Cargando…

Efficacy of 5-FU Combined to Na[trans-RuCl(4)(DMSO)Im], A Novel Selective Antimetastatic Agent, on the Survival Time of Mice With P388 Leukemia, P388/DDP subline and MCa Mammary Carcinoma

The combinational treatment between the selective antimetastatic agent, sodium-trans-rutheniumtetrachloridedimethylsulfoxideimidazole, Na[trans-RuCl(4)(DMSO)Im], and the cytotoxic drug 5-fluorouracil (5-FU) on primary tumor growth and on the survival time of experimental tumors results in an effect...

Descripción completa

Detalles Bibliográficos
Autores principales: Coluccia, M., Sava, G., Salerno, G., Bergamo, A., Pacor, S., Mestroni, G., Alessio, E.
Formato: Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 1995
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2364973/
https://www.ncbi.nlm.nih.gov/pubmed/18472766
http://dx.doi.org/10.1155/MBD.1995.195
Descripción
Sumario:The combinational treatment between the selective antimetastatic agent, sodium-trans-rutheniumtetrachloridedimethylsulfoxideimidazole, Na[trans-RuCl(4)(DMSO)Im], and the cytotoxic drug 5-fluorouracil (5-FU) on primary tumor growth and on the survival time of experimental tumors results in an effect significantly greater than that of each single agent used alone either with the solid metastasizing MCa mammary carcinoma of the CBA mouse or with the lymphocytic leukemia P388 and its platinum resistant P388/DDP subline. Thus the inorganic compound Na[trans-RuCl(4)(DMSO)Im], known for its potent and selective antimetastatic effects, positively interacts with the antitumor action of an organic anticancer agent such as 5-FU on both a solid metastasizing tumor and a tumor of lymphoproliferative type. In particular, the effects of the combinational treatment on the survival time of tumor bearing mice seem to be related to the selective antimetastatic activity of the ruthenium complex that joins the potent cytotoxicity of 5-FU for the tumor. Moreover, these data show that Na[trans-RuCl(4)(DMSO)Im] is almost as effective on the subline of P388 made resistant to cisplatin as it was on the parental line.