Association Between Dna Repair Enzyme and Somatostatin Receptor in Glioblastoma Multiforme

Aim: Glioblastoma multiforme (GBM) by its nature is radio-resistant because with postoperative radiotherapy only short-term stabilization of the disease can be achieved. Prior studies suggest that a higher level of DNA repair enzyme DNA-PK in GBM cells is one cause of the resistance. In current study we tried to identify factors that are associated with higher levels of DNA-PK in GBM. Somatostatin has been shown to be involved in many anti-tumor biological processes, such as inhibition of cell proliferation and the promotion of apoptosis. Therefore, we studied the expression of somatostatin receptor 1 (SSTR1) in GBM tissue and surrounding microenvironment. Methods: Surgically excised GBM tissues (n = 42) were immunohistochemically stained according to standard procedure. Staining intensity of DNA-PK was determined using an arbitrary score (0-3). For SSTR1, the proportion (%) of SSTR-positive (SSTR1+) tumor cells, the number of SSTR1+ blood vessels (per microscopic field) and endothelial SSTR1 staining intensity (score 0-3) were assessed. All individual parameters were characterized by the average value of 10 microscope fields. DNA-PK expression was correlated to SSTR1. Results: All markers were evaluated by two independent investigators whose results were in good accordance (R = 0.8, p Conclusions: The level of DNA repair enzyme DNA-PK in GMB tissue depends on SSTR1 expression in tumor and surrounding microenvironment. The potential of somatostatin in modulating DNA-PK levels and thereby cytotoxic treatment sensitivity has to be clarified in further studies. This work was supported by grant IUT2-4 and by Novartis Pharma unrestricted grant. Disclosure: All authors have declared no conflicts of interest.