Abstract
Fusion of the high-mobility group protein gene HMGIC to other genes
due to chromosomal rearrangements occurs in a variety of human benign
tumors. In contrast to genes clearly derived from other chromosomes,
some of the ectopic sequences fused to HMGIC have been assigned to
chromosome 12 by CASH (chromosome assignment using somatic cell hybrids)
analyses and thus can be assumed either to result from alternative
splicing or to represent true ectopic sequences derived from other
genes on chromosome 12. In an attempt to identify the ectopic sequences
fused to this exon, we have sequenced the entire intron 4. Four of
seven ectopic sequences previously described to be fused to exon
4 of HMGIC in different tumors were found to be located within intron
4 of the gene and thus are due to abnormal splicing. As for a mechanism
explaining this observation, it can be suggested that breakpoints
of chromosomal aberrations not directly disrupting HMGIC may induce
small genomic alterations in their vicinity and thus facilitate abnormal
splicing. The latter mechanism may underlie the development of part
of the neoplasms characterized by 12q14--15 rearrangements.
- alternative_splicing,_genetics
- chromosomes,_human,_pair_12,_genetics
- chromosome_aberrations,_genetics
- high_mobility_group_proteins,_genetics
- hmga1a_protein
- humans
- introns,_genetics
- molecular_sequence_data
- neoplasm_proteins,_genetics
- oncogene_proteins,_fusion,_genetics
- transcription_factors,_genetics
- translocation,_genetic,_genetics
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