Deletion of HMG17 in uterine leiomyomas with ring chromosome 1.

Abstract Uterine leiomyomas are characterized by several subgroups with characteristic chromosomal aberrations, mainly 12q14–15, 6p21, or interstitial deletions of chromosomes 3 and 7. For the first two subgroups, aberrations of the HMGIC and HMGIY genes have been described and are held responsible for tumor initiation. For other subgroups no molecular findings have been described as of yet. We focus here on a smaller subgroup of uterine leiomyomas with a ring chromosome 1 either as the only karyotypic deviation or occurring along with other abnormalities. In the p-arm of chromosome 1 HMG17 , another member of the high-mobility group of proteins has been localized to the short arm of chromosome 1 (1p35) with two PAC clones on metaphase spreads of a uterine leiomyoma ring(1). Hybridization signals for these probes were not detected within the ring chromosome consistent with loss or deletion of HMG17. These findings suggest that HMG17 does not play a mechanistic role in leiomyoma similar to that observed with other high-mobility proteins.