PO-330 Prevention of worsening in glioma relapse

Introduction Gliomas are primary tumours, which have aggressively and resiliency characteristics. Even in the last years having proposals of new therapies, the results continue frustrating for this tumour, so developing biocompounds with view to glioma adjuvant will bring very useful to increase therapeutic response to the recurrences. Hydrolysed Rutin (HR), biocompound modified from the de-glycolization of rutin, already demonstrated antiproliferative capacity in vitro for this tumour type. This study intends to confirm the HR antiproliferative action and antitumor activity on human glioblastoma/U251 and to investigate the mechanism related to its action as a potential agent modifying the tumour aggressiveness, with a view to its application in the primary tumour, also as on recurrences. Material and methods After the obtainment of HR, it was used on antiproliferative assays and flow cytometry to verify the cell cycle and apoptosis induction on human glioblastoma/U251 in vitro . On animal glioblastoma model, divided in groups treated (prophylactic and therapy) and untreated, was measured lipid peroxidation, genotoxicity and verified HR antitumoral and the modification of aggressively pattern by histopathological and immunohistoquemistry analysis. The data was analysed adopting p-value lower than 5% (p Results and discussions TGI was 3.6 µg/mL. G1/S delay was observed in treated groups. Large proliferation of undifferentiated cells, with anaplastic degree and high index of atypical mitoses, forming solid neoplastic blocks was found. Tumour growth inhibition can be observed both in prophylactic (p=0.00) and in the therapeutic use of HR (p=0.03). Three cellular patterns were observed that were randomly distributed among groups, which characterises the multiple histological glioblastoma presentations. The HR decrease mitosis and anaplasia. There was a decrease in mitoses, as well as the expression of MDA, without induction of genotoxicity in the tumours submitted to HR treatment when compared to the untreated. In the control group 20% of necrosis was observed, whereas in the prophylactic and treatment groups no necrosis was observed. The number of mitoses was lower in the prophylactic groups (p=0.00) than in the control group. Mutated p53 expression remained the same in all groups, treated or not. Conclusion The de-glycolization of rutin has potential to be used not only as adjuvant, but also as modifier of tumour aggressively, especially important as a new therapeutic weapon in glioma relapse.