Nature Communications (Oct 2019)
Antitumor immunity augments the therapeutic effects of p53 activation on acute myeloid leukemia
- Yasutaka Hayashi,
- Susumu Goyama,
- XiaoXiao Liu,
- Moe Tamura,
- Shuhei Asada,
- Yosuke Tanaka,
- Tomofusa Fukuyama,
- Mark Wunderlich,
- Eric O’Brien,
- Benjamin Mizukawa,
- Satoshi Yamazaki,
- Akiko Matsumoto,
- Satoshi Yamasaki,
- Tatsuhiro Shibata,
- Koichi Matsuda,
- Goro Sashida,
- Hitoshi Takizawa,
- Toshio Kitamura
Affiliations
- Yasutaka Hayashi
- Division of Cellular Therapy, The Institute of Medical Science, The University of Tokyo
- Susumu Goyama
- Division of Cellular Therapy, The Institute of Medical Science, The University of Tokyo
- XiaoXiao Liu
- Division of Cellular Therapy, The Institute of Medical Science, The University of Tokyo
- Moe Tamura
- Division of Cellular Therapy, The Institute of Medical Science, The University of Tokyo
- Shuhei Asada
- Division of Cellular Therapy, The Institute of Medical Science, The University of Tokyo
- Yosuke Tanaka
- Division of Cellular Therapy, The Institute of Medical Science, The University of Tokyo
- Tomofusa Fukuyama
- Division of Cellular Therapy, The Institute of Medical Science, The University of Tokyo
- Mark Wunderlich
- Cancer & Blood Diseases Institute, Cincinnati Children’s Hospital Medical Center, University of Cincinnati College of Medicine
- Eric O’Brien
- Cancer & Blood Diseases Institute, Cincinnati Children’s Hospital Medical Center, University of Cincinnati College of Medicine
- Benjamin Mizukawa
- Cancer & Blood Diseases Institute, Cincinnati Children’s Hospital Medical Center, University of Cincinnati College of Medicine
- Satoshi Yamazaki
- Division of Stem Cell Therapy, The Institute of Medical Science, The University of Tokyo
- Akiko Matsumoto
- Laboratory of Molecular Medicine, The Institute of Medical Science, The University of Tokyo
- Satoshi Yamasaki
- Laboratory of Molecular Medicine, The Institute of Medical Science, The University of Tokyo
- Tatsuhiro Shibata
- Laboratory of Molecular Medicine, The Institute of Medical Science, The University of Tokyo
- Koichi Matsuda
- Laboratory of Clinical Genome Sequencing, Department of Computational biology and medical Sciences, Graduate school of Frontier Sciences, The University of Tokyo
- Goro Sashida
- Laboratory of Transcriptional Regulation in Leukemogenesis, International Research Center for Medical Sciences, Kumamoto University
- Hitoshi Takizawa
- Laboratory of Stem Cell Stress, International Research Center for Medical Sciences, Kumamoto University
- Toshio Kitamura
- Division of Cellular Therapy, The Institute of Medical Science, The University of Tokyo
- DOI
- https://doi.org/10.1038/s41467-019-12555-1
- Journal volume & issue
-
Vol. 10,
no. 1
pp. 1 – 14
Abstract
MDM2 is frequently overexpressed in acute myeloid leukaemia leading to p53 inactivation. Here, the authors are demonstrating that an inhibitor of p53-MDM2 interaction, DS-5272, induce in vivo tumour regression through immune response regulation.
