The PISSLRE Gene: structure, exon skipping, and exclusion as tumor suppressor in breast cancer
Date
1999
Authors
Crawford, J.
Ianzano, L.
Savino, M.
Whitmore, S.
Cleton-Jansen, A.M.
Settasatian, C.
d'Apolito, M.
Seshadri, R.
Pronk, J.
Auerbach, A.
Editors
Advisors
Journal Title
Journal ISSN
Volume Title
Type:
Journal article
Citation
Genomics, 1999; 56(1):90-97
Statement of Responsibility
Joanna Crawford, Leonarda Ianzano, Maria Savino, Scott Whitmore, Anne-Marie Cleton-Jansen, Chatri Settasatian, Maria d'Apolito, Ram Seshadri, Jan C. Pronk, Arleen D. Auerbach, Peter C. Verlander, Christopher G. Mathew, Alex J. Tipping, Norman A. Doggett, Leopoldo Zelante, David F. Callen and Anna Savoia
Conference Name
Abstract
In sporadic breast cancer, loss of heterozygosity (LOH) frequently occurs in three discrete regions of the long arm of chromosome 16q, the most telomeric of which is located at 16q24.3. Among the genes mapped to this region,PISSLREis a plausible candidate tumor suppressor gene. It codes for a putative cyclin-dependent kinase that, as with other members of this family, is likely to be involved in regulating the cell cycle and therefore may have a role in oncogenesis. We characterized the genomic structure ofPISSLREand found that the splicing of this gene is complex. A variety of different transcripts were identified, including those due to cryptic splice sites, exon skipping, insertion of intronic sequences, and exon scrambling. The last phenomenon was observed in a rarePISSLREtranscript in which exons are joined at a nonconsensus splice site in an order different from that predicted by the genomic sequence. To screen thePISSLREgene in breast tumors with ascertained LOH at 16q24.3, we have analyzed each exon by single-strand conformational polymorphism. No variation was found in the coding sequence, leading us to conclude that another tumor suppressor must be targeted by LOH in sporadic breast cancer.
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Copyright © 1999 Academic Press