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Home > Genichiro Ishii, MD, PhD

Genichiro Ishii, MD, PhD


Cancer microenvironment is created not only by malignant epithelial cells, but also by several kinds of stromal cells. The main compartment of host stromal cells is fibroblasts (Cancer-Associated Fibroblasts; CAFs) which play important roles in several aspects of the tumor progression process and the chemotherapeutic process. However, CAFs have heterogeneous origins, phenotypes, and functions under these conditions. We isolate cancer cells and CAFs from surgically resected specimens and generate novel in vitro models mimicking the cancer microenvironment by using fluorescence imaging, time-lapse imaging and organoid culture. My major aim is to clarify the novel biological mechanisms of cancer progression and drug sensitivity based on the microenvironment context.

Official Title

  • Chief, Division of Pathology
  • Visiting professor, University of Tokyo

Areas of research

  • Cancer biology based on the microenvironment context


  • Tumor microenvironment
  • Lung cancer
  • Cancer associated fibroblasts (CAFs)


gishii●east.ncc.go.jp(Replace ● to @)

Brief History


  • 1984-1990  School of medicine, Kanazawa University
  • 1990-1994  1st Department of Pathology, School of Medicine, Chiba University


  • 1994-2000  Research Associate, School of Medicine, Chiba University
  • 2000-2001  Lecturer, School of Medicine, Chiba University
  • 2001-2005  Head, Pathology Division, National Cancer Center Research Institute East 
  • 2015-          Visiting Professor, Graduate School of Frontier Sciences, The University of Tokyo
  • 2016-          Chief, Division of Pathology, Exploratory Oncology Research & Clinical Trial Center, National Cancer Center

Major affiliated societies

  • The Japanese Society of Pathology
  • The Japanese Cancer Association
  • The Japan Lung Cancer Society

Major Publications 

  1. Ishii G, Sangai T, Sugiyama K, Ito T, Hasebe T, Endoh Y, Magae J, Ochiai A. In vivo characterization of bone marrow-derived fibroblasts recruited into fibrotic lesions. Stem Cells, 23:699-706, 2005
  2. Ishii G, Ito TK, Aoyagi K, Fujimoto H, Chiba H, Hasebe T, Fujii S, Nagai K, Sasaki H, Ochiai A. Presence of human circulating progenitor cells for cancer stromal fibroblasts in the blood of lung cancer patients. Stem Cells, 25:1469-1477, 2007                                   
  3. Hoshino A, Ishii G, Ito T, Aoyagi K, Ohtaki Y, Nagai K, Sasaki H, Ochiai A. Podoplanin-positive fibroblasts enhance lung adenocarcinoma tumor formation: podoplanin in fibroblast functions for tumor progression. Cancer Res, 71:4769-4779, 2011
  4. Yoshida T, Ishii G, Goto K, Neri S, Hashimoto H, Yoh K, Niho S, Umemura S, Matsumoto S, Ohmatsu H, Iida S, Niimi A, Nagai K, Ohe Y, Ochiai A. Podoplanin-positive cancer-associated fibroblasts in the tumor microenvironment induce primary resistance to EGFR-TKIs in lung adenocarcinoma with EGFR mutation. Clin Cancer Res, 21:642-651, 2015                                  
  5. Ishii G, Ochiai A, Neri S. Phenotypic and functional heterogeneity of cancer-associated fibroblast within the tumor microenvironment.Adv Drug Deliv Rev, 2015 [Epub ahead of print]
  6. Miyashita T, Higuchi Y, Kojima M, Ochiai A, Ishii G. Single cell time-lapse analysis reveals that podoplanin enhances cell survival and colony formation capacity of squamous cell carcinoma cells. Sci Rep. 2017 21;7:39971
  7. Neri S, Miyashita T, Hashimoto H, Suda Y, Ishibashi M, Kii H, Watanabe H, Kuwata T, Tsuboi M, Goto K, Menju T, Sonobe M, Date H, Ochiai A, Ishii G. Fibroblast-led cancer cell invasion is activated by epithelial-mesenchymal transition through platelet-derived growth factor BB secretion of lung adenocarcinoma. Cancer Lett. 2017                                                         
  8. Ishibashi M, Neri S, Hashimoto H, Miyashita T, Yoshida T, Nakamura Y, Udagawa H, Kirita K, Matsumoto S, Umemura S, Yoh K, Niho S, Tsuboi M, Masutomi K, Goto K, Ochiai A, Ishii G.  CD200-positive cancer associated fibroblasts augment the sensitivity of Epidermal Growth Factor Receptor mutation-positive lung adenocarcinomas to EGFR Tyrosine kinase inhibitors. Sci Rep. 2017 21;7:46662