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Yoshinori Hasegawa MD, PhDProfessor, Department of Respiratory Medicine, Nagoya University Graduate School of Medicine
Specialized field
Molecular biology of the pulmonary diseases and Lung cancer, Pharmacogenomics of cancer chemotherapy
Career Summary
- 1980
- M.D., University of Tokushima
- 1980-1983
- Resident, Social Insurance Chukyo Hospital
- 1983-1987
- Postgraduate School, Nagoya University
- 1987-1989
- Research Fellow, Dept. Microbiology and Immunology, UCLA
- 1989-1994
- Clinical Fellow, 1st. Dept Internal Medicine, Nagoya University
- 1994-2002
- Research Associate, 1st. Dept Internal Medicine, Nagoya University
- 2002-2007
- Assistant Professor, Dept Respiratory Medicine, Nagoya University
- 2007-present
- Professor of Medicine, Dept Respiratory Medicine, Nagoya
Research Theme
Common molecular target of tissue repair and cancer
Research Summary
Recent progress in medical science revealed the crucial role of epithelial to mesenchymal cell transition (EMT) or mesenchymal to epithelial cell transition (MET) in not only inflammatory tissue repair but tumor development and progression. Injury models have suggested that several origins of epithelial cell progenitors in addition to the functionally distinct epithelial stem cell populations plays an important role for the tissue repair. We have been studied on the molecular mechanisms of pulmonary fibrosis. The accumulation of fibroblasts, excess collagen, and other matrix components at sites of chronic inflammation lead to scar-tissue formation and progressive tissue injury. These fibroblasts derive from the bone marrow, but also arise from an EMT of cells at injury sites. We speculate that EMT is likely involved in the progressive fibrotic diseases of the lung. On the other hand, progression toward malignancy is accompanied by loss of epithelial differentiation and a shift towards a mesenchymal phenotype. Therefore, EMT has been speculated to be requisite for acquiring the capacity to infiltrate surrounding tissue and to metastasize to distant sites. Research of molecular targets that regulate or mediate the EMT signal pathway has been widely started. In this global COE project, we will focus on the molecular targets such as NOTCH, TWIST and SNAIL, which have been speculated to regulate the EMT signal pathway. This project will provide us evidences of the common molecular target for both inflammatory tissue repair and cancer control.
Principal Research Achievement
- Ando Y et al. UGT1AI*6 and UGT1A1*27 for individualized irinotecan chemotherapy. Curr Opin Mol Ther 9: 258-262 (2007)
- Mori K et al. Bronchoscope tracking without fiducial markers using ultra-tiny electromagnetic tracking system and its evaluation in different environments. Med Image Comput Comput Assist Interv Int Conf Med Image Comput Comput Assist Interv. 10: 644-651 (2007)
- Okamoto M et al. Macrophage-derived chemokine in malignant and tuberculous pleurisy. Respirology 12: 581?584 (2007)
- Hasegawa Y et al. Screening for adverse reactions to irinotecan treatment using the lnvader UGT1A1 molecular assay. Expert Rev Mol Diagn 6: 527-533 (2006)
- Yokoyama T et al. EGFR point mutation in non-small cell lung cancer is occasionally accompanied by a second mutation or amplification. Cancer Sci 97: 753-759 (2006)
- Kitagawa C et al. Genetic polymorphisms in the phenobarbital-responsive enhancer module of the UDP-glucuronosyltransferase 1A1 gene and irinotecan toxicity. Pharmacogenet Genomics 15: 35-41 (2005)
- Ando Y et al. Clinical pharmacogenetics of irinotecan. Drug Metab Rev 37: 565-574 (2005)
- Ito G et al. Krupple-like factor 6 is frequently down-regulated and induces apoptosis in non-small cell lung cancer cells. Cancer Res 64: 3838-3843 (2004)
- Hasegawa Y et al. Rapid Detection of UGT1A1 Gene Polymorphisms by Newly Developed Invader Assay. Clin Chem 50: 1479-1480 (2004)
- Jinnai N et al. Polymorphisms in the prostaglandin E2 receptor subtype 2 gene confer susceptibility to aspirin induced asthma: a candidate gene approach. Hum Mol Genet 13: 3203-3217 (2004)
- Hashimoto N et al. CD40 plays a crucial role in lipopolysaccharide-induced acute lung injury. Am J Respir Cell Mol Biol 30: 808-815 (2004)
- Usami N et al. b-catenin inhibits cell growth of a malignant mesothelioma cell line, NCI-H28,with a 3p21.3 homozygous deletion. Oncogene 22: 5978-5986 (2003)
- Uno Y et al. Characterization of six base pair deletion in the putative HNF1-binding site of human PXR promoter. J Hum Genet 48: 594-597 (2003)
- Sato M et al. The expression of DNA methyltransferases and methyl-CpG-binding proteins is not associated with the methylation status of p14ARF, p16INK4a and RASSF1A in human lung cancer cell lines. Oncogene 21: 4822-4829 (2002)
- Ando Y et al. Polymorphisms of UDP-glucuronosyltransferase gene and irinotecan toxicity: a pharmacogenetic analysis. Cancer Res 60: 6921-6926 (2000)
- Ando Y et al. Modification of clinical presentation of prostate tumors by a novel genetic variant in CYP3A4. J Natl Cancer Inst 91: 1587-1588 (1999)
- Takada Y et al. 12-O-tetradecanoylphorbol-13-acetate-induced apoptosis is mediated by tumor necrosis factor a in human monocytic U937 cells. J Biol Chem 274: 28286-28292 (1999)
- Ando Y et al. Prediction equation for glomerular filtration rate. Ann Intern Med 131: 629-630 (1999)
- Isobe K et al. Induction of antitumor immunity in mice by allo-major histocompatibility complex class I gene transfectant with strong antigen expression. J Natl Cancer Inst 81: 1823-1828 (1989)
- Hasegawa Y et al. Calcium-independent pathway of tumor necrosis factor-mediated lysis of target cells. J Immunol 142: 2670-2676 (1989)
- Ando K et al. Induction and characterization of minor histocompatibility antigens: specific primary cyotoxic T lymphocyte responses in vitro. J Immunol 140: 723-729 (1988)

