419P - Association between DNA repair enzyme and somatostatin receptor in glioblastoma multiforme

Date 28 September 2014
Event ESMO 2014
Session Poster Display session
Topics Central Nervous System Malignancies
Translational Research
Basic Principles in the Management and Treatment (of cancer)
Presenter Madis Joonsalu
Citation Annals of Oncology (2014) 25 (suppl_4): iv137-iv145. 10.1093/annonc/mdu330
Authors M. Joonsalu1, T. Jogi2, M. Kase3, A. Minajeva4, J. Lukjanova5, T. Metsaots5, M. Vardja2, T. Asser6, J. Jaal7
  • 1Hematology And Oncology, Tartu University Clinics, 51003 - Tartu/EE
  • 2Dept Of Radiotherapy And Oncological Therapy, Tartu University Hospital, Haematology and Oncology Clinic, Tartu/EE
  • 3Center Of Oncology, East Tallinn Central Hospital, Tallinn/EE
  • 4Faculty Of Medicine, University of Tartu, Tartu/EE
  • 5Faculty Of Medicine, University of Tartu, 51014 - Tartu/EE
  • 6Dept Of Neurosurgery, Tartu University Hospital, Tartu/EE
  • 7Dept Of Radiotherapy And Oncological Therapy, Haematology and Oncology Clinic, 51003 - Tartu/EE



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.


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.


All markers were evaluated by two independent investigators whose results were in good accordance (R = 0.8, p < 0.01). Group mean values for DNA-PK expession, SSTR1+ tumor cell proportion, SSTR1+ blood vessel numbers and endothelial SSTR1 staining intensity were 2.0 ± 0.5 (mean ± SD), 61.6 ± 29.8%, 4.0 ± 1.3, 1.4 ± 0.9 respectively. Statistically significant correlation was found between the levels of DNA-PK expression and the proportion of SSTR1+ tumor cells (p = 0.01), between the levels of DNA-PK and SSTR1+ blood vessels count (p < 0.01) as well as between the levels of DNA-PK and endothelial SSTR1 staining intensity (p = 0,04).


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.


All authors have declared no conflicts of interest.