JaLCDOI 10.18926/AMO/56934
FullText URL 73_4_325.pdf
Author Ueno, Tsuyoshi| Maki, Yuho| Sugimoto, Ryujiro| Suehisa, Hiroshi| Yamashita, Motohiro| Harada, Daijiro| Kozuki, Toshiyuki| Nogami, Naoyuki|
Abstract Therapeutic approaches to bronchopleural fistula (BPF) closure after lung resection are surgical or endoscopic interventions. We evaluated therapeutic outcomes to determine the optimal approach. We reviewed 15 patients who had developed BPF after lung resection for thoracic malignant diseases at our institution in the 10 years since 2008. The patients were 11 men and 4 women (mean age 68 years). We performed one pneumonectomy, 6 lobectomies, 7 segmentectomies, and one partial resection for malignant diseases. The median interval from lung resection to the BPF diagnosis was 46 days. The BPF-associated mortality rate was 26.7% (4/15). The rate of successful BPF closure was 66.6% (10/15). The endoscopic and surgical intervention success rates were 14.2% (1/7) and 69.2% (9/13), respectively (p<0.01). Of 5 patients who had failed BPF treatments, 4 died, and one transferred out without BPF closure. The therapeutic outcomes were related to preoperative comorbidities, performance status at the BPF diagnosis, time intervals from lung resection to BPF diagnosis, and presence of active pneumonia. The difference between endoscopic and surgical outcomes was nonsignificant, although the surgical intervention success rate was somewhat higher. The selection of endoscopic or surgical intervention for BPF does not significantly affect therapeutic outcomes.
Keywords bronchopleural fistula endoscopic intervention surgical intervention
Amo Type Original Article
Published Date 2019-08
Publication Title Acta Medica Okayama
Volume volume73
Issue issue4
Publisher Okayama University Medical School
Start Page 325
End Page 331
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
Copyright Holders CopyrightⒸ 2019 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 31439955
JaLCDOI 10.18926/AMO/55588
FullText URL 71_6_513.pdf
Author Sawada, Shigeki| Sugimoto, Ryujiro| Ueno, Tsuyoshi| Yamashita, Motohiro|
Abstract We evaluated the feasibility of maintenance treatment using UFT (a combination of tegafur and uracil) after adjuvant platinum-based chemotherapy in patients with resected lung cancer. A prospective feasibility trial was conducted. Between 2010 and 2014, UFT was administered for 2 years sequentially after platinum-based adjuvant chemotherapy in 24 patients with resected Stage IIA-IIIA non-small cell lung cancer. The safety of UFT and the rate of treatment completion were then evaluated. The prior platinum-based chemotherapy regimens consisted of cisplatin+vinorelbine in 16 patients, carboplatin+paclitaxel in 5 and carboplatin+S-1 in one. During the subsequent UFT administration, a total of 3 patients required a dose reduction because of Grade 1 blood-stained sputum, Grade 2 numbness, and Grade 2 constipation, in one patient each. Eleven patients underwent the planned 2-year UFT administration, but 12 patients could not because of the recurrence of lung cancer in 5 patients, metachronous malignancy in one, and toxicities in 6. The completion rate for UFT administration was 64.7% (11/17). The most common type of toxicity was gastrointestinal toxicities. All of the toxicities were grade 1 or 2, and no severe toxicities were observed. UFT treatment after platinum-based chemotherapy was revealed to be feasible.
Keywords UFT adjuvant chemotherapy lung cancer resection
Amo Type Original Article
Published Date 2017-12
Publication Title Acta Medica Okayama
Volume volume71
Issue issue6
Publisher Okayama University Medical School
Start Page 513
End Page 518
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 29276224
JaLCDOI 10.18926/AMO/54417
FullText URL 70_3_183.pdf
Author Sawada, Shigeki| Hiroshi, Suehisa| Ueno, Tsuyoshi| Yamashita, Motohiro|
Abstract We reviewed post-operative complication and mortality rates from 1995 through 2014 and evaluated the changes in those rates across that 20-year period. Two thousand and three hundred sixteen patients with lung cancer underwent resection at our institution between 1995 and 2014. This timespan was divided into four 5-year periods. Each patientʼs age, Charlson comorbidity index score, and extent of surgery in each 5-year period were summarized, and the changes in these factors over the 20-year span were evaluated. The complication and mortality rates were calculated for each 5-year period, and the changes in those rates over the 20-years were evaluated. The number of patients with higher Charlson comorbidity index scores increased during the 20-year period. Of the 455 patients who developed complications, 97 developed life-threating complications. There were 16 post-operative deaths and 23 in-hospital deaths. There were no significant changes in the complication rate or mortality rate during the 20-year period. Both rates were significantly correlated with the extent of resection. Although the number of patients with comorbidities increased in the 20-year period, the post-operative complication and mortality rates, as well as in-hospital mortality, did not change significantly.
Keywords post-operative complication post-operative mortality lung cancer surgery outcomes
Amo Type Original Article
Published Date 2016-06
Publication Title Acta Medica Okayama
Volume volume70
Issue issue3
Publisher Okayama University Medical School
Start Page 183
End Page 188
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 27339207
Web of Sience KeyUT 000379406100005
JaLCDOI 10.18926/AMO/53911
FullText URL 69_6_361.pdf
Author Suehisa, Hiroshi| Ueno, Tsuyoshi| Sawada, Shigeki| Yamashita, Motohiro| Teramoto, Norihiro|
Abstract A 35-year-old Japanese manʼs routine chest radiography revealed an abnormal opacity. Chest computed tomography and magnetic resonance imaging showed a 5.5cm in dia. cystic tumor located at the left anterior mediastinum. The tumor was suspected to be an asymptomatic thymic cyst, and we chose observation for the tumor. At the 3-year follow up, the cystic tumor had gradually enlarged to 7.5cm in dia. and we thus performed a surgical resection via left video-assisted thoracic surgery. An immunohistochemical analysis showed that the cystic tumor was not a thymic cyst but rather a mediastinal cystic lymphangioma. Mediastinal cystic lymphangiomas are very rare, and they are difficult to diagnose preoperatively. Complete surgical resection is proposed for the treatment of such tumors.
Keywords mediastinal tumor mediastinal cystic lymphangioma thymic cyst
Amo Type Case Reports
Published Date 2015-12
Publication Title Acta Medica Okayama
Volume volume69
Issue issue6
Publisher Okayama University Medical School
Start Page 361
End Page 363
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
Copyright Holders CopyrightⒸ 2015 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 26690247
Web of Sience KeyUT 000368434500006
JaLCDOI 10.18926/AMO/53124
FullText URL 69_1_65.pdf
Author Ueno, Tsuyoshi| Yamashita, Motohiro| Sawada, Shigeki| Suehisa, Hiroshi| Kawamoto, Hiroaki| Takahata, Hiroyuki|
Abstract Inflammatory myofibroblastic tumor (IMT) is a rare neoplasm that occurs at different sites in the body. Pleural IMT in particular is especially rare. IMTs infrequently tend to have malignancy. We report a rare case of advanced diaphragmatic parietal pleural IMT with dissemination. A 30-year-old woman complained of right upper abdominal pain. Computed tomography showed a large lobulated mass over the right diaphragm, but no disseminated nodules were noted. Intraoperatively, we found the primary tumor arising from the diaphragmatic parietal pleura and a dozen disseminated nodules, and we removed them completely. The histopathological and immunohistochemical diagnosis was IMT.
Keywords inflammatory myofibroblastic tumor pleura dissemination
Amo Type Case Report
Published Date 2015-02
Publication Title Acta Medica Okayama
Volume volume69
Issue issue1
Publisher Okayama University Medical School
Start Page 65
End Page 68
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
Copyright Holders CopyrightⒸ 2015 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 25703173
Web of Sience KeyUT 000349740300008
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 Science KeyUT 000331592800004
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 Science KeyUT 000316829900003
Related Url http://ousar.lib.okayama-u.ac.jp/metadata/52534
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 Science KeyUT 000292017500004