Background and objectives: Gemcitabine (GEM) is a pyrimidine nucleoside analogue that is a new chemotherapeutic agent used for treating various cancers. Because accumulating evidence indicates that GEM may activate host immune responses, its potential as an immune modulator in cancer chemotherapy has generated considerable interest.

Methods: In the present study, we sought to identify the antitumor immune effects of GEM in a mouse oral cancer model using immunological analyses.

Results: In vivo GEM administration markedly augmented maturation and stimulatory capacity of tumor-infiltrating dendritic cells (DCs). Moreover, GEM treatment upregulated tumor-cell surface expressions of several immune accessory molecules and adhesion molecules, including CD80, CD86, CD40, ICAM-1, VCAM-1, and P-selectin. Remarkably, these tumor cells augmented tumor-specific T-cell responses.

Conclusions: These results suggest that GEM can induce host antitumor immune responses, which would facilitate antitumor effects in the treatment of oral cancer.

Key words : gemcitabine; chemotherapy; oral cancer; antitumor immune response; mouse model of oral cancer