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Molecular Human Reproduction Vol. 2, NUMBER 4 pp. 277-283, 1996
© European Society of Human Reproduction and Embryology 1996

research-article

Diagnosing and preventing inheirted disease

Rearrangements of the high mobility group protein family genes and the molecular genetic origin of uterine leiomyomas and endometrial polyps

Yvonne Hennig1, Sylke Wanschura1, Ulrich Deichert2, Sabine Bartnitzke1 and Jörn Bullerdiek1,3

1Center for Human Genetics and Genetic Counselling, University of Bremen Leobener Str. ZHG, D-28359 Bremen 2Central Hospital St. Jürgen Strasse, Women's Clinic, D-28205 Bremen, Germany

To whom correspondence should be addressed at: 3To whom correspondence should be addressed

The results of cytogenetic studies of uterine leiomyomas have revealed that ~50% of these tumours are characterized by clonal chromosomal alterations. These karyotypic deviations are dominated by rearrangements involving a particular part of chromosome 12, i.e. region 12q13–15. We recently showed that the multiple aberration region on chromosome 12q15 harbours recurrent breakpoints frequently found in a variety of benign solid tumours. Within this region a gene encoding for a member of the so called high mobility group family proteins (HMG) was mapped. Further investigation revealed that this gene i.e. HMGI-C is often truncated by the chromosomal aberrations and fused to ectopic DNA sequences leading to fusion genes. Therefore, the results suggest a causal relationship between mutations of the HMGI-C gene and the development of uterine leiomyomas. Apparently identical mutations have been found also in endometrial polyps. Furthermore, there is an obvious coincidence between the chromosomal assignment of other members of the HMG family and the breakpoints of other non-random chromosome abnormalities seen in uterine leiomyomas.

endometrial polyps/gene rearrangement/high mobility group proteins/uterine leiomyomas


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[Abstract] [Full Text]


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