Abstract
Alterations of chromosomes 7 and 11 have been involved in the progression of atherosclerosis.
Twenty-three carotid endarterectomy specimens were studied for the presence of alterations
in chromosomes 7 and 11, and fibroblastic growth factor-3 (FGF-3) gene amplification.
Besides classic histological stainings, immunophenotyping of cellular and vascular
components and fluorescence in situ hybridization (FISH) were performed. At the caps,
unstable plaques (n=18) showed inflammatory infiltration of macrophages, smooth muscle cells, and T-lymphocytes.
Specifically in these regions, the FISH showed varying percentages of trisomy (15/18)
and tetrasomy (8/15) of chromosome 7. In four cases polisomy 7 was noted in some nuclei.
Monosomy of chromosome 11 and gene amplification of FGF-3 gene was observed. The FISH
of the five stable plaques and normal arterial walls showed no chromosome alterations;
furthermore, chromosome 3, which is not involved in atherosclerotic progression, presented
a normal ploidy of smooth muscle cells in stable and unstable plaques and normal arterial
walls. In conclusion, chromosome 7 and 11 alterations and FGF-3 gene amplification
are components of unstable plaques, and might contribute to the evolution of stable
plaques into complicated plaques.
Keywords
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Article info
Publication history
Accepted:
March 29,
2000
Received in revised form:
March 8,
2000
Received:
April 13,
1998
Identification
Copyright
© 2001 Elsevier Science Ireland Ltd. Published by Elsevier Inc. All rights reserved.
