Naoko Ohtani, M.D., Ph.D.


Cancer Institute, Cancer Biology Senior Staff Scientist


Division of Cancer Biology, The Cancer Institute of Japanese Foundation for Cancer Research 3-8-31 Ariake, Koto-ku, Tokyo 135-8550 Japan
Tel:+81-3-3520-0111 (ext: 5353, 5355)

Education & Professional Career

1988.3   M.D.  Kyoto Prefectural University of  Medicine (Japan)
1988.6  Internal MedicineTrainee Doctor:  West Japan Railway Company Hospital (Japan)
1990.4   Research fellow: Harvard Medical School, Massachusetts Eye and Ear Infirmary (USA)
1995.3   Ph.D.  Kyoto Prefectural University of  Medicine Graduate School (Japan)
1995.4   Assistant Professor:  Kyoto Prefectural University of  Medicine (Japan)
1998.4   Postdoctoral fellow: Kyoto University, Institute for Virus Research (Japan)
1998.12   Postdoctoral fellow: Paterson Institute for Cancer Research (UK)
2003.8   Lecturer:  Institute for Genome Research, University of Tokushima (Japan)
2005.2  Associate Professor:  Institute for Genome Research, University of Tokushima (Japan)
2008.1   Senior Staff Scientist: Cancer Institute, Japanese Foundation for Cancer Research (Japan)

Area of Research

・Molecular oncology
・Cellular senescence
・Cell cycle regulation


・Japanese Cancer Association (Board member)
・Japan Gastroenterological Endoscopy Society
・Molecular Biology Society of Japan
・Astellas Foundation for Research on Metabolic Disorders (Scientific committee member)


1995.3   Shouren Award of Kyoto Prefectural University of  Medicine (Japan)
1997.2  Inoue Research Award for Young Scientists (Japan)
2003.12   Uemura Shusaburo Cancer Research Award for Young Investigators (Japan)

Research Projects

In normal tissue, cell division is carefully regulated to maintain the correct proliferative balance.  Abnormal cell division underlies many hypo-and hyper-proliferative disorders, including cancer, and a better understanding of the mechanisms involved could lead to new strategies for treatment and prevention.  Cellular senescence, a state of irreversible growth arrest, was first described as a limit to the replicative life span of somatic cells after serial cultivation in vitro.  Recently, however, cellular senescence has also been shown to be triggered prematurely by potentially oncogenic stimuli such as telomere dysfunction, oxidative stress and DNA damage in cell culture studies.  These data suggest that cellular senescence is therefore acting as a tumor-protective fail-safe mechanism. Recently, we have developed a real-time in vivo imaging system for visualizing the expression of senescence-related genes, such as p21Waf1/Cip1 and p16INK4a in mice. Visualizing the dynamics of cellular senescence responses in vivo in the context of living animals is likely to be a useful tool in the identification of the location and the timing of the gene expression and hence their likely roles in cellular senescence in vivo.

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