Literature DB >> 9790751

Characterization and screening for mutations of the growth arrest-specific 11 (GAS11) and C16orf3 genes at 16q24.3 in breast cancer.

S A Whitmore1, C Settasatian, J Crawford, K M Lower, B McCallum, R Seshadri, C J Cornelisse, E W Moerland, A M Cleton-Jansen, A J Tipping, C G Mathew, M Savnio, A Savoia, P Verlander, A D Auerbach, C Van Berkel, J C Pronk, N A Doggett, D F Callen.   

Abstract

Loss of heterozygosity involving the long arm of chromosome 16 is a frequent event seen in a number of human carcinomas, including breast, prostate, hepatocellular, and ovarian cancers. A region found to be commonly deleted in breast and prostate carcinomas is located at 16q24.3, which suggests the presence of a tumor suppressor gene that may be altered in these two malignancies. A detailed physical and transcription map of this region that includes the loci defining the smallest region of deletion has been constructed. This report describes the characterization of a transcript located in this region, the growth arrest-specific 11 (GAS11) gene, which was viewed as a potential tumor suppressor gene due to the expression of its mouse homolog specifically during growth arrest. The gene consists of 11 exons spanning approximately 25 kb. Northern blot analysis identified two ubiquitously expressed mRNAs of 3.4 and 1.8 kb produced by the use of alternative polyadenylation sites. Another gene, C16orf3 (chromosome 16 open reading frame 3), was found to lie within intron 2 of GAS11. This gene appears intronless, is transcribed in the orientation opposite to that of GAS11, and is expressed at low levels. These genes were examined for mutations in breast tumor DNA, and both were excluded as tumor suppressor genes involved in breast cancer. Copyright 1998 Academic Press.

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Year:  1998        PMID: 9790751     DOI: 10.1006/geno.1998.5457

Source DB:  PubMed          Journal:  Genomics        ISSN: 0888-7543            Impact factor:   5.736


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