Bonatz G, Frahm S O, Andreas S, Heidorn K, Jonat W, Parwaresch R
Department of Obstetrics and Gynecology, University of Kiel, Germany.
Am J Obstet Gynecol. 1998 Sep;179(3 Pt 1):591-6. doi: 10.1016/s0002-9378(98)70050-x.
To gain a better understanding of proliferation control mechanisms in a common benign tumor, we investigated the mean telomere length and the clonality of uterine leiomyomas.
Deoxyribonucleic acid from uterine leiomyomas and from the adjacent normal myometrium of 51 patients (total number of uterine leiomyomas 107; 28 patients with single leiomyoma, 23 patients with multiple leiomyomas ranging from 2 to 8 myoma nodules per case) was hybridized to a telomeric oligonucleotide probe by Southern blot and chemiluminescent detection. The mean telomere length was evaluated by densitometry. Clonality was assessed with use of the phosphoglycerokinase gene polymorphism.
The mean telomere length was significantly shorter in uterine leiomyomas (median 7950 bp, interquartile range 7261 to 8372 bp) than in normal myometrium (median 9688 bp, interquartile range 8528 to 10535 bp) (P < .001). There was no correlation between tumor size and telomere attrition. Multiple uterine leiomyomas were found to have an independent clonal origin.
Telomere attrition in uterine leiomyomas reflects enhanced proliferation activity in the course of tumor evolution. The basic telomere lengths differ in the myocytes from which the uterine leiomyomas originate, probably explaining the lack of correlation between telomere attrition and tumor size.
