title: Enhancement of antitumor activity by combination of tumor lysate-pulsed dendritic cells and celecoxib in a rat glioma model.
abstract: Using dendritic cell (DC)-based vaccines for treatment of gliomas has emerged as a meaningful and feasible treatment approach for inducing long-term survival, but this approach so far has failed to generate significant clinical responses. In the present study, we demonstrated that glioma lysate-pulsed DCs in combination with celecoxib, a selective cyclooxygenase 2 (COX-2) inhibitor, showed more significantly enhanced antitumor activity with increased apoptosis of tumor cells, reduced neovascularization, and developed a strong cytotoxic T lymphocyte (CTL) response in tumor-bearing rats. Celecoxib may reduce production of prostaglandin E2 and modulate the balance between T helper 1 (Th1) cytokines and T helper 2 (Th2) cytokines by increasing the pivotal Thl cytokine interleukin-12 and reducing Th2 cytokine interleukin-10. Taken together, our results demonstrated that selective inhibition of COX-2 using celecoxib combined with DC-based immunotherapy could act as an important novel strategy for improving future treatment of malignant gliomas.
authors.affiliation: Department of Neurosurgery, Yantai Yuhuangding Hospital Affiliated to Qingdao University School of Medicine, Yantai, Shandong, China.
authors.forename: Hongtao
authors.initials: H
authors.lastname: Zhang
authors.forename: Miao
authors.initials: M
authors.lastname: Tian
authors.forename: Chunming
authors.initials: C
authors.lastname: Xiu
authors.forename: Yunbo
authors.initials: Y
authors.lastname: Wang
authors.forename: Guotai
authors.initials: G
authors.lastname: Tang
mesh_terms: D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects; D001932:Brain Neoplasms / Q000201:enzymology / Q000276:immunology / Q000473:pathology / Q000628:therapy*; D019496:Cancer Vaccines; D000068579:Celecoxib; D045744:Cell Line, Tumor; D017024:Chemotherapy, Adjuvant; D051546:Cyclooxygenase 2 / Q000378:metabolism; D052246:Cyclooxygenase 2 Inhibitors / Q000494:pharmacology*; D003713:Dendritic Cells / Q000276:immunology / Q000637:transplantation*; D015232:Dinoprostone / Q000378:metabolism; D004195:Disease Models, Animal; D005260:Female; D005910:Glioma / Q000201:enzymology / Q000276:immunology / Q000473:pathology / Q000628:therapy*; D007167:Immunotherapy / Q000379:methods*; D018664:Interleukin-12 / Q000378:metabolism; D016246:Lymphocytes, Tumor-Infiltrating / Q000187:drug effects / Q000276:immunology; D011720:Pyrazoles / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D013449:Sulfonamides / Q000494:pharmacology*; D013602:T-Lymphocytes, Cytotoxic / Q000187:drug effects / Q000276:immunology; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D000970:Antineoplastic Agents; D019496:Cancer Vaccines; D052246:Cyclooxygenase 2 Inhibitors; D011720:Pyrazoles; D013449:Sulfonamides; D014409:Tumor Necrosis Factor-alpha; D018664:Interleukin-12; D051546:Cyclooxygenase 2; C489691:Ptgs2 protein, rat; D000068579:Celecoxib; D015232:Dinoprostone