In:
Gynecologic and Obstetric Investigation, S. Karger AG, Vol. 81, No. 2 ( 2016), p. 186-192
Abstract:
〈 b 〉 〈 i 〉 Background: 〈 /i 〉 〈 /b 〉 Leiomyomatosis peritonealis disseminata (LPD) is a rare disease characterised by the subperitoneal proliferation of smooth muscle cells that form benign nodules. A few studies have aimed to reveal the pathogenesis of LPD without reaching a clear explanation. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 Karyotype analysis and array-comparative genomic hybridization (aCGH) of a human LPD case were performed to evaluate the role of chromosomal abnormalities in LPD pathogenesis. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 The LPD nodules showed a 45, XX, del(7p), t(11; 17) (q23;q25),-22 de novo karyotype, and the aCGH analysis confirmed these deletions at 7p22.3-p12.1 (1,862,362-52,766,911 bp) and 22q11.23-q13.33 (21,973,915-49,265,116 bp) with lengths of 50.9 Mb and 27.3 Mb, respectively. 〈 b 〉 〈 i 〉 Conclusion: 〈 /i 〉 〈 /b 〉 In this study, we described two large novel aberrations - deletions in chromosome 7 and 22 - that might play an important role in LPD disease. These findings might contribute to new insights to unravel the pathogenesis of LPD and develop further clinical treatments.
Type of Medium:
Online Resource
ISSN:
0378-7346
,
1423-002X
Language:
English
Publisher:
S. Karger AG
Publication Date:
2016
detail.hit.zdb_id:
1482695-1
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