GLIAL CELLSEffects of retinoic acid and tumor necrosis factor alpha on GL-15 glioblastoma cellsChambaut-Guérin, Anne-Marie1,2,4; Costa, Silvia L.3; Lefrançois, Thierry3; Fages, Christiane3; Gauthereau, Xavier1,2; Tardy, Marcienne3Author Information 1INSERM U282, Hôpital Henri Mondor, 94010 Créteil, France; 2Present address: UPRES-A 7079, 15 rue de l'Ecole de Médecine, 75270 Paris Cedex 06, France 3INSERM U421, IM3, Faculté de Médecine, 8 rue du Général Sarrail, 94010 Créteil, France 4Corresponding Author: Anne-Marie Chambaut-Guérin Received 6 October 1999; accepted 24 November 1999 Acknowledgments: We are indebted to Dr V. Bocchini (University of Perugia, Italy) for her kind gift of the GL-15 cell line she had established; Dr M. Brockhaus for providing the mAbs utrl and htr9, and Dr H. Loetscher for the 55 kDa TNFR β cDNA (Hoffmann-La Roche, Basel); Drs S. Gillis and C.A. Smith (Immunex Research & Development Corporation, Seattle) for the p80 TNFR cDNA. We thank Dr N. Boord for proofreading the manuscript and correcting the English. NeuroReport: February 7, 2000 - Volume 11 - Issue 2 - p 389-393 Buy Abstract Glioblastomas are particularly resistant to classical antitumor treatments. Retinoids, which proved effective in the treatment of promyelocytic leukemia, have been used for clinical assays on glioma tumors with only moderate effects; however in some cases they were active in combination with another therapy. These observations prompted us to analyse the efficacy of combining retinoic acid (RA) with a cytokine on a clonal human glioma cell line. On GL-15 cells, RA and tumor necrosis factor alpha (TNFα) both reduced the glial fibrillary acidic protein level and DNA synthesis and induced apoptotic pathways, but they were significantly more effective when used together. The up-regulation of the p55 TNF receptors observed during RA exposure might explain this cooperative effect. © 2000 Lippincott Williams & Wilkins, Inc.