Experimental Chemotherapy

Update : 2018-04-02


Cancer treatments have dramatically improved during past 2 decades, we are still facing problems to surmount in prevention and therapy of cancers. Recent advances in molecular-targets of cancers have provided the rationale for the molecular-targeted therapy to treat cancer, and often showed market tumor shrinkage. The aim of this research division is to identify possible targets, to clarify the function of molecular targets by analyzing cancer patients derived specimens including pre-treatment and treatment refractory tumors, and ultimately to develop an effective molecular-targeted therapy of cancer. For this purpose, we are investigating the molecular mechanisms of anti-cancer drug resistance, apoptosis resistance, and tumor metastasis. In addition, we are investigating the nature of cancer stem cells.


  1. Resistance mechanisms to molecular targeted therapy, and therapeutic strategies to overcome the resistance
  2. Aggrus: a platelet aggregation-inducing factor that is associated with hematogenous metastasis
  3. Targeting cancer stem cells and their regulation
  4. Molecular mechanisms of survival signaling pathways



Ariyasu R, Nishikawa S, Uchibori K, Oh-Hara T, Yoshizawa T, Dotsu Y, Koyama J, Saiki M, Sonoda T, Kitazono S, Yanagitani N, Horiike A, Inase N, Kasahara K, *Nishio M, *Katayama R.
High ratio of T790M to EGFR activating mutations correlate with the osimertinib response in non-small-cell lung cancer. Lung Cancer, 117: 1-6 (2018)
Katayama R.
Drug resistance in anaplastic lymphoma kinase-rearranged lung cancer. Cancer Science. 109:572-580. (2018)
Fuse, M. J., Okada, K., Oh-hara, T., Ogura, H., Fujita, N. and Katayama, R.
Mechanisms of resistance to NTRK inhibitors and therapeutic strategies in NTRK1-rearranged cancers.
Mol. Cancer Ther., 16:2130-2143. (2017)
Takemoto, A., Miyata, K. and Fujita, N.
Platelet-activating factor podoplanin: from discovery to drug development.
Cancer and metastasis reviews, 36, 225-234 (2017)
Ogura, H., Nagatake-Kobayashi, Y., Adachi, J., Tomonaga, T., Fujita, N. and Katayama, R.
TKI-addicted ROS1-rearranged cells are destined to survival or death by the intensity of ROS1 kinase activity.
Sci. Rep., 7, 5519 (2017)
Miyata, K., Takemoto, A., Okumura, S., Nishio, M. and Fujita, N.
Podoplanin enhances lung cancer cell growth in vivo by inducing platelet aggregation.
Sci. Rep., 7, 4059 (2017)
Uchibori K, Inase N, Araki M, Kamada M, Sato S, Okuno Y, Fujita N, Katayama R.*. Brigatinib
combined with anti-EGFR antibody overcomes osimertinib resistance in EGFR-mutated non-small-cell lung cancer. Nature Commun., 2017 Mar 13;8:14768., *:corresponding author
R. Katayama.
Therapeutic strategies and mechanisms of drug resistance in Anaplastic Lymphoma Kinase (ALK)-rearranged lung cancer.
Pharmacol. Ther., 117, 1-8 (2017)
Katayama, R., Sakashita, T., Yanagitani, N., Ninomiya, H., Horiike, A., Gainor, J.F., Motoi, N., Dobashi, A., Tambo, Y., Kitazono, S., Sato, S., Koike, S., lafrate, A.J., Mino-Kenudson, M., Ishikawa, Y., Shaw, A.T., Engelman, J.A., Takeuchi, K., Nishio, M., Fujita, N.
P-glycoprotein mediates ceritinib resistance in ALK-rearranged non-small-cell lung cancer. EBioMedicine, 3: 54-66, 2016.
Sekiguchi, T., Takemoto, A., Takagi, S, Takatori, K., Sato, S., Takami, M., Fujita, N.
Targeting a novel domain in podoplanin for inhibiting platelet-mediated tumor metastasis.
Oncotarget, 7: 3934-3946, 2016.
Katayama, R., Kobayashi, Y., Friboulet, L., Lockerman, E.L., Koike, S., Shaw, A.T., Engelman, J.A., Fujita, N.
Cabozantinib overcomes crizotinib resistance in ROS1 fusion positive cancer.
Clin. Cancer Res., 21. 166-174, 2015.
Katayama, R., Friboulet, L., Koike, S., Lockerman, E.L., Khan, T.M., Gainor, J.F., Iafrate, A.J., Takeuchi, K., Taiji, M., Okuno, Y., Fujita, N., Engelman, J.A., Shaw, A.T.
Two novel ALK mutations mediate acquired resistance to the next-generation ALK inhibitor alectinib.
Clin. Cancer Res., 20, 5686-5696 (2014)
Katayama, R., Aoyama, A., Yamori, T., Qi, J., Oh-Hara, T., Song, Y., Engelman, J.A., Fujita, N.
Cytotoxic activity of Tivanitib (ARQ 197) is not due solely to c-MET inhibition.
Cancer Res, 73, 3087-3096 (2013)


Ryohei Katayama(Chief)
3-8-31, Ariake, Koto-ku, Tokyo 135-8550, Japan
Tel:81-3-3520-0111 Fax:81-3-3570-0484


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