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Effect of Co‐administration of Granulocyte Colony‐stimulating Factor on Interferon Therapy

The effect of co‐administration of granulocyte colony‐stimulating factor (G‐CSF), as an anti‐neutropenia agent, on interferon therapy was examined in a mouse model, in anticipation of an enhancement of interferon efficacy, because neutrophils induced by G‐CSF are thought to act as antitumor effector...

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Detalles Bibliográficos
Autores principales: Segawa, Kotaro, Suhara, Yasuji, Ueno, Yoshio, Kataoka, Tateshi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Blackwell Publishing Ltd 1991
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5918389/
https://www.ncbi.nlm.nih.gov/pubmed/1708757
http://dx.doi.org/10.1111/j.1349-7006.1991.tb01852.x
Descripción
Sumario:The effect of co‐administration of granulocyte colony‐stimulating factor (G‐CSF), as an anti‐neutropenia agent, on interferon therapy was examined in a mouse model, in anticipation of an enhancement of interferon efficacy, because neutrophils induced by G‐CSF are thought to act as antitumor effectors. G‐CSF was intraperitoneally co‐administered with human interferon α A/D (IFN) on Day 6 to Day 10 after intradermal inoculation of Meth A fibrosarcoma. Although the co‐administration of G‐CSF could protect against neutropenia and leukopenia induced by IFN, it did not enhance the regression of tumor, and rather reduced the prolongation of survival time and the long‐term survival incidence of IFN therapy. The subsequent in vitro study showed that the antiproliferative activity of peripheral blood leukocytes from Meth A‐bearing mice given both IFN and G‐CSF was much weaker than that of mice given IFN alone. Whether the observed nullifying effect of G‐CSF on IFN therapy is also the case with tumors other than Meth A is open to further study.