APLASIA RAS HOMOLOGOUS MEMBER I GENE AND DEVELOPMENT OF GLIAL TUMORS
Yakut S1, Tuncer MR2,* Berker M3, Goksu E2, Gurer I4, Ozes ON1, Luleci G1, Karauzum SB1
*Corresponding Author: Sibel Berker Karauzum, Department of Medical Biology and Genetics, Faculty of Medicine, Akdeniz University Antalya, Turkey; Tel.: +90 242 2496971; Fax: +90 242 2274482; E-mail: sibelkarauzum@akdeniz.edu.tr
page: 37

RESULTS

We found decreased ARHI gene expression in seven of the tumors (33.3%). Three of these (samples 3, 11 and 14) were GBM (23.1%), three (samples 15, 16 and 17) were O (60%) and one (sample 9) was AA. We found increased ARHI gene expression in 14 of the tumors (66.7%) of which 10 (samples 4, 5, 6, 8, 10, 12, 13, 18, 19 and 20) were GBM (77.0%), two (samples 1 and 2) were O (40.0%), one (sample 7) was AA and one (sample 21) was AOA (Figure 1). The LOH analysis revealed allelic loss in two tumors which were O (samples 15 and 17) (Figure 2, Table 1). Both of these also showed decreased ARHI gene expression in real time RT-PCR. To determine whether epigenetic events contributed to ARHI silencing, we studied promoter methylation of for CpG island I, II and III from the tumors. Only two (samples 9 and 17) had hypermethylation in CpG island I ( ure 3 and Table 2). Both of these also showed decreased ARHI gene expression as measured by real time RT-PCR.



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