Canevari, R. A.Pontes, Anaglória [UNESP]Rosa, F. E.Rainho, C. A.Rogatto, Silvia Regina [UNESP]2014-05-202014-05-202005-10-01American Journal of Obstetrics and Gynecology. St Louis: Mosby, Inc., v. 193, n. 4, p. 1395-1403, 2005.0002-9378http://hdl.handle.net/11449/13425Objective: In an attempt to clarify the clonality and genetic relationships that are involved in the tumorigenesis of uterine leiomyomas, we used a total of 43 multiple leiomyomas from 14 patients and analyzed the allelic status with 15 microsatellite markers and X chromosome inactivation analysis.Study design: We have used a set of 15 microsatellite polymorphism markers mapped on 3q, 7p, 11, and 15q by automated analysis. The X chromosome inactivation was evaluated by the methylation status of the X-linked androgen receptor gene.Results: Loss of heterozygosity analysis showed a different pattern in 7 of the 8 cases with allelic loss for at least 1 of 15 microsatellite markers that were analyzed. A similar loss of heterozygosity findings at 7p22-15 was detected in 3 samples from the same patient. X chromosome inactivation analysis demonstrated the same inactivated allele in all tumors of the 9 of 12 informative patients;. different inactivation patterns were observed in 3 cases.Conclusion: Our data support the concept that uterine leiomyomas are derived from a single cell but are generated independently in the uterus. Loss of heterozygosity findings at 7p22-15 are consistent with previous data that suggested the relevance of chromosomal aberrations at 7p that were involved in individual uterine leiomyomas. (C) 2005 Mosby, Inc. All rights reserved.1395-1403engloss of heterozygosityX chromosome inactivationclonalityuterine leiomyomaArtigo10.1016/j.ajog.2005.02.097WOS:000232408000017Acesso restrito0514178654667684225998654626557988148235451595040000-0002-0285-1162