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[Cancer Research 59, 19-23, January 1, 1999]
© 1999 American Association for Cancer Research
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[Cancer Research 59, 19-23, January 1, 1999]
© 1999 American Association for Cancer Research

Advances in Brief

Allelic Knockout of Novel Splice Variants of Human Recombination Repair Gene RAD51B in t(12;14) Uterine Leiomyomas1

Eric F. P. M. Schoenmakers2, Christel Huysmans and Wim J. M. Van de Ven

Laboratory for Molecular Oncology, Center for Human Genetics, University of Leuven, and Flanders Interuniversity Institute for Biotechnology, B-3000 Leuven, Belgium

Recently, the high mobility group protein gene HMGIC was identified as the chromosome 12q15 target gene in a variety of benign solid tumors. Here, we report that the recombinational repair gene RAD51B on chromosome 14q23–24 is the preferential translocation partner of HMGIC in uterine leiomyomas. The pathogenetically critical sequences seem to reside in the last coding exon of a novel RAD51B isoform, which encode a domain containing a putative transmembrane anchor and are expressed in the uterus but not in a wide variety of other tissues tested. By fluorescence in situ hybridization, rapid amplification of 3' cDNA ends, and reverse transcription-PCR analysis, we demonstrated consistent chromosomal rearrangements within RAD51B and expression of fusion transcripts, structurally resulting in an allelic knockout of the uterine isoform of RAD51B and confirming a pleiotropic function of this gene.




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Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
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Copyright © 1999 by the American Association for Cancer Research.