Bockhorn M, Frilling A, Clauer U, Hertl M, Broelsch C E
Dept. of General and Transplantation Surgery, University Hospital Essen, Germany.
Int J Surg Investig. 2000;2(3):219-25.
Neuroendocrine tumors span a rather heterogenic group of tumors, which differ in malignant potential. Very few is known about the tumorigenesis of neuroendocrine tumors. Telomeres seem to stabilize chromosomes and prevent DNA degradation and provide a signal of cellular senescence. During each cell cycle of replication, telomeres are progressively shortened. Non-diseased somatic cells, when the telomere length is reduced to a critical point, exit from the cell cycle and become senescent. In tumor cells, telomere shortening is prevented by the DNA-complex telomerase. Aim of this study was to evaluate the role of telomerase activity in the pathogenesis of neuroendocrine tumors and whether it can be a clinically useful marker for malignant potential.
Telomerase activity was determined in frozen tissue samples of 31 patients with neuroendocrine tumors by means of the "telomeric repeat amplification protocol" (TRAP)-assay. Classification of the tumors was done by the clinical course and histologic examination. There were 11 benign and 20 malignant neuroendocrine tumors. Telomerase activity was expressed as percentage of the positive control.
25 tumors had a telomerase activity between 0-5% of the positive control (group I), 5 tumors between 5-20% (group II) and 1 tumor over 20% (group II). We were not able to distinct malignant from benign tissue by means of the telomerase activity assay. There was no association with telomerase activity and clinicopathological parameters.
The data indicate that telomerase activity does not seem to be associated with the tumorigenesis of neuroendocrine tumors and can therefore not be used as a suitable marker for malignancy.
