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Thus, these findings prompt us to investigate the genomic and transcriptomic profilingin ULs using CONEXIC, an algorithm recently described [17]. In addition, functionalanalysis of networks and canonical pathways of modulators was applied to uncover molecularpathways involving in ULs pathogenesis that can be useful to select molecular markers anddefine target therapies.MATERIAL AND METHODSTissue sample collection. Fifty-one fresh ULs samples were collected from 34 patientsand stored at -80°C. These samples were collected from patients that undergone tohysterectomy procedure at the Department of Gynecology and Obstetrics, School ofMedicine, Sao Paulo State University, São Paulo, Brazil, between October 1995 and February2004. All the patients were advised of the procedures and thus provided informed consent.This study was approved by the Institutional Ethics Committee 146/2007-CEP.Clinical and histopathological parameters. Nine patients (n=9) had one UL tumor.Twenty-five patients had multiple tumors: 13 of them had one sample evaluated (n=13),seven had two samples evaluated (n=14) and five had three samples evaluated (n=15). Allwomen were premenopausal, showing regular menstrual cycles prior to diagnosis of UL, andthey no received exogenous hormones or hormone suppression therapy at least three monthsbefore surgery. At surgery, 13 patients were in proliferative menstrual cycle phase and 21 insecretory period [21]. The medical records from patients were examined in 2011 to retrieveclinical and pathological data (Table S1). The age ranged from 35 to 51 years with mean age45 years. All of the tumors were histopathologically diagnosed as usual ULs.Array CGH. Genomic DNA from 51 ULs were prepared by standard sodium dodecylsulfate/proteinase K digestion followed by phenol and chloroform extraction and ethanolprecipitation and were stored at -20°C. The samples were treated with RNaseA 20µg/ml4