PT - JOURNAL ARTICLE AU - NAKAZAWA, TSUTOMU AU - MURAKAMI, TOSHIHARU AU - NATSUME, ATSUSHI AU - NISHIMURA, FUMIHIKO AU - MORIMOTO, TAKAYUKI AU - MATSUDA, RYOSUKE AU - NAKAMURA, MITSUTOSHI AU - YAMADA, SHUICHI AU - NAKAGAWA, ICHIRO AU - PARK, YOUNG-SOO AU - MOTOYAMA, YASUSHI AU - TSUJIMURA, TAKAHIRO AU - WAKABAYASHI, TOSHIHIKO AU - NAKASE, HIROYUKI TI - KHYG-1 Cells With EGFRvIII-specific CAR Induced a Pseudoprogression-like Feature in Subcutaneous Tumours Derived from Glioblastoma-like Cells AID - 10.21873/anticanres.14304 DP - 2020 Jun 01 TA - Anticancer Research PG - 3231--3237 VI - 40 IP - 6 4099 - http://ar.iiarjournals.org/content/40/6/3231.short 4100 - http://ar.iiarjournals.org/content/40/6/3231.full SO - Anticancer Res2020 Jun 01; 40 AB - Background/Aim: We previously established a novel type of epidermal growth factor receptor variant III (EGFRvIII)-specific chimeric antigen receptor (CAR)-expressing natural killer (NK) cell line, designated EvCAR-KHYG-1, which inhibited the growth of glioblastoma (GBM) cells in vitro via apoptosis. Materials and Methods: We investigated the cytokine-producing effect of EvCAR-KHYG-1 cells on GBM-like cell lines and their antitumour effect using in vivo xenograft assays. Results: EvCAR-KHYG-1 cells produced interleukin-2, interferon-γ, and tumour necrosis factor-α on EGFRvIII-expressing U87MG cells. In vivo xenograft assays showed that EvCAR-KHYG-1 cells did not reduce the volume of subcutaneous tumours derived from EGFRvIII-expressing U87MG cells but did reduce tumour cell occupancy. Conclusion: EvCAR-KHYG-1 cells led to expression of cellular immunity-related cytokines on EGFRvIII-expressing U87MG in vitro but did not inhibit tumour progression due to the induction of a pseudo progression-like pathological feature. Future studies investigating the effect of different conditions in vivo are required to study the inhibition of tumour progression in GBM.