Author Miyoshi, Shinichiro|
Published Date 2009-12-01
Publication Title 岡山医学会雑誌
Volume volume121
Issue issue3
Content Type Journal Article
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
JaLCDOI 10.18926/AMO/46852
FullText URL 65_4_265.pdf
Author Kojima, Katsuhide| Kato, Katsuya| Oto, Takahiro| Mitsuhashi, Toshiharu| Shinya, Takayoshi| Sei, Tetsuro| Okumura, Yoshihiro| Sato, Shuhei| Miyoshi, Shinichiro| Kanazawa, Susumu|
Abstract To determine the effectiveness of living-donor lobar lung transplantation (LDLLT), it is necessary to predict the recipient's postoperative lung function. Traditionally, Date's formula, also called the segmental ratio, has used the number of lung segments to estimate the forced vital capacity (FVC) of grafts in LDLLT. To provide a more precise estimate of graft FVC, we calculated the volumes of the lower lobe and total lung using three-dimensional computed tomography (3D-CT) and the volume ratio between them. We calculated the volume ratio in 52 donors and tested the difference between the segmental volume ratios with a one-tailed t-test. We also calculated the predicted graft FVC in 21 LDLLTs using the segmental ratio pFVC(c) and the volume ratio pFVC(v), and then found the Pearson's correlation coefficients for both pFVC(c) and pFVC(v) with the recipients' actual FVC (rFVC) measured spirometrically 6 months after surgery. Significant differences were found between the segmental ratio and the average volume ratio for both sides (right, p=0.03;left, p=0.0003). Both pFVC(c) and pFVC(v) correlated significantly with rFVC at 6 months after surgery (p=0.007 and 0.006). Both the conventional and the volumetric methods provided FVC predictions that correlated significantly with measured postoperative FVC.
Keywords living-donor lobar lung transplantation 3D-CT volumetry
Amo Type Original Article
Published Date 2011-08
Publication Title Acta Medica Okayama
Volume volume65
Issue issue4
Publisher Okayama University Medical School
Start Page 265
End Page 268
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 21860533
Web of Sience KeyUT 000294236700007
Author Miyoshi, Kentaroh| Oto, Takahiro| Otani, Shinji| Tanaka, Shin| Harada, Masaaki| Kakishita, Tomokazu| Hori, Shiro| Waki, Naohisa| Yamane, Masaomi| Miyoshi, Shinichiro|
Published Date 2011-12-01
Publication Title 岡山医学会雑誌
Volume volume123
Issue issue3
Content Type Journal Article
Author Yamamoto, Sumiharu| Okazaki, Mikio| Yamane, Masaomi| Miyoshi, Kentaro| Otani, Shinji| Kakishita, Tomokazu| Yoshida, Osamu| Waki, Naohisa| Toyooka, Shinichi| Oto, Takahiro| Sano, Yoshifumi| Miyoshi, Shinichiro|
Published Date 2012-03
Publication Title Transplant Immunology
Volume volume26
Issue issue2-3
Content Type Journal Article
Author Nogami, Tomohiro| Shien, Tadahiko| Tanaka, Takehiro| Nishiyama, Keiko| Mizoo, Taeko| Iwamto, Takayuki| Ikeda, Hirokuni| Taira, Naruto| Doihara, Hiroyoshi| Miyoshi, Shinichiro|
Published Date 2012-03-10
Publication Title Breast Cancer
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 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 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
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/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
Author Kubo, Takafumi| Toyooka, Shinichi| Miyoshi, Shinichiro|
Published Date 2012-12-03
Publication Title 岡山医学会雑誌
Volume volume124
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
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/49669
FullText URL 67_2_105.pdf
Author Alafate, Aierken| Shinya, Takayoshi| Okumura, Yoshihiro| Sato, Shuhei| Hiraki, Takao| Ishii, Hiroaki| Gobara, Hideo| Kato, Katsuya| Fujiwara, Toshiyoshi| Miyoshi, Shinichiro| Kaji, Mitsumasa| Kanazawa, Susumu|
Abstract We retrospectively evaluated the accumulation of fluorodeoxy glucose (FDG) in pulmonary malignancies without local recurrence during 2-year follow-up on positron emission tomography (PET)/computed tomography (CT) after radiofrequency ablation (RFA). Thirty tumors in 25 patients were studied (10 non-small cell lung cancers;20 pulmonary metastatic tumors). PET/CT was performed before RFA, 3 months after RFA, and 6 months after RFA. We assessed the FDG accumulation with the maximum standardized uptake value (SUVmax) compared with the diameters of the lesions. The SUVmax had a decreasing tendency in the first 6 months and, at 6 months post-ablation, FDG accumulation was less affected by inflammatory changes than at 3 months post-RFA. The diameter of the ablated lesion exceeded that of the initial tumor at 3 months post-RFA and shrank to pre-ablation dimensions by 6 months post-RFA. SUVmax was more reliable than the size measurements by CT in the first 6 months after RFA, and PET/CT at 6 months post-RFA may be more appropriate for the assessment of FDG accumulation than that at 3 months post-RFA.
Keywords fluorodeoxy glucose (FDG) positron emission tomography (PET) standardized uptake value (SUV) radiofrequency ablation (RFA) non-small cell lung cancer (NSCLC)
Amo Type Original Article
Published Date 2013-04
Publication Title Acta Medica Okayama
Volume volume67
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Ⓒ 2013 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 23603927
Web of Sience KeyUT 000317801700005
Related Url http://ousar.lib.okayama-u.ac.jp/metadata/50688
Author Nishikawa, Hitoshi| Oto, Takahiro| Otani, Shinji| Harada, Masaaki| Iga, Norichika| Miyoshi, Kentaroh| Miyoshi, Shinichiro|
Published Date 2013-12
Publication Title The Journal of Thoracic and Cardiovascular Surgery
Volume volume146
Issue issue6
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
Author Mizoo, Taeko| Taira, Naruto| Nishiyama, Keiko| Nogami, Tomohiro| Iwamoto, Takayuki| Motoki, Takayuki| Shien, Tadahiko| Matsuoka, Junji| Doihara, Hiroyoshi| Ishihara, Setsuko| Kawai, Hiroshi| Kawasaki, Kensuke| Ishibe, Youichi| Ogasawara, Yutaka| Komoike, Yoshifumi| Miyoshi, Shinichiro|
Published Date 2013-12-01
Publication Title BMC Cancer
Volume volume13
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