JaLCDOI 10.18926/AMO/54978
FullText URL 71_2_105.pdf
Author Shinya, Takayoshi| Tanaka, Takashi| Soh, Junichi| Matsushita, Toshi| Sato, Shuhei| Toyooka, Shinichi| Yoshino, Tadashi| Miyoshi, Shinichiro| Kanazawa, Susumu|
Abstract We retrospectively assessed the dual-time-point (DTP) F-18 FDG PET/CT findings of thymic epithelial neoplasms (TENs) and investigated the diagnostic capacity of PET/CT compared to that of CT for predicting carcinoma. We calculated the ratio of the standardized uptake value of the tumor and that of the aortic arch (T/M ratio) for both the 90-min early scan and the 2-h delayed scan in 56 TEN patients. We used a multivariate logistic regression (MLR) analysis to estimate the CT features of carcinoma. We compared the diagnostic capacities of PET/CT and chest CT using receiver operating characteristic (ROC) analyses. The ROC curve revealed that the appropriate cut-off T/M ratio value for the highest accuracy was 2.39 with 75.0% accuracy. The area under the curve (AUC) was 0.855. The statistical analyses for DTP scans of 35 TEN patients demonstrated 74.3% accuracy and 0.838 AUC for the early scan versus 82.9% and 0.825 for the delayed scan. The MLR analysis indicated that mediastinal fat infiltration was a predictor of carcinoma. The ROC curve obtained for the model yielded an AUC of 0.853. Delayed scanning could improve the diagnostic capacity for carcinoma. The T/M ratio and mediastinal fat infiltration are predictive of carcinoma with moderate diagnostic accuracy.
Keywords thymic epithelial neoplasm thymic carcinoma thymoma dual-time-point PET/CT chest CT
Amo Type Original Article
Published Date 2017-04
Publication Title Acta Medica Okayama
Volume volume71
Issue issue2
Publisher Okayama University Medical School
Start Page 105
End Page 112
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 28420891
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/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/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
Author Hayashi, Tatsuro| Asano, Hiroaki| Toyooka, Shinichi| Tsukuda, Kazunori| Soh, Junichi| Shien, Tadahiko| Taira, Naruto| Maki, Yuho| Tanaka, Norimitsu| Doihara, Hiroyoshi| Nasu, Yasutomo| Huh, Nam-ho| Miyoshi, Shinichiro|
Published Date 2012-05
Publication Title Journal of Cancer Research and Clinical Oncology
Volume volume138
Issue issue5
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
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
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 Ueno, Tsuyoshi| Tsukuda, Kazunori| Toyooka, Shinichi| Ando, Midori| Takaoka, Munenori| Soh, Junichi| Asano, Hiroaki| Maki, Yuho| Muraoka, Takayuki| Tanaka, Norimitsu| Shien, Kazuhiko| Furukawa, Masashi| Yamatsuji, Tomoki| Kiura, Katsuyuki| Naomoto, Yoshio| Miyoshi, Shinichiro|
Published Date 2012-04
Publication Title Lung Cancer
Volume volume76
Issue issue1
Content Type Journal Article
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 Shien, Kazuhiko| Toyooka, Shinichi| Ichimura, Kouichi| Soh, Junichi| Furukawa, Masashi| Maki, Yuho| Muraoka, Takayuki| Tanaka, Norimitsu| Ueno, Tsuyoshi| Asano, Hiroaki| Tsukuda, Kazunori| Yamane, Masaomi| Oto, Takahiro| Kiura, Katsuyuki| Miyoshi, Shinichiro|
Published Date 2012-07
Publication Title Lung Cancer
Volume volume77
Issue issue1
Content Type Journal Article
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/48691
FullText URL 66_4_357.pdf
Author Shien, Kazuhiko| Shien, Tadahiko| Soh, Junichi| Ikeda, Hirokuni| Nogami, Tomohiro| Taira, Naruto| Doihara, Hiroyoshi| Miyoshi, Shinichiro|
Abstract Ectopic thymoma is considered to arise from ectopic thymus tissue deposited as a result of the abnormal mislocalization of thymus tissue during the embryonic stage. An 86-year-old man visited our hospital with chief complaints of hoarseness and a mass in his anterior neck. A preoperative needle biopsy of the mass did not yield a definitive diagnosis. A positron emission tomography (PET) study revealed heterogeneous accumulation of <sup>18</sup>F-fluorodeoxyglucose (FDG) in the tumor. The tumor, affecting the left sternocleidomastoid muscle, the recurrent laryngeal nerve, the internal carotid vein, and the brachiocephalic vein, was resected using a combination of a collar incision in the neck and a median incision in the sternum. Immunohistochemically, the tumor was diagnosed as an ectopic thymoma of the neck. To date, only a few cases of ectopic thymoma presenting with FDG accumulation have been reported. Our experience indicates that ectopic thymoma should be kept in mind during the differential diagnosis of neck tumors with FDG accumulation appearing on PET images.
Keywords ectopic thymoma thyroid tumor positron emission tomography (PET)
Amo Type Case Report
Published Date 2012-08
Publication Title Acta Medica Okayama
Volume volume66
Issue issue4
Publisher Okayama University Medical School
Start Page 357
End Page 361
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
Copyright Holders CopyrightⒸ 2012 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 22918209
JaLCDOI 10.18926/AMO/46629
FullText URL 65_3_179.pdf
Author Teramen, Hirotake| Tsukuda, Kazunori| Tanaka, Norimitsu| Ueno, Tsuyoshi| Kubo, Takafumi| Ando, Midori| Soh, Junichi| Asano, Hiroaki| Pass, Harvery I.| Toyooka, Shinichi| Miyoshi, Shinichiro|
Abstract Suppression of p21 has been implicated in the genesis and progression of many human malignancies. DNA methylation is an important mechanism of gene silencing in human malignancies. In this study, we examined the expression status and aberrant methylaion of p21 in lung cancers and malignant pleural mesotheliomas (MPM). We used 12 small cell lung cancer (SCLC) cell lines, 13 non-small cell lung cancer (NSCLC) cell lines, 50 primary NSCLCs, 6 MPM cell lines and 10 primary MPMs. The expression and methylation of p21 was examined by reverse transcription-PCR (RT-PCR), Western blotting and methylation-specific PCR (MSP) assay. Loss of p21 protein expression was observed in 7 SCLC cell lines (58.3%), 5 NSCLC cell lines (38.5%) and 3 MPM cell lines (50%) while mRNA expression was lost in 2 SCLC cell lines (16.7%), 2 NSCLC cell lines (15.4%) and none of the MPM cell lines. Aberrant methylation of p21 was found in 8.3% of SCLC cell lines, 30.2% of NSCLCs and 6.3% of MPMs. Among primary NSCLCs, methylation in adenocarcinomas was significantly more frequent than in squamous cell carcinomas. Loss of p21 expression was frequently observed in lung cancers and MPMs and aberrant methylation was one of the mechanisms of suppression of p21, especially in NSCLCs.
Keywords p21 methylation lung cancer mesothelioma
Amo Type Original Article
Published Date 2011-06
Publication Title Acta Medica Okayama
Volume volume65
Issue issue3
Publisher Okayama University Medical School
Start Page 179
End Page 184
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
Copyright Holders CopyrightⒸ 2011 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 21709715
Web of Sience KeyUT 000292017500004
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 So, Jun-ichi|
Published Date 2007-03-23
Publication Title
Content Type Thesis or Dissertation