RT Journal Article SR Electronic T1 Chemotherapy-induced Bystander Effect in Response to Several Chloroethylnitrosoureas: An Origin Independent of DNA Damage? JF Anticancer Research JO Anticancer Res FD International Institute of Anticancer Research SP 21 OP 27 VO 28 IS 1A A1 PATRICK MERLE A1 DANIEL MORVAN A1 DENIS CAILLAUD A1 AICHA DEMIDEM YR 2008 UL http://ar.iiarjournals.org/content/28/1A/21.abstract AB Chloroethylnitrosourea (CENU) chemotherapy is used for the treatment of melanoma tumors. The main mechanism of action of this anticancer agent is via DNA damage. We recently showed in murine experiments using a parental double B16 melanoma tumor model that, after treatment of primary tumors with cystemustine (CENU agent), untreated secondary tumors exhibited growth inhibition and metabolism disorders. The response of secondary untreated tumor was called the chemotherapy-induced bystander effect. To see whether chemotherapy-induced bystander effects were induced with other members of the CENU family, we compared three CENU(s) used in melanoma treatment: cystemustine, carmustine and fotemustine. Our results demonstrate that fotemustine, like cystemustine, but not carmustine induced a protective effect against secondary untreated tumors including alterations in phospholipid derivative and glutathione which are the metabolic signature of the bystander effect. From these data we may conclude that DNA damage to the primary tumor is not sufficient to explain chemotherapy-induced bystander effects.