Independent clonal origin of multiple uterine leiomyomas that was determined by X chromosome inactivation and microsatellite analysis
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Data
2005-10-01
Autores
Canevari, R. A.
Pontes, Anaglória [UNESP]
Rosa, F. E.
Rainho, C. A.
Rogatto, Silvia Regina [UNESP]
Título da Revista
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Editor
Mosby, Inc
Resumo
Objective: 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.
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Palavras-chave
loss of heterozygosity, X chromosome inactivation, clonality, uterine leiomyoma
Como citar
American Journal of Obstetrics and Gynecology. St Louis: Mosby, Inc., v. 193, n. 4, p. 1395-1403, 2005.