In an approach comprising three different cancer-prone model systems—(1) treatment with CCl4 (carbon tetrachloride), (2) treatment with DEN (diethylnitrosamine) and (3) a genetic model (urokinase plasminogen activator transgenic mice) in Terc−/− mice—it could be shown that telomere dysfunction has a differential impact on tumor initiation and tumor progression. Here, PLAU is linked to neoplasm.