Toshiro Migita

Affiliation

Cancer Chemotherapy Center Molecular Biotherapy Attending Scientist

Contact

Division of Molecular Biotherapy, Cancer Chemotherapy Center Japanese Foundation for Cancer Research 3-8-31 Ariake, Koto-ku, Tokyo 135-8550, Japan
Tel：+81-3-3520-0111 ext 5745
Fax：+81-3-3570-0484
Mail：toshiro.migita@jfcr.or.jp

Education & Professional Career

1992 M.D., Nagasaki University School of Medicine
1992-1996 Resident, Kidney Center, Tokyo Women’s Medical University Hospital
1996-2002 Resident, Department of Urology, Kyushu University
2002 Ph.D., Department of Anatomic Pathology, Kyushu University
2002-2007 Postdoctoral Fellow, Dana-Farber Cancer Institute, Boston, USA
2007-2009 Research Scientist, Division of Pathology, Japanese Foundation for Cancer Research
2009- Present post

Area of Research

・Cancer metabolism
・Carcinogenesis
・Cell death

Membership

・The Japanese Urological Association
・Japanese Cancer Association
・American Association for Cancer Research
・The Molecular Society of Japan
・The Japanese Association for Molecular Target Therapy of Cancer

Awards

2010 Jan　Outstanding performance award at Kanto-Hormone and Cancer Research

Research Projects

Abnormal metabolism is one of hallmarks of malignancies. Otto Warburg described that tumor cells catalyze glucose and secreted lactate either in the presence or absence of oxygen in the 1920s (Warburg effect). In 1950s Sidney Weinhouse found that tumors derive almost all their fatty acids from de novo synthesis despite adequate nutritional supply. De novo lipogenesis is processed by lipogenic enzymes including ATP citrate lyase (ACLY), Acetyl-CoA carboxylase (ACAC), and fatty acid synthase (FASN). Accumulating evidence shows that these enzymes are overexpressed in a wide variety of cancers. In vitro and in vivo experiments demonstrated that their inhibition induced growth suppression and/or cell death of cancer cells, whereas little effects on normal cells.
I am involved in the project to define their biological significance in cancer, and to address the molecular mechanisms of cell death mediated by lipogenesis inhibition utilizing molecular biology, biochemistry, and pathology methodologies.