RT Journal Article
SR Electronic
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
FD International Institute of Anticancer Research
SP 3231
OP 3237
DO 10.21873/anticanres.14304
VO 40
IS 6
A1 NAKAZAWA, TSUTOMU
A1 MURAKAMI, TOSHIHARU
A1 NATSUME, ATSUSHI
A1 NISHIMURA, FUMIHIKO
A1 MORIMOTO, TAKAYUKI
A1 MATSUDA, RYOSUKE
A1 NAKAMURA, MITSUTOSHI
A1 YAMADA, SHUICHI
A1 NAKAGAWA, ICHIRO
A1 PARK, YOUNG-SOO
A1 MOTOYAMA, YASUSHI
A1 TSUJIMURA, TAKAHIRO
A1 WAKABAYASHI, TOSHIHIKO
A1 NAKASE, HIROYUKI
YR 2020
UL http://ar.iiarjournals.org/content/40/6/3231.abstract
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.