TY - JOUR T1 - KHYG-1 Cells With EGFRvIII-specific CAR Induced a Pseudoprogression-like Feature in Subcutaneous Tumours Derived from Glioblastoma-like Cells JF - Anticancer Research JO - Anticancer Res SP - 3231 LP - 3237 DO - 10.21873/anticanres.14304 VL - 40 IS - 6 AU - TSUTOMU NAKAZAWA AU - TOSHIHARU MURAKAMI AU - ATSUSHI NATSUME AU - FUMIHIKO NISHIMURA AU - TAKAYUKI MORIMOTO AU - RYOSUKE MATSUDA AU - MITSUTOSHI NAKAMURA AU - SHUICHI YAMADA AU - ICHIRO NAKAGAWA AU - YOUNG-SOO PARK AU - YASUSHI MOTOYAMA AU - TAKAHIRO TSUJIMURA AU - TOSHIHIKO WAKABAYASHI AU - HIROYUKI NAKASE Y1 - 2020/06/01 UR - http://ar.iiarjournals.org/content/40/6/3231.abstract N2 - 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. ER -