| Author | Tanaka, Norimitsu| Toyooka, Shinichi| Soh, Junichi| Kubo, Takafumi| Yamamoto, Hiromasa| Maki, Yuho| Muraoka, Takayuki| Shien, Kazuhiko| Furukawa, Masashi| Ueno, Tsuyoshi| Asano, Hiroaki| Tsukuda, Kazunori| Aoe, Keisuke| Miyoshi, Shinichiro| |
|---|---|
| Published Date | 2012-04 |
| Publication Title | Lung Cancer |
| Volume | volume76 |
| Issue | issue1 |
| Content Type | Journal Article |
| Author | Maki, Yuho| Soh, Junichi| Ichimura, Kouichi| Shien, Kazuhiko| Furukawa, Masashi| Muraoka, Takayuki| Tanaka, Norimitsu| Ueno, Tsuyoshi| Yamamoto, Hiromasa| Asano, Hiroaki| Tsukuda, Kazunori| Toyooka, Shinichi| Miyoshi, Shinichiro| |
|---|---|
| Published Date | 2013-01 |
| Publication Title | Oncology Reports |
| Volume | volume29 |
| Issue | issue1 |
| Content Type | Journal Article |
| Author | Muraoka, Takayuki| Soh, Junichi| Toyooka, Shinichi| Aoe, Keisuke| Fujimoto, Nobukazu| Hashida, Shinsuke| Maki, Yuho| Tanaka, Norimitsu| Shien, Kazuhiko| Furukawa, Masashi| Yamamoto, Hiromasa| Asano, Hiroaki| Tsukuda, Kazunori| Kishimoto, Takumi| Otsuki, Takemi| Miyoshi, Shinichiro| |
|---|---|
| Published Date | 2013-12 |
| Publication Title | Lung Cancer |
| Volume | volume82 |
| Issue | issue3 |
| Content Type | Journal Article |
| JaLCDOI | 10.18926/AMO/52140 |
|---|---|
| FullText URL | 68_1_23.pdf |
| Author | Ueno, Tsuyoshi| Toyooka, Shinichi| Fukazawa, Takuya| Kubo, Takafumi| Soh, Junichi| Asano, Hiroaki| Muraoka, Takayuki| Tanaka, Norimitsu| Maki, Yuho| Shien, Kazuhiko| Furukawa, Masashi| Sakaguchi, Masakiyo| Yamamoto, Hiromasa| Tsukuda, Kazunori| Miyoshi, Shinichiro| |
| Abstract | The microRNA-34s (miR-34s) have p53 response elements in their 5ʼ-flanking regions and demonstrate tumor-suppressive functions. In malignant pleural mesothelioma (MPM), we previously reported that expression of miR-34b and miR-34c (miR-34b/c) was frequently downregulated by methylation in MPM cell lines and primary tumors. The forced overexpression of miR-34b/c showed significant antitumor effects with the induction of apoptosis in MPM cells. In this study, we examined the in vivo antitumor effects of miR-34b/c using adenovirus vector on MPM. We subcutaneously transplanted NCI-H290, a human MPM cell line, into BALB/C mice and injected adenovirus vector expressing miR-34b/c, luciferase driven by the cytomegalovirus promoter (Ad-miR-34b/c or Ad-Luc), or PBS control into tumors over 5mm in diameter. A statistically significant growth inhibition of the tumor volume was observed in the Ad-miR-34b/c group from day 6 onward compared to the Ad-Luc group. The inhibition rate of Ad-miR-34b/c, compared to the tumor volume treated with Ad-Luc, was 58.6% on day 10 and 54.7% on day13. Our results indicate that adenovirus-mediated miR-34b/c gene therapy could be useful for the clinical treatment of MPM. |
| Keywords | mesothelioma microRNA microRNA-34b/c p53 |
| Amo Type | Original Article |
| Published Date | 2014-02 |
| Publication Title | Acta Medica Okayama |
| Volume | volume68 |
| Issue | issue1 |
| Publisher | Okayama University Medical School |
| Start Page | 23 |
| End Page | 26 |
| ISSN | 0386-300X |
| NCID | AA00508441 |
| Content Type | Journal Article |
| language | 英語 |
| Copyright Holders | CopyrightⒸ 2014 by Okayama University Medical School |
| File Version | publisher |
| Refereed | True |
| PubMed ID | 24553485 |
| Web of Sience KeyUT | 000331592800004 |
| JaLCDOI | 10.18926/AMO/52785 |
|---|---|
| FullText URL | 68_4_191.pdf |
| Author | Shien, Kazuhiko| Yamamoto, Hiromasa| Soh, Junichi| Miyoshi, Shinichiro| Toyooka, Shinichi| |
| Abstract | Non-small cell lung cancer (NSCLC) harboring an activating mutation within the epidermal growth factor receptor (EGFR) was defined as a clinically distinct molecular group. These lesions show oncogene addiction to EGFR and dramatic responses to the EGFR tyrosine kinase inhibitors (TKIs). Several large Phase III trials have shown that EGFR-TKIs improved the progression-free survival of patients with EGFR mutant NSCLC compared to conventional chemotherapy. However, the long-term effectiveness of EGFR-TKIs is usually limited because of acquired drug resistance. To overcome this resistance to EGFR-TKIs, it will be essential to identify the specific mechanisms underlying the resistance. Many investigators have attempted to identify the mechanisms using preclinical models and drug-resistant clinical samples. As a result, several mechanisms have been showed to be responsible for the resistance, but not all of the relevant mechanisms have been uncovered. In this review, we provide an overview of mechanisms underlying drug-resistance to EGFR-TKIs, focusing on results obtained with preclinical models, and we present some possible strategies to overcome the EGFR-TKI resistance. |
| Keywords | non-small cell lung cancer EGFR mutation tyrosine-kinase inhibitor drug resistance cancer stem cell |
| Amo Type | Review |
| Published Date | 2014-08 |
| Publication Title | Acta Medica Okayama |
| Volume | volume68 |
| Issue | issue4 |
| Publisher | Okayama University Medical School |
| Start Page | 191 |
| End Page | 200 |
| ISSN | 0386-300X |
| NCID | AA00508441 |
| Content Type | Journal Article |
| language | 英語 |
| Copyright Holders | CopyrightⒸ 2014 by Okayama University Medical School |
| File Version | publisher |
| Refereed | True |
| PubMed ID | 25145405 |
| Web of Sience KeyUT | 000340687500001 |
| Title Alternative | The 2013 Incentive Award of the Okayama Medical Association in General Medical Science (2013 Yuuki Prize) |
|---|---|
| FullText URL | 126_187.pdf |
| Author | Yamamoto, Hiromasa| |
| Abstract | 受賞対象論文: Yamamoto H, Higasa K, Sakaguchi M, Shien K, Soh J, Ichimura K, Furukawa M, Hashida S, Tsukuda K, Takigawa N, Matsuo K, Kiura K, Miyoshi S, Matsuda F, Toyooka S：Novel germline mutation in the transmembrane domain of HER2 in familial lung adenocarcinomas. J Natl Cancer Inst (2014) 106, djt338 |
| Publication Title | 岡山医学会雑誌 |
| Published Date | 2014-12-01 |
| Volume | volume126 |
| Issue | issue3 |
| Start Page | 187 |
| End Page | 190 |
| ISSN | 0030-1558 |
| language | 日本語 |
| Copyright Holders | Copyright (c) 2014 岡山医学会 |
| File Version | publisher |
| DOI | 10.4044/joma.126.187 |
| NAID | 130004903235 |
| Author | Yasuda, Yukiko| Sakai, Akiko| Ito, Sachio| Sasai, Kaori| Yamamoto, Hiromasa| Matsubara, Nagahide| Ouchida, Mamoru| Katayama, Hiroshi| Shimizu, Kenji| |
|---|---|
| Published Date | 2017-02 |
| Publication Title | Acta Medica Okayama |
| Volume | volume71 |
| Issue | issue1 |
| Content Type | Journal Article |
| JaLCDOI | 10.18926/AMO/54826 |
| JaLCDOI | 10.18926/AMO/49253 |
|---|---|
| FullText URL | 67_1_19.pdf |
| Author | Furukawa, Masashi| Soh, Junichi| Yamamoto, Hiromasa| Ichimura, Kouichi| Shien, Kazuhiko| Maki, Yuho| Muraoka, Takayuki| Tanaka, Norimitsu| Ueno, Tsuyoshi| Asano, Hiroaki| Tsukuda, Kazunori| Toyooka, Shinichi| Miyoshi, Shinichiro| |
| Abstract | Nuclear factor of κ-light polypeptide gene enhancer in B cells inhibitor α (NFKBIA), which is a tumor suppressor gene, was found to be silenced in lung adenocarcinomas. We examined NFKBIA expression, mutations in the EGFR and K-ras genes, and EML4-ALK fusion in 101 resected lung adenocarcinoma samples from never-smokers. NFKBIA expression was evaluated using immunohistochemistry. NFKBIA expression was negative in 16 of the 101 samples (15.8%). EGFR and K-ras mutations and EML4-ALK fusion were detected in 61 (60.5%), 1 (1.0%), and 2 (2.0%) of the 101 samples, respectively, in a completely mutually exclusive manner. Negative NFKBIA expression was observed significantly more frequently among the tumors with none of the three genetic alterations compared to those with such alterations (p＝0.009). In addition, negative NFKBIA expression was significantly more frequent among the EGFR-wild type samples compared to the EGFR-mutant samples (p＝0.013). In conclusion, NFKBIA expression was silenced in adenocarcinomas without EGFR/K-ras mutations or EML4-ALK fusion, suggesting that the silencing of NFKBIA may play an important role in the carcinogenesis of adenocarcinomas independent of EGFR/K-ras mutations or EML4-ALK fusion. |
| Keywords | never-smoker lung cancer adenocarcinoma nuclear factor of κ-light polypeptide gene enhancer in B cells inhibitor α epidermal growth factor receptor |
| Amo Type | Original Article |
| Published Date | 2013-02 |
| Publication Title | Acta Medica Okayama |
| Volume | volume67 |
| Issue | issue1 |
| Publisher | Okayama University Medical School |
| Start Page | 19 |
| End Page | 24 |
| ISSN | 0386-300X |
| NCID | AA00508441 |
| Content Type | Journal Article |
| language | 英語 |
| Copyright Holders | CopyrightⒸ 2013 by Okayama University Medical School |
| File Version | publisher |
| Refereed | True |
| PubMed ID | 23439505 |
| Web of Sience KeyUT | 000316829900003 |
| Related Url | http://ousar.lib.okayama-u.ac.jp/metadata/52534 |
| 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 |
| Published Date | 2016-08 |
| Publication Title | Acta Medica Okayama |
| 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 | 英語 |
| Copyright Holders | CopyrightⒸ 2016 by Okayama University Medical School |
| File Version | publisher |
| Refereed | True |
| PubMed ID | 27549683 |
| Web of Sience KeyUT | 000384748600018 |
| JaLCDOI | 10.18926/AMO/54816 |
|---|---|
| FullText URL | 70_6_507.pdf |
| Author | Torigoe, Hidejiro| Toyooka, Shinichi| Yamamoto, Hiromasa| Soh, Junichi| Miyoshi, Shinichiro| |
| Abstract | We present the case of a 65-year-old Japanese man diagnosed with chronic empyema (without a bronchopleural fistula) that occurred 7 months after he underwent an extrapleural pneumonectomy for right malignant pleural mesothelioma (MPM). Following thoracic drainage and irrigation for 1 month, we performed surgery by a thoracoscopic approach, in light of his general condition. We performed debridement and removal of the Gore-Tex polytetrafluoroethylene (PTFE) patch that had been used for the reconstruction of the diaphragm and the pericardium. The empyema had not relapsed when he died from recurrence of the MPM at 4 months after the thoracoscopic surgery. This patientʼs case suggests that thoracoscopic debridement and patch removal can be a therapeutic option for not only early-stage (exudative or fibrinopurulent) empyema but also late-stage (organized and chronic) empyema without a bronchopleural fistula, particularly for patients in poor general condition. |
| Keywords | empyema chronic extrapleural pneumonectomy thoracoscopic debridement patch removal |
| Amo Type | Case Report |
| Published Date | 2016-12 |
| Publication Title | Acta Medica Okayama |
| Volume | volume70 |
| Issue | issue6 |
| Publisher | Okayama University Medical School |
| Start Page | 507 |
| End Page | 510 |
| ISSN | 0386-300X |
| NCID | AA00508441 |
| Content Type | Journal Article |
| language | 英語 |
| Copyright Holders | CopyrightⒸ 2016 by Okayama University Medical School |
| File Version | publisher |
| Refereed | True |
| PubMed ID | 28003678 |
| JaLCDOI | 10.18926/AMO/55210 |
|---|---|
| FullText URL | 71_3_259.pdf |
| Author | Kawana, Shinichi| Yamamoto, Hiromasa| Maki, Yuho| Sugimoto, Seiichiro| Toyooka, Shinichi| Miyoshi, Shinichiro| |
| Abstract | Primary sternal chondrosarcoma is a rare malignant tumor that is refractory to chemotherapy and radiation. Effective therapy is radical resection of the tumor. We present two patients with primary sternal chondrosarcoma who underwent a radical resection of the lower half of the sternum and bilateral ribs, followed by reconstruction with 2 sheets of polypropylene mesh layered orthogonally. The patients have maintained almost the same pulmonary function as preoperative values, with stability of the chest wall. Although there are various ways to reconstruct the anterior chest wall, reconstruction with polypropylene mesh layered orthogonally is an easy-to-use and sufficient method. |
| Keywords | chondrosarcoma sternum reconstruction polypropylene mesh |
| Amo Type | Case Report |
| Published Date | 2017-06 |
| Publication Title | Acta Medica Okayama |
| Volume | volume71 |
| Issue | issue3 |
| Publisher | Okayama University Medical School |
| Start Page | 259 |
| End Page | 262 |
| ISSN | 0386-300X |
| NCID | AA00508441 |
| Content Type | Journal Article |
| language | 英語 |
| Copyright Holders | CopyrightⒸ 2017 by Okayama University Medical School |
| File Version | publisher |
| Refereed | True |
| PubMed ID | 28655947 |
