dc.contributor | Universidade Estadual Paulista (UNESP) | |
dc.creator | Canevari, R. A. | |
dc.creator | Pontes, Anaglória | |
dc.creator | Rosa, F. E. | |
dc.creator | Rainho, C. A. | |
dc.creator | Rogatto, Silvia Regina | |
dc.date | 2014-05-20T13:38:44Z | |
dc.date | 2016-10-25T16:54:49Z | |
dc.date | 2014-05-20T13:38:44Z | |
dc.date | 2016-10-25T16:54:49Z | |
dc.date | 2005-10-01 | |
dc.date.accessioned | 2017-04-05T20:35:51Z | |
dc.date.available | 2017-04-05T20:35:51Z | |
dc.identifier | American Journal of Obstetrics and Gynecology. St Louis: Mosby, Inc., v. 193, n. 4, p. 1395-1403, 2005. | |
dc.identifier | 0002-9378 | |
dc.identifier | http://hdl.handle.net/11449/13425 | |
dc.identifier | http://acervodigital.unesp.br/handle/11449/13425 | |
dc.identifier | 10.1016/j.ajog.2005.02.097 | |
dc.identifier | WOS:000232408000017 | |
dc.identifier | http://dx.doi.org/10.1016/j.ajog.2005.02.097 | |
dc.identifier.uri | http://repositorioslatinoamericanos.uchile.cl/handle/2250/860761 | |
dc.description | 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. | |
dc.language | eng | |
dc.publisher | Mosby, Inc | |
dc.relation | American Journal of Obstetrics and Gynecology | |
dc.rights | info:eu-repo/semantics/closedAccess | |
dc.subject | loss of heterozygosity | |
dc.subject | X chromosome inactivation | |
dc.subject | clonality | |
dc.subject | uterine leiomyoma | |
dc.title | Independent clonal origin of multiple uterine leiomyomas that was determined by X chromosome inactivation and microsatellite analysis | |
dc.type | Otro | |