par Dupressoir, Thierry;Vanacker, Jean-Marc;Cornells, Jan J.J.;Duponchel, Nadine;Rommelaere, Jean
Référence Cancer research, 49, 12, page (3203-3208)
Publication Publié, 1989-06
Référence Cancer research, 49, 12, page (3203-3208)
Publication Publié, 1989-06
Article révisé par les pairs
Résumé : | The formation of tumors in adult nude mice from transformed human mammary epithelial cells was drastically inhibited (>80%) both after coinjection of tumoral cells and virus or after a single s.c. injection of parvovirus H-l at the site of cell implantation prior to tumor formation. Moreover, when injected i.v. in animals bearing preformed tumors, H-1 virus was able to slow down and even in some cases to revert neoplastic growth. Thus, H-1 virus achieved the suppression of implanted tumors of human origin under conditions where the immune antitumor mechanisms of the recipient animals were dramatically impaired. Viral infection was not accompanied by detectable deleterious side effects. Imprints of H-l virus DNA were found in one residual tumor. Normal human mammary epithelial cells were also compared with homologous transformed cells, either derived from tumors (three lines) or containing simian virus 40 (one line), for their susceptibility to the lytic replication of H-l virus in vitro. Transformed cell lines were more sensitive to virus-induced killing than secondary cultures of normal cells. Moreover, the former had much greater abilities than the latter to amplify viral DNA and to express the viral nonstructural protein NS-1. Altogether, these results are compatible with the idea that the oncosuppressive activity exerted by H-1 virus may be mediated, at least in part, by virus replication in developing tumors. © 1989, American Association for Cancer Research. All rights reserved. |