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Kundrát, P. ; Bauer, G.* ; Jacob, P. ; Friedland, W.

Mechanistic modelling suggests that the size of preneoplastic lesions is limited by intercellular induction of apoptosis in oncogenically transformed cells.

Carcinogenesis 33, 253-259 (2012)
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Selective removal of oncogenically transformed cells by apoptosis induced via signalling by surrounding cells has been suggested to represent a natural anticarcinogenic process. To investigate its potential effect in detail, a mechanistic model of this process is proposed. The model is calibrated against in vitro data on apoptosis triggered in transformed cells by defined external inducers as well as through signalling by normal cells under coculture conditions. The model predicts that intercellular induction of apoptosis is capable of balancing the proliferation of oncogenically transformed cells and limiting the size of their populations over long times, even if their proliferation per se were unlimited. Experimental research is desired to verify whether the predicted stable population of transformed cells corresponds to a kind of dormancy during early-stage carcinogenesis (dormant preneoplastic lesions), and how this process relates to other anticarcinogenic mechanisms taking place under in vivo conditions.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter reactive oxygen; nontransformed fibroblasts; lipid-peroxidation; tumor-cells; cancer; carcinogenesis; superoxide; radiation; catalase
ISSN (print) / ISBN 0143-3334
e-ISSN 1460-2180
Zeitschrift Carcinogenesis
Quellenangaben Band: 33, Heft: 2, Seiten: 253-259 Artikelnummer: , Supplement: ,
Verlag Oxford University Press
Begutachtungsstatus Peer reviewed