Prof. Jitsuo Usuda Profile

Prof. Jitsuo Usuda

at Nippon Medical School

SPIE Involvement:

Author

Proceedings Article | 14 August 2019 Presentation

Management of multiple primary lung cancer in patients with centrally located early lung cancer lesions (Conference Presentation)

Takumi Sonokawa, Takuma Matsui, Kyoshiro Takegahara, Tatsuya Inoue, Jitsuo Usuda

Proceedings Volume 11070, 110700T (2019) https://doi.org/10.1117/12.2527439

KEYWORDS: Lung cancer, Photodynamic therapy, Surgery, Bronchoscopy, Cell biology

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Proceedings Article | 14 August 2019 Presentation

Combination therapy with photodynamic therapy in lung cancer (Conference Presentation)

Kinya Furukawa, Jitsuo Usuda, Masakazu Kimura, Kuniharu Miyajima, Taisuke Matsubara, Shotaro Ono, Eiji Nakajima, Norihiko Ikeda, Harubumi Kato

Proceedings Volume 11070, 110702N (2019) https://doi.org/10.1117/12.2527891

KEYWORDS: Photodynamic therapy, Lung cancer, Surgery, Chromium, Patents

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Proceedings Article | 12 February 2018 Presentation + Paper

The NPe6 fluorescence measurements by using a fluorescence sensing system for skin photosensitivity risk assessment after photodynamic therapy

Keishi Ohtani, Jitsu Usuda, Emiyu Ogawa, Sachio Maehara, Kentaro Imai, Tatsuya Inoue, Masaru Hagiwara, Masatoshi Kakihana, Naohiro Kajiwara, Tatsuo Ohira, Tsunenori Arai, Norihiko Ikeda

Proceedings Volume 10476, 104760D (2018) https://doi.org/10.1117/12.2287677

KEYWORDS: Luminescence, Skin, Photodynamic therapy, Sensing systems, Lung cancer, Surgery

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Proceedings Article | 8 February 2017 Paper

3-compartment dynamic model of talaporfin sodium pharmacokinetics in silico

Emiyu Ogawa, Yuko Uno, Keishi Ohtani, Sachio Maehara, Kentaro Imai, Shotaro Ono, Jitsuo Usuda, Tsunenori Arai

Proceedings Volume 10047, 100470Y (2017) https://doi.org/10.1117/12.2250716

KEYWORDS: Sodium, Plasma, Laser ablation, Laser irradiation, Luminescence, Data modeling, Oxygen, Fluorescence spectroscopy, Polymer optical fibers

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Proceedings Article | 13 June 2003 Paper

From molecular PDT damage to cellular PDT responses: attempts at bridging the gap on the role of Bcl-2

Jitsuo Usuda, Liang-yan Xue, Song-mao Chiu, Kashif Azizuddin, Rachel Morris, John Mulvihill, Nancy Oleinick

Proceedings Volume 4952, (2003) https://doi.org/10.1117/12.488633

KEYWORDS: Photodynamic therapy, Proteins, Cell death, Green fluorescent protein, Cancer, Flow cytometry, Photosensitizer targeting, Tumors, Breast cancer, Therapeutics

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Expression of the anti-apoptotic proteins Bcl-2 and/or Bcl-xL is greatly elevated in many advanced cancers, especially those resistant to standard therapies, such as radiation or chemotherapy. It has been suggested that those two proteins would be attractive targets for the development of new cancer treatments. Photodynamic therapy (PDT) with photosensitizers that localize in or target mitochondria, such as the phthalocyanine Pc 4, specifically attack the anti-apoptotic protein Bcl-2, generating a variety of oxidized, complexed, and cleaved photoproducts. The closely related protein Bcl-xL is also a target of Pc 4-PDT. In a recent study employing transient transfection of an expression vector encoding deletion mutants of Bcl-2, we identified the membrane anchorage regions of the protein that are required to form the photosensitive target. In spite of the demonstrated photodamage to Bcl-2 (and Bcl-xL), how the photodamage translates into changes in the sensitivity of cells to PDT-induced apoptosis or other modes of cell death is not clear, and it also remains unclear how elevated amounts of anti-apoptotic proteins in tumors might make them more or less responsive to PDT. In the present study, we have studied the PDT response of MCF7 human breast cancer cells overexpressing wild-type Bcl-2 or certain deletion mutants either in a transient or stable mode. We show that cells expressing modestly elevated amounts (<10-fold increase) of Bcl-2 and in which the pro-apoptotic protein Bax is not upregulated do not differ from the parental cells with respect to PDT-induced cell killing. In contrast, cells expressing higher amounts (>50-fold increase) of Bcl-2 or certain mutants are made significantly more resistant to the induction of apoptosis and the loss of clonogenicity upon exposure to Pc 4-PDT. In the presence of high levels of Bcl-2, extensive photodamage requires higher PDT doses. We conclude that Pc 4-PDT targets Bcl-2 and Bcl-xL, eliminating one mechanism that protects the tumor cells from other types of therapy. However, it is possible that cells expressing very high levels of the anti-apoptotic proteins might still be resistant to PDT. The data suggest that PDT with a non-vascular-targeting photosensitizer might be effective in a combination treatment in which Bcl-2 and Bcl-xL are first photodamaged before delivery of a second agent.

Proceedings Article | 6 June 2002 Paper

Mitochondrial targets of photodynamic therapy and their contribution to cell death

Nancy Oleinick, Jitsuo Usuda, Liang-yan Xue, Kashif Azizuddin, Song-mao Chiu, Minh Lam, Rachel Morris, Anna-Liisa Nieminen

Proceedings Volume 4612, (2002) https://doi.org/10.1117/12.469339

KEYWORDS: Proteins, Photodynamic therapy, Cell death, Molecules, Oxygen, Photosensitizer targeting, Cancer, Breast cancer, Tumors, Medicine

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Proceedings Article | 2 April 1996 Paper

Fluorescence photodiagnosis for malignant tumor

Tetsuya Okunaka, Kinya Furukawa, Kouichi Tanaka, Hideaki Shimatani, Masahiko Harada, Hiroshi Shibuya, Shinya Okada, Jitsuo Usuda, Chimori Konaka, Katsuo Aizawa, Harubumi Kato

Proceedings Volume 2675, (1996) https://doi.org/10.1117/12.237525

KEYWORDS: Luminescence, Tumors, Lung cancer, Cancer, Image analysis, Excimer lasers, Imaging systems, Tissues, Endoscopy, Excimers

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Showing 5 of 7 publications

Conference Committee Involvement (1)

17th International Photodynamic Association World Congress

28 June 2019 | Cambridge, Massachusetts, United States

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