Translocation breakpoints upstream of the HMGIC gene in uterine leiomyomata suggest dysregulation of this gene by a mechanism different from that in lipomas
✍ Scribed by Marlena Schoenberg Fejzo; Hena R. Ashar; Kenneth S. Krauter; W. Lee Powell; Mitchell S. Rein; Stanislawa Weremowicz; Sung-Joo Yoon; Raju S. Kucherlapati; Kiran Chada; Cynthia C. Morton
- Book ID
- 102655773
- Publisher
- John Wiley and Sons
- Year
- 1996
- Tongue
- English
- Weight
- 537 KB
- Volume
- 17
- Category
- Article
- ISSN
- 1045-2257
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✦ Synopsis
Uterine leiomyomata are the most common pelvic tumors in women and are the indication for more than 200.000 hysterectomies annually in the United States. Rearrangement of chromosome I2 in bands q 14-q I 5 is characteristic of uterine leiomyomata and other benign mesenchymal tumors, and we identified a yeast artificial chromosome (YAC) spanning chromosome I 2 translocation breakpoints in a uterine leiomyoma, a pulmonary chondroid hamartoma, and a lipoma. Recently, we demonstrated that HMGIC, which is an architectural factor mapping within the YAC, is disrupted in lipomas, resulting in novel fusion transcripts. Here, we report on the localization of translocation breakpoints in seven uterine leiomyomata from I0 t o > I00 kb upstream of HMGIC by use of fluorescence in situ hybridization. Our findings suggest a different pathobiologic mechanism in uterine leiomyomata from that in lipomas. HMGIC is the first gene identified in chromosomal rearrangements in uterine leiomyomata and has important implications for an understanding of benign mesenchymal proliferation and differentiation. Genes Chromosom Cancer 17:l-6 (1996).