Human Molecular Genetics, Vol 8, 515-521, Copyright © 1999 by Oxford University Press
S Ding, GP Larson, K Foldenauer, G Zhang and TG Krontiris
DNA sequence analysis of 130 alleles of the HRAS1 minisatellite has
demonstrated that breast cancer-associated variants arise as a consequence
of both replication errors and gene conversions. Unlike mutations at other
variable number of tandem repeats (VNTRs), high-risk variants of the HRAS1
minisatellite do not demonstrate positional polarity. Instead, most
mutations occur at three hotspots, with replication errors confined to one
hotspot, gene conversions to a second and a mixed pattern of mutation at
the third. DNA sequence analysis of 66 low-risk a1 alleles revealed no
evidence for hypermutation. Therefore, while the HRAS1 minisatellite may
serve as a reporter for a broad-based group of mutational mechanisms, these
results are consistent with a direct pathogenetic contribution by high-
risk alleles as the biological basis underlying cancer association of this
VNTR.
ARTICLES
Distinct mutation patterns of breast cancer-associated alleles of the HRAS1 minisatellite locus
Division of Molecular Medicine, Beckman Research Institute of the City of Hope National Medical Center, 1500 East Duarte Road, Duarte, CA 91010, USA.
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