97th DOG Annual Meeting 1999
TELOMERASE ACTIVITY IN UVEAL MELANOMAS
J. M. Rohrbach1, C. Riedinger1, M. Wild1, M. Partsch2
Background: According to current concepts the maximum number of cell divisions of a certain cell population is genetically fixed so that aging cells become non-dividing (senescent) at least (1). This "barrier of cell division", also known as "Hayflick-limit", is probably defined by a "critical" length of the telomeres. Telomeres are special DNA-sequences located at the four ends of the chromosomes which are reduced in length with each cell cycle. Various non-ocular tumours but not their normal cellular counterparts activate the enzyme telomerase so that telomeres can be reconstructed, "Hayflick-limit" can be overcome, and unlimited capability of cell division (with theoretically unrestricted tumour growth) can be established (1). However, telomerase is very likely not required for growth of all malignant tumours. Aim of the study was to elucidate whether uveal melanoma cells activate telomerase or not.
Material and methods: Eight eyes with uveal melanoma without prior radiotherapy were enucleated. Thereafter, tumour tissue was excised immediately under sterile conditions and stored at -80º Celsius. Telomerase activity was determined using a PCR ELISA according to the Telomeric Repeat Amplification Protocol (TRAP) (1). Normal conjunctival tissue served as non-tumorous negative control.
Results: While the control specimens were negative telomerase activity was detectable in 7 of the 8 uveal melanomas.
Conclusions: Telomeres and telomerase seem to play a role for uveal melanoma growth. Thus, telomerase inhibition could perhaps offer a therapeutical approach not only for many non-ocular malignant tumours but also for intraocular melanomas.
1. Harley CB, Kim NW. Telomerase and Cancer. In: DeVita VT, Hellman S, Rosenberg SA (Eds.): Important Advances in Oncology. Lippincott-Raven, Philadelphia (1996) 57-67
2. Eye Clinic Dept.I (1) und III (2), Eberhard-Karls-University, Schleichstr.12, D-72076 Tübingen
Supported by Fortüne-Program (Project F1221132)