Name: Hitoshi Nakagama, M.D., D.M.Sc.
Position:President, Japan Agency for Medical Research and Development (AMED) / Honorary President, National Cancer Center (NCC)
Education:
1982 University of Tokyo, Faculty of Medicine, M.D.,
1992 University of Tokyo, Faculty of Medicine, D. M.Sc.,

Positions and Employment:
1984 Clinical Staff, The 3rd Department of Internal Medicine, University of
Tokyo, Faculty of Medicine
1988 Research Associate, University of Tokyo, Faculty of Medicine
1991 Postdoctoral Fellow, Center for Cancer Research, MIT, U.S.A.
1995 Section Head, Carcinogenesis Division, National Cancer Center Research
Institute (NCCRI)
1997 Chief, Biochemistry Division, NCCRI
2007 Deputy Director, NCCRI
2011 Director, NCCRI
2012 Executive Director, National Cancer Center (NCC)
2016-April 1, 2025-March President, NCC
2025- April 1, President, Japan Agency for Medical Research and Development (AMED) / Honorary President, National Cancer Center (NCC)
 

Expertise: Molecular oncology, Cancer genomics, Environmental carcinogenesis

Biography---Hitoshi Nakagama has served as President of the Japan Agency for Medical Research and Development (AMED) since April 2025 and concurrently served as Honorary President of National Cancer Center (NCC) since April 2025. He earned his medical degree from the University of Tokyo Faculty of Medicine in 1982 and received his Ph.D. in 1992. He then joined the Center for Cancer Research at the Massachusetts Institute of Technology (MIT), where he worked with Prof. D.E. Housman on the functional analysis of the tumor suppressor gene WT1. After returning back to Japan in 1995, he joined the NCC Research Institute (NCCRI), where he held key leadership roles: Chief of the Biochemistry Division (1997), Deputy Director (2007), Director of NCCRI (2011), and President of NCC (2016). His research at NCCRI focused on animal models of colon carcinogenesis induced by various environmental carcinogens as well as comprehensive studies on DNA adductomics to elucidate genetic/epigenetic alterations that play pivotal roles in driving cancer development. He also identified several tumor-suppressive microRNAs that regulate cell cycle arrest and/or apoptosis in response t exposure to environmental insults.