Mediators of wound healing response are suspected to put premalignant MSC in a transformed state and contribute to the development of desmoids. In addition to the Wnt signalling, constitutively activated in FAP patients, a synergism with the wound healing induced proliferation stimulus for mesenchymal cells, mediated through TGF-β, would present a possible explanation. In vitro, primary MSC can be cultivated only for a short period of time. SV-40 large T antigen may inhibit or prevent cellular apoptosis processes. As a contribution to a better understanding of the possible pathogenesis,in this preclinical study, MSC were stably transduced with LT-Ag using a lentiviral expression system to prevent an oncogenic-induced senescence. The resulting transgenic cell lines have significantly higher cumulative PD as their origin cells. The LT-positive MSC did not show any significant differences compared to the cells of origin concerning the characteristic surface markers of MSCand their response to standard differentiation protocols. A malignant transformation of transgenic MSC was excluded.