| Author | Kiura, Katsuyuki| Tanimoto, Mitsune| |
|---|---|
| Published Date | 2013-04-01 |
| Publication Title | 岡山医学会雑誌 |
| Volume | volume125 |
| Issue | issue1 |
| Content Type | Journal Article |
| Author | Rai, Kammei| Takigawa, Nagio| Ito, Sachio| Kashihara, Hiromi| Ichihara, Eiki| Yasuda, Tatsuji| Shimizu, Kenji| Tanimoto, Mitsune| Kiura, Katsuyuki| |
|---|---|
| Published Date | 2012-12-03 |
| Publication Title | 岡山医学会雑誌 |
| Volume | volume124 |
| Issue | issue3 |
| Content Type | Journal Article |
| Author | Taniguchi, Akihiko| Miyahara, Nobuaki| Nakahara, Atsushi| Takata, Saburo| Sakugawa, Ryo| Nagano, Osamu| Tanimoto, Yasushi| Kanehiro, Arihiko| Kiura, Katsuyuki| Ujike, Yoshito| Tanimoto, Mitsune| |
|---|---|
| Published Date | 2011-12-01 |
| Publication Title | 岡山医学会雑誌 |
| Volume | volume123 |
| Issue | issue3 |
| Content Type | Journal Article |
| Author | Nogami, Naoyuki| Hotta, Katsuyuki| Kuyama, Shoichi| Kiura, Katsuyuki| Takigawa, Nagio| Chikamori, Kenichi| Shibayama, Takuo| Kishino, Daizo| Hosokawa, Shinobu| Tamaoki, Akihiko| Harita, Shingo| Tabata, Masahiro| Ueoka, Hiroshi| Shinkai, Tetsu| Tanimoto, Mitsune| |
|---|---|
| Published Date | 2011-10 |
| Publication Title | Lung Cancer |
| Volume | volume74 |
| Issue | issue1 |
| Content Type | Journal Article |
| Author | Ichihara, Eiki| Ohashi, Kadoaki| Takigawa, Nagio| Osawa, Masahiro| Ogino, Atsuko| Tanimoto, Mitsune| Kiura, Katsuyuki| |
|---|---|
| Published Date | 2011-04-01 |
| Publication Title | 岡山医学会雑誌 |
| Volume | volume123 |
| Issue | issue1 |
| Content Type | Journal Article |
| Author | Ichihara, Eiki| Matsuoka, Junji| Takigawa, Nagio| Matsuzaki, Takashi| Katsui, Kuniaki| Kiura, Katsuyuki| Tanimoto, Mitsune| |
|---|---|
| Published Date | 2009-12-01 |
| Publication Title | 岡山医学会雑誌 |
| Volume | volume121 |
| Issue | issue3 |
| Content Type | Journal Article |
| Author | Suehisa, Hiroshi| Toyooka, Shinichi| Hotta, Katsuyuki| Uchida, Akiko| Soh, Junichi| Fujiwara, Yoshiro| Matsuo, Keitaro| Ouchida, Mamoru| Takata, Minoru| Kiura, Katsuyuki| Date, Hiroshi| |
|---|---|
| Published Date | 2008-12-01 |
| Publication Title | 岡山医学会雑誌 |
| Volume | volume120 |
| Issue | issue3 |
| Content Type | Journal Article |
| Author | 木浦 勝行| 谷本 安| 田端 雅弘| 金廣 有彦| 上岡 博| 谷本 光音| 渡邊 都貴子| 草野 展周| 小出 典男| |
|---|---|
| Published Date | 2005-05-30 |
| Publication Title | 岡山医学会雑誌 |
| Volume | volume115 |
| Issue | issue1 |
| Content Type | Journal Article |
| Author | 谷本 安| 佐久川 亮| 木浦 勝行| 谷本 光音| |
|---|---|
| Published Date | 2005-01-31 |
| Publication Title | 岡山医学会雑誌 |
| Volume | volume116 |
| Issue | issue3 |
| Content Type | Journal Article |
| Author | Kiura, Katsuyuki| Takigawa, Nagio| Oze, Isao| Yasugi, Masayuki| Ochi, Nobuaki| Harada, Daijiro| Tanimoto, Mitsune| |
|---|---|
| Published Date | 2008-01-04 |
| Publication Title | 岡山医学会雑誌 |
| Volume | volume119 |
| Issue | issue3 |
| Content Type | Journal Article |
| Author | Kiura, Katsuyuki| |
|---|---|
| Published Date | 1993-09-30 |
| Publication Title | |
| Content Type | Thesis or Dissertation |
| JaLCDOI | 10.18926/AMO/64363 |
|---|---|
| FullText URL | 77_1_65.pdf |
| Author | Sato, Ken| Takigawa, Nagio| Kubo, Toshio| Katayama, Hideki| Kishino, Daizo| Okada, Toshiaki| Hisamoto, Akiko| Mimoto, Junko| Ochi, Nobuaki| Yoshino, Tadashi| Ueoka, Hiroshi| Tanimoto, Mitsune| Maeda, Yoshionobu| Kiura, Katsuyuki| |
| Abstract | We investigated the effects of celecoxib combined with (−)-epigallocatechin-3-gallate (EGCG) or polyphenon E in a cisplatin-induced lung tumorigenesis model. Four-week-old female A/J mice were divided into seven groups: (i) Control, (ii) 150 mg/kg celecoxib (150Cel), (iii) 1,500 mg/kg celecoxib (1500Cel), (iv) EGCG+150 mg/kg celecoxib (EGCG+150Cel), (v) EGCG+1,500 mg/kg celecoxib (EGCG+1500Cel), (vi) polyphenon E+150 mg/kg celecoxib (PolyE+150Cel), and (vii) polyphenon E+1,500 mg/kg celecoxib (PolyE+1500Cel). All mice were administered cisplatin (1.62 mg/kg of body weight, i.p.) 1×/week for 10 weeks and sacrificed at week 30; the numbers of tumors on the lung surface were then determined. The tumor incidence and multiplicity (no. of tumors/mouse, mean±SD) were respectively 95% and 2.15±1.50 in Control, 95% and 2.10±1.29 in 150Cel, 86% and 1.67±1.20 in 1500Cel, 71% and 1.38±1.24 in EGCG+150Cel, 67% and 1.29±1.38 in EGCG+1500Cel, 80% and 1.95±1.36 in PolyE+150Cel, and 65% and 1.05±0.10 in PolyE+1500Cel. The combination of high-dose celecoxib with EGCG or polyphenon E significantly reduced multiplicity in cisplatin-induced lung tumors. |
| Keywords | celecoxib cisplatin EGCG lung tumor polyphenon E |
| Amo Type | Original Article |
| Publication Title | Acta Medica Okayama |
| Published Date | 2023-02 |
| Volume | volume77 |
| Issue | issue1 |
| Publisher | Okayama University Medical School |
| Start Page | 65 |
| End Page | 70 |
| ISSN | 0386-300X |
| NCID | AA00508441 |
| Content Type | Journal Article |
| language | English |
| Copyright Holders | Copyright Ⓒ 2023 by Okayama University Medical School |
| File Version | publisher |
| Refereed | True |
| PubMed ID | 36849147 |
| Web of Science KeyUT | 000952992100004 |
| JaLCDOI | 10.18926/AMO/61429 |
|---|---|
| FullText URL | 75_1_15.pdf |
| Author | Katsui, Kuniaki| Ogata, Takeshi| Tada, Akihiro| Sugiyama, Soichi| Yoshio, Kotaro| Kuroda, Masahiro| Kiura, Katsuyuki| Maeda, Yoshinobu| Toyooka, Shinichi| Hiraki, Takao| Kanazawa, Susumu| |
| Abstract | The aim of this study was to investigate whether volumetric positron emission tomography (PET) parameters are prognostic predictors in stage III non-small cell lung cancer patients receiving definitive concurrent chemo-radiotherapy (CCRT) with cisplatin/docetaxel. Cases involving definitive CCRT were reviewed retrospectively, and the maximum standardized uptake value, metabolic tumor volume (MTV) and total lesion glycolysis (TLG) were calculated. The relationships between these PET parameters and prognosis were analyzed. MTV and TLG were significant predictors of distant metastasis-free survival (DMFS) (p = 0.0003 and 0.0005, respectively) and progression-free survival (PFS) (p = 0.001 and 0.0007, respectively). The three-year DMFS rates in patients with low and high MTV were 13.3% and 64.6%, respectively, and the corresponding values in those with low and high TLG were 13.3% and 65.2%, respectively. The three-year PFS rates in patients with low and high MTV were 13.3% and 57.8%, respectively, and the corresponding values in patients with low and high TLG were 13.3% and 57.8%, respectively. However, MTV and TLG were not predictors of local control or overall sur-vival. We demonstrated that volumetric PET parameters were predictors of patients receiving definitive CCRT. Our findings contradict the findings of previous reports and warrant further research to validate them. |
| Keywords | volumetric positron emission tomography parameters distant metastasis-free survival chemoradiotherapy cisplatin/docetaxel non-small cell lung cancer |
| Amo Type | Original Article |
| Publication Title | Acta Medica Okayama |
| Published Date | 2021-02 |
| Volume | volume75 |
| Issue | issue1 |
| Publisher | Okayama University Medical School |
| Start Page | 15 |
| End Page | 23 |
| ISSN | 0386-300X |
| NCID | AA00508441 |
| Content Type | Journal Article |
| language | English |
| Copyright Holders | CopyrightⒸ 2021 by Okayama University Medical School |
| File Version | publisher |
| Refereed | True |
| PubMed ID | 33649609 |
| JaLCDOI | 10.18926/AMO/60802 |
|---|---|
| FullText URL | 74_5_423.pdf |
| Author | Hirabae, Atsuko| Ichihara, Eiki| Sunami, Ryota| Ota, Moeko| Iwamoto, Yoshitaka| Maeda, Yoshinobu| Kiura, Katsuyuki| |
| Abstract | We report a case of late-onset hyperprogressive disease after cessation of a PD-1 inhibitor. A male was diagnosed with metastatic lung adenocarcinoma with little progression for 2 months before treatment. He received pembrolizumab as a second-line treatment and was subsequently prescribed docetaxel for 3 months until a slight increase in pleural effusion. At the time of progression to docetaxel, he commenced prednisolone because of immune-system-related diarrhea. After that, his general condition rapidly worsened with severe fatigue and hypoxia. Computed tomography revealed a massive increase of pleural effusion and replacement of almost the entire liver with cancer over a period of 5 weeks. |
| Keywords | lung cancer immune checkpoint inhibitors pembrolizumab hyperprogression |
| Amo Type | Case Report |
| Publication Title | Acta Medica Okayama |
| Published Date | 2020-10 |
| Volume | volume74 |
| Issue | issue5 |
| Publisher | Okayama University Medical School |
| Start Page | 423 |
| End Page | 425 |
| ISSN | 0386-300X |
| NCID | AA00508441 |
| Content Type | Journal Article |
| language | English |
| Copyright Holders | CopyrightⒸ 2020 by Okayama University Medical School |
| File Version | publisher |
| Refereed | True |
| PubMed ID | 33106698 |
| Web of Science KeyUT | 000581970100007 |
| NAID | 120006892928 |
| JaLCDOI | 10.18926/AMO/60796 |
|---|---|
| FullText URL | 74_5_371.pdf |
| Author | Makimoto, Go| Ohashi, Kadoaki| Maeda, Yoshinobu| Kiura, Katsuyuki| |
| Abstract | The prognosis of advanced non-small cell lung cancer (NSCLC) patients has improved in recent decades, especially for patients with an oncogenic driver mutation. Anaplastic lymphoma kinase (ALK) tyrosine kinase inhibitors (TKIs) are effective for patients with the echinoderm microtubule-associated protein-like 4-ALK fusion gene. Several ALK-TKIs have been established: the first-generation ALK-TKI, crizotinib; second-generation ALK-TKIs, alectinib and ceritinib; and third-generation ALK-TKI, lorlatinib. Some ALK-TKIs are effective for tumors that are resistant to other ALK-TKIs; however, as is known in epidermal growth factor receptormutant lung cancer, tumor resistance is inevitable. ALK-positive NSCLCs acquire resistance via various mechanisms, making it a heterogeneous disease. Therefore, it is necessary to develop next-generation treatment strategies, such as the use of next-generation ALK-TKIs for secondary mutations, or combination therapies with ALK-TKIs and other TKIs. In this review, we summarize the development and use of ALK-TKIs, prior pivotal clinical trials, and resistance mechanisms. |
| Keywords | lung cancer anaplastic lymphoma kinase tyrosine kinase inhibitors resistance mechanism |
| Amo Type | Review |
| Publication Title | Acta Medica Okayama |
| Published Date | 2020-10 |
| Volume | volume74 |
| Issue | issue5 |
| Publisher | Okayama University Medical School |
| Start Page | 371 |
| End Page | 379 |
| ISSN | 0386-300X |
| NCID | AA00508441 |
| Content Type | Journal Article |
| language | English |
| Copyright Holders | CopyrightⒸ 2020 by Okayama University Medical School |
| File Version | publisher |
| Refereed | True |
| PubMed ID | 33106692 |
| Web of Science KeyUT | 000581970100001 |
| NAID | 120006892922 |
| JaLCDOI | 10.18926/AMO/55446 |
|---|---|
| FullText URL | 71_5_453.pdf |
| Author | Taniguchi, Akihiko| Miyahara, Nobuaki| Oda, Naohiro| Morichika, Daisuke| Ichihara, Eiki| Oze, Isao| Tanimoto, Yasushi| Ichikawa, Hirohisa| Fujii, Utako| Tanimoto, Mitsune| Kanehiro, Arihiko| Kiura, Katsuyuki| |
| Abstract | Although recent retrospective studies suggested that the use of β-blockers appears to help improve the mortality rate and decrease the rate of exacerbation in chronic obstructive pulmonary disease (COPD) patients with heart failure, the effects of β-blockers on COPD patients without heart failure have not been established. Based on previous reports, we have launched a multicenter, prospective, single-arm phase II study to evaluate the preventive effect of the cardioselective β-blocker bisoprolol in COPD exacerbation, in Japanese individuals with moderate-to-severe COPD who do not have heart failure but do have hypertension requiring the use of medication. The primary endpoint is the rate of mild-to-severe COPD exacerbation. The results of this study will clarify whether bisoprolol can prevent exacerbation in COPD patients without heart failure. |
| Keywords | chronic obstructive pulmonary disease β-blocker bisoprolol exacerbation heart failure |
| Amo Type | Clinical Study Protocol |
| Publication Title | Acta Medica Okayama |
| Published Date | 2017-10 |
| Volume | volume71 |
| Issue | issue5 |
| Publisher | Okayama University Medical School |
| Start Page | 453 |
| End Page | 457 |
| ISSN | 0386-300X |
| NCID | AA00508441 |
| Content Type | Journal Article |
| language | English |
| Copyright Holders | CopyrightⒸ 2017 by Okayama University Medical School |
| File Version | publisher |
| Refereed | True |
| PubMed ID | 29042706 |
| JaLCDOI | 10.18926/AMO/54514 |
|---|---|
| FullText URL | 70_4_327.pdf |
| Author | Watanabe, Mototsugu| Yamamoto, Hiromasa| Eikawa, Shingo| Shien, Kazuhiko| Shien, Tadahiko| Soh, Junichi| Hotta, Katsuyuki| Wada, Jun| Hinotsu, Shiro| Fujiwara, Toshiyoshi| Kiura, Katsuyuki| Doihara, Hiroyoshi| Miyoshi, Shinichiro| Udono, Heiichiro| Toyooka, Shinichi| |
| Abstract | A study to evaluate the effect of metformin on the immune system was commenced in July 2014. Metformin is one of the most commonly prescribed drugs for type 2 diabetes, and previous studies have reported that metformin has an anti-tumor effect. The aim of this study is to evaluate the efficacy of metformin on the immune system in human cancer patients in vivo. The primary outcome parameter will be the rate change in the population of CD8＋ T cells, which produce multiple cytokines. |
| Keywords | metformin CD8＋ T cells cancer immunology |
| Amo Type | Clinical Study Protocols |
| Publication Title | Acta Medica Okayama |
| Published Date | 2016-08 |
| Volume | volume70 |
| Issue | issue4 |
| Publisher | Okayama University Medical School |
| Start Page | 327 |
| End Page | 330 |
| ISSN | 0386-300X |
| NCID | AA00508441 |
| Content Type | Journal Article |
| language | English |
| Copyright Holders | CopyrightⒸ 2016 by Okayama University Medical School |
| File Version | publisher |
| Refereed | True |
| PubMed ID | 27549683 |
| Web of Science KeyUT | 000384748600018 |
| JaLCDOI | 10.18926/AMO/54503 |
|---|---|
| FullText URL | 70_4_273.pdf |
| Author | Makimoto, Go| Miyahara, Nobuaki| Yoshikawa, Mao| Taniguchi, Akihiko| Kanehiro, Arihiko| Tanimoto, Mitsune| Kiura, Katsuyuki| |
| Abstract | Heerfordtʼs syndrome is a rare manifestation of sarcoidosis and is defined as a combination of facial palsy, parotid swelling, and uveitis, associated with a low-grade fever. We report a case of Heerfordtʼs syndrome presenting with a high fever and increased serum tumor necrosis factor alpha (TNF-α) levels. The patient had facial palsy, parotid swelling, uveitis, and swelling of the right supraclavicular and hilar lymph nodes. Corticosteroid therapy was initiated, and her symptoms soon resolved completely, in tandem with a decrease in TNF-α serum levels. |
| Keywords | Heerfordtʼs syndrome sarcoidosis TNF-α |
| Amo Type | Case Report |
| Publication Title | Acta Medica Okayama |
| Published Date | 2016-08 |
| Volume | volume70 |
| Issue | issue4 |
| Publisher | Okayama University Medical School |
| Start Page | 273 |
| End Page | 277 |
| ISSN | 0386-300X |
| NCID | AA00508441 |
| Content Type | Journal Article |
| language | English |
| Copyright Holders | CopyrightⒸ 2016 by Okayama University Medical School |
| File Version | publisher |
| Refereed | True |
| PubMed ID | 27549672 |
| Web of Science KeyUT | 000384748600007 |
| JaLCDOI | 10.18926/AMO/54499 |
|---|---|
| FullText URL | 70_4_243.pdf |
| Author | Osawa, Masahiro| Ohashi, Kadoaki| Kubo, Toshio| Ichihara, Eiki| Takata, Saburo| Takigawa, Nagio| Takata , Minoru| Tanimoto, Mitsune| Kiura, Katsuyuki| |
| Abstract | Vandetanib (ZactimaTM) is a novel, orally available inhibitor of both vascular endothelial growth factor receptor-2 (VEGFR-2) and epidermal growth factor receptor (EGFR) tyrosine kinase. In the present study, a line of transgenic mice with a mouse Egfr gene mutation (delE748-A752) corresponding to a human EGFR mutation (delE746-A750) was established. The transgenic mice developed atypical adenomatous hyperplasia to adenocarcinoma of the lung at around 5 weeks of age and died of lung tumors at approximately 17 weeks of age. In the mice treated with vandetanib (6mg/kg/day), these lung tumors disappeared and the phosphorylations of EGFR and VEGFR-2 were reduced in lung tissues to levels comparable to those of non-transgenic control mice. The median overall survival time of the transgenic mice was 28 weeks in the vandetanib-treated group and 17 weeks in the vehicle-treated group. Vandetanib significantly prolonged the survival of the transgenic mice (log-rank test, p＜0.01); resistance to vandetanib occurred at 20 weeks of age and the animals died from their lung tumors at about 28 weeks of age. These data suggest that vandetanib could suppress the progression of tumors harboring an activating EGFR mutation. |
| Keywords | vandetanib VEGFR EGFR nonsmall cell lung cancer transgenic mouse |
| Amo Type | Original Article |
| Publication Title | Acta Medica Okayama |
| Published Date | 2016-08 |
| Volume | volume70 |
| Issue | issue4 |
| Publisher | Okayama University Medical School |
| Start Page | 243 |
| End Page | 253 |
| ISSN | 0386-300X |
| NCID | AA00508441 |
| Content Type | Journal Article |
| language | English |
| Copyright Holders | CopyrightⒸ 2016 by Okayama University Medical School |
| File Version | publisher |
| Refereed | True |
| PubMed ID | 27549668 |
| Web of Science KeyUT | 000384748600003 |
| JaLCDOI | 10.18926/AMO/53671 |
|---|---|
| FullText URL | 69_5_261.pdf |
| Author | Nojima, Daisuke| Fujimoto, Nobukazu| Kato, Katsuya| Fuchimoto, Yasuko| Kiura, Katsuyuki| Kishimoto, Takumi| Tanimoto, Mitsune| |
| Abstract | We investigated the clinical features of asbestos-induced diffuse pleural thickening (DPT) with severe respiratory compromise. We conducted a retrospective study of consecutive subjects with asbestos-induced DPT. Medical data such as initial symptoms, radiological findings, respiratory function test results, and clinical course were collected and analyzed. There were 24 patients between 2003 and 2012. All were men, and the median age at the development of DPT was 74 years. The top occupational category associated with asbestos exposure was dockyard workers. The median duration of asbestos exposure was 35.0 years, and the median latency from first exposure to the onset of DPT was 49.0 years. There were no significant differences in respiratory function test results between the higher and lower Brinkman index groups or between unilateral and bilateral DPT. Thirteen patients had a history of benign asbestos pleural effusion (BAPE), and the median duration from pleural fluid accumulation to DPT with severe respiratory compromise was 28.4 months. DPT with severe respiratory compromise can develop after a long latency following occupational asbestos exposure and a history of BAPE. |
| Keywords | asbestos pleural thickening MRC dyspnea scale respiratory function test costophrenic angle |
| Amo Type | Original Article |
| Publication Title | Acta Medica Okayama |
| Published Date | 2015-10 |
| Volume | volume69 |
| Issue | issue5 |
| Publisher | Okayama University Medical School |
| Start Page | 261 |
| End Page | 266 |
| ISSN | 0386-300X |
| NCID | AA00508441 |
| Content Type | Journal Article |
| language | English |
| Copyright Holders | CopyrightⒸ 2015 by Okayama University Medical School |
| File Version | publisher |
| Refereed | True |
| PubMed ID | 26490022 |
| Web of Science KeyUT | 000365519600001 |
