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 Bièche, I. Articles by Lidereau, R. Search for Related Content PubMed PubMed Citation Articles by Bièche, I. Articles by Lidereau, R.

A Tumor Suppressor Gene on Chromosome 1p32-pter Controls the Amplification of MYC Family Genes in Breast Cancer¹

Laboratoire d'Oncogénétique, Centre René Huguenin, 35 rue Dailly, F-92211 St. Cloud, France

To investigate the possibility of collaboration between telomeric deletion on the short arm of chromosome 1 and genetic amplification similar to that described in human neuroblastoma, 122 human primary breast tumors were examined by restriction fragment length polymorphism analysis for loss of heterozygosity on 1p32-pter and for the three most frequently amplified genetic regions in breast carcinomas (MYC and ERBB2 protooncogenes and the chromosomal region 11q13). Allelic losses at one or more loci on the telomeric part of the short arm of chromosome 1 was observed in 57 (47%) of 122 informative tumors. MYC, ERBB2, and the 11q13 region were amplified in 23, 20, and 21% of breast tumors, respectively. A correlation was found between loss of heterozygosity on chromosome 1p32-pter and amplification of the MYC (formerly c-myc) protooncogene (P = 0.003), suggesting that these two genetic events may collaborate during tumor progression in human breast cancer.

These results, together with those obtained in human neuroblastoma, suggest that the distal part of the short arm of chromosome 1 harbors an unidentified tumor suppressor gene(s), whose inactivation may be involved in MYC family gene amplification (an example of genetic instability) in tumors of various cellular origins.

¹ This work was supported by the Ligue Nationale de Lutte Contre le Cancer; the Comités Régionaux des Hauts de Seine, du Val d'Oise et des Yvelines; and the Association pour la Recherche sur le Cancer. R. L. is a research director with the Institut National de la Santé et de la Recherche Médicale.

² To whom requests for reprints should be addressed.

Received 5/24/94. Accepted 7/ 5/94.

This article has been cited by other articles:

				M. Wang, Y. E. Liu, I. D. Goldberg, and Y. E. Shi Induction of Mammary Gland Differentiation in Transgenic Mice by the Fatty Acid-binding Protein MRG J. Biol. Chem., November 21, 2003; 278(47): 47319 - 47325. [Abstract] [Full Text] [PDF]

				E. H. Radany, K. Hong, S. Kesharvarzi, E. S. Lander, and J. M. Bishop Mouse mammary tumor virus/v-Ha-ras transgene-induced mammary tumors exhibit strain-specific allelic loss on mouse chromosome 4 PNAS, August 5, 1997; 94(16): 8664 - 8669. [Abstract] [Full Text] [PDF]

				T F Lane, C Deng, A Elson, M S Lyu, C A Kozak, and P Leder Expression of Brca1 is associated with terminal differentiation of ectodermally and mesodermally derived tissues in mice. Genes & Dev., November 1, 1995; 9(21): 2712 - 2722. [Abstract] [PDF]

				K L Guan, C W Jenkins, Y Li, M A Nichols, X Wu, C L O'Keefe, A G Matera, and Y Xiong Growth suppression by p18, a p16INK4/MTS1- and p14INK4B/MTS2-related CDK6 inhibitor, correlates with wild-type pRb function. Genes & Dev., December 15, 1994; 8(24): 2939 - 2952. [Abstract] [PDF]