Kazuko Kaneda-Nakashima, ZiJian Zhang, Yoshiyuki Manabe, Atsushi Shimoyama, Kazuya Kabayama, Tadashi Watabe, Yoshikatsu Kanai, Kazuhiro Ooe, Atsushi Toyoshima, Yoshifumi Shirakami, Takashi Yoshimura, Mitsuhiro Fukuda, Jun Hatazawa, Takashi Nakano, Koichi Fukase, Atsushi Shinohara
Cancer science 2021 Marα-Methyl-l-tyrosine (AMT) has a high affinity for the cancer-specific l-type amino acid transporter 1 (LAT1). Therefore, we established an anti-cancer therapy, with 211 At-labeled α-methyl-l-tyrosine (211 At-AAMT) as a carrier of 211 At into tumors. 211 At-AAMT had high affinity for LAT1, inhibited tumor cell growth, and induced DNA double-stranded breaks in vitro. We evaluated the accumulation of 211 At-AAMT in vivo and the role of LAT1. Treatment with 0.4 MBq/mouse 211 At-AAMT inhibited tumor growth in the PANC-1 tumor model and 1 MBq/mouse 211 At-AAMT inhibited metastasis in the lung of the B16F10 metastasis model. Our results suggested that 211 At would be useful for anti-cancer therapy and that LAT1 is suitable as a target for radionuclide therapy. © 2020 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.
Kazuko Kaneda-Nakashima, ZiJian Zhang, Yoshiyuki Manabe, Atsushi Shimoyama, Kazuya Kabayama, Tadashi Watabe, Yoshikatsu Kanai, Kazuhiro Ooe, Atsushi Toyoshima, Yoshifumi Shirakami, Takashi Yoshimura, Mitsuhiro Fukuda, Jun Hatazawa, Takashi Nakano, Koichi Fukase, Atsushi Shinohara. α-Emitting cancer therapy using 211 At-AAMT targeting LAT1. Cancer science. 2021 Mar;112(3):1132-1140
PMID: 33277750
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