Adriana Camargo Ferrasi
São Paulo State University, Brazil
Title: Genetic variations of interleukin 28B (IL28B) in meningioma
Biography
Biography: Adriana Camargo Ferrasi
Abstract
Meningioma is the most common tumor of the central nervous system and despite of their benign characteristic and slow growth, they frequently recur after surgical removal. Interleukin 28B seems to be involved in antiviral and antitumor immune response. Recently, IL28B rs12979860 C/T polymorphism was associated with outcome of treatment with IFNα and ribavirin in patients with Hepatitis C virus. Also, patients with CC genotype have higher chances of viral depuration than those with other genotypes. However, there are few data on this polymorphism in tumors, especially in meningioma. Thus, the aim of this study was to analyze allele and genotype frequencies of this polymorphism in patients affected by meningioma and healthy individuals (control) and to sequencing IL28b gene, searching for novel genetic variations. Sixty patients treated by UNESP Neurosurgery Service were included in this study. The Research Ethics Committee approved this study and each subject signed an informed consent form before tissue was obtained. Analysis of rs12979860 C/T polymorphism was performed by PCR-RFLP (PCR - Restriction Fragment Length Polymorphism) and the complete sequencing of the IL28B gene was performed by Sanger Sequencing Capillary Electrophoresis (Applied Biosystems™). The present study showed unpublished results that evidenced a greater frequency of TT genotype in the meningioma patients when compared to healthy individuals. Novel genetic variations (missense and silent) were detected in IL28B gene and only three have been reported in the scientific literature, but not in tumor samples. Amino acids exchanged as consequence of the missense variations are located mainly in the binding domains of IL28B protein to its receptor, reinforcing the probable importance of these alterations in protein function. These results suggest that IL28B protein and its geneticvariations may participate in the molecular mechanisms of meningioma.