumor Spectrum of p53-Deficient Mice Am. J. Pathol., November 1, 2001; 159(5): 1949 - 1956. [Abstract] [Full Text] [PDF]

				P. Robbins p53 and Breast Cancer International Journal of Surgical Pathology, October 1, 1996; 4(2): 93 - 110. [Abstract] [PDF]