start-ver=1.4
cd-journal=joma
no-vol=128
cd-vols=
no-issue=2
article-no=
start-page=117
end-page=120
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2016
dt-pub=20160801
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Incisional hernia repair after wide excision of the iliac bone
kn-title=腸骨広範囲切除術後に発生した腹壁瘢痕ヘルニアに対しメッシュ修復術を行った一例
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract= The patient was a 46-year old Japanese female who had undergone wide excision of the iliac bone and hip transposition at our institute's orthopedics department 2 years earlier. She presented with a growing incisional hernia and was transferred to our gastroenterological surgery department for surgical treatment. We planned a mesh repair for the incisional hernia, which protruded over the right iliac bone. The dimensions of the abdominal defect were 15×9 cm, and we used prolene mesh to repair the defect. The mesh was fixed at the inner part of the iliac bone, folded back at the iliac horn and fixed to the abdominal oblique muscles. The postoperative course was smooth, and recurrence was not seen at 3.5 years after the operation. An incisional hernia as seen in this patient's case is very rare, but we found that the underlay technique and prolene mesh were very useful for the three-dimensional hernia repair.
en-copyright=
kn-copyright=
en-aut-name=TsukudaKazunori
en-aut-sei=Tsukuda
en-aut-mei=Kazunori
kn-aut-name=佃和憲
kn-aut-sei=佃
kn-aut-mei=和憲
aut-affil-num=1
ORCID=
en-aut-name=AsanoHiroaki
en-aut-sei=Asano
en-aut-mei=Hiroaki
kn-aut-name=浅野博昭
kn-aut-sei=浅野
kn-aut-mei=博昭
aut-affil-num=2
ORCID=
en-aut-name=MandaiYasuhiro
en-aut-sei=Mandai
en-aut-mei=Yasuhiro
kn-aut-name=万代康弘
kn-aut-sei=万代
kn-aut-mei=康弘
aut-affil-num=3
ORCID=
en-aut-name=FujiwaraToshiyoshi
en-aut-sei=Fujiwara
en-aut-mei=Toshiyoshi
kn-aut-name=藤原俊義
kn-aut-sei=藤原
kn-aut-mei=俊義
aut-affil-num=4
ORCID=
affil-num=1
en-affil=Minimally Invasive Therapy Center, Okayama University Hospital
kn-affil=岡山大学病院 低侵襲治療センター
affil-num=2
en-affil=Minimally Invasive Therapy Center, Okayama University Hospital
kn-affil=岡山大学病院 低侵襲治療センター
affil-num=3
en-affil=Center of the Development and Health Care Education, Okayama University
kn-affil=岡山大学医療教育統合開発センター
affil-num=4
en-affil=Department of Gastrointestinal Sugery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=岡山大学大学院医歯薬総合研究科 消化器外科学
en-keyword=腹壁瘢痕ヘルニア（incisional hernia）
kn-keyword=腹壁瘢痕ヘルニア（incisional hernia）
en-keyword=腸骨軟骨肉腫（chondrosarcoma of the iliac bone）
kn-keyword=腸骨軟骨肉腫（chondrosarcoma of the iliac bone）
en-keyword=腸骨広範囲切除術（wide excision of the iliac bone）
kn-keyword=腸骨広範囲切除術（wide excision of the iliac bone）
en-keyword=プロリーンメッシュ（prolene mesh）
kn-keyword=プロリーンメッシュ（prolene mesh）
END
start-ver=1.4
cd-journal=joma
no-vol=138
cd-vols=
no-issue=5
article-no=
start-page=799
end-page=809
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2012
dt-pub=201205
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=DNA methylation status of REIC/Dkk-3 gene in human malignancies
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The REIC (reduced expression in immortalized cells)/Dkk-3 is down-regulated in various cancers and considered to be a tumor suppressor gene. REIC/Dkk-3 mRNA has two isoforms (type-a,b). REIC type-a mRNA has shown to be a major transcript in various cancer cells, and its promoter activity was much stronger than that of type-b. In this study, we examined the methylation status of REIC/Dkk-3 type-a in a broad range of human malignancies.
We examined REIC/Dkk-3 type-a methylation in breast cancers, non-small-cell lung cancers, gastric cancers, colorectal cancers, and malignant pleural mesotheliomas using a quantitative combined bisulfite restriction analysis assay and bisulfate sequencing. REIC/Dkk-3 type-a and type-b expression was examined using reverse transcriptional PCR. The relationships between the methylation and clinicopathological factors were analyzed.
The rate of REIC/Dkk-3 type-a methylation ranged from 26.2 to 50.0% in the various primary tumors that were examined. REIC/Dkk-3 type-a methylation in breast cancer cells was significantly heavier than that in the other cell lines that we tested. REIC/Dkk-3 type-a methylation was inversely correlated with REIC/Dkk-3 type-a expression. There was a correlation between REIC/Dkk-3 type-a and type-b mRNA expression. REIC/Dkk-3 type-a expression was restored in MDA-MB-231 cells using 5-aza-2'-deoxycytidine treatment. We found that estrogen receptor-positive breast cancers were significantly more common among the methylated group than among the non-methylated group.
REIC/Dkk-3 type-a methylation was frequently detected in a broad range of cancers and appeared to play a key role in silencing REIC/Dkk-3 type-a expression in these malignancies.
en-copyright=
kn-copyright=
en-aut-name=HayashiTatsuro
en-aut-sei=Hayashi
en-aut-mei=Tatsuro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=AsanoHiroaki
en-aut-sei=Asano
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=ToyookaShinichi
en-aut-sei=Toyooka
en-aut-mei=Shinichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=TsukudaKazunori
en-aut-sei=Tsukuda
en-aut-mei=Kazunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=SohJunichi
en-aut-sei=Soh
en-aut-mei=Junichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=ShienTadahiko
en-aut-sei=Shien
en-aut-mei=Tadahiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
en-aut-name=TairaNaruto
en-aut-sei=Taira
en-aut-mei=Naruto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=
en-aut-name=MakiYuho
en-aut-sei=Maki
en-aut-mei=Yuho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
en-aut-name=TanakaNorimitsu
en-aut-sei=Tanaka
en-aut-mei=Norimitsu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=
en-aut-name=DoiharaHiroyoshi
en-aut-sei=Doihara
en-aut-mei=Hiroyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=
en-aut-name=NasuYasutomo
en-aut-sei=Nasu
en-aut-mei=Yasutomo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=
en-aut-name=HuhNam-ho
en-aut-sei=Huh
en-aut-mei=Nam-ho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=
en-aut-name=MiyoshiShinichiro
en-aut-sei=Miyoshi
en-aut-mei=Shinichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=
affil-num=1
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Canc & Thorac Surg
affil-num=2
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Canc & Thorac Surg
affil-num=3
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Canc & Thorac Surg
affil-num=4
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Canc & Thorac Surg
affil-num=5
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Canc & Thorac Surg
affil-num=6
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Canc & Thorac Surg
affil-num=7
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Canc & Thorac Surg
affil-num=8
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Canc & Thorac Surg
affil-num=9
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Canc & Thorac Surg
affil-num=10
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Canc & Thorac Surg
affil-num=11
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Urol
affil-num=12
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Cell Biol
affil-num=13
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Canc & Thorac Surg
en-keyword=DNA methylation
kn-keyword=DNA methylation
en-keyword=REIC/Dkk-3
kn-keyword=REIC/Dkk-3
en-keyword=Breast cancer
kn-keyword=Breast cancer
en-keyword=Lung cancer
kn-keyword=Lung cancer
en-keyword=Mesothelioma
kn-keyword=Mesothelioma
END
start-ver=1.4
cd-journal=joma
no-vol=68
cd-vols=
no-issue=1
article-no=
start-page=23
end-page=26
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2014
dt-pub=201402
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Preclinical Evaluation of MicroRNA-34b/c Delivery for Malignant Pleural Mesothelioma
en-subtitle=
kn-subtitle=
en-abstract=
kn-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.
en-copyright=
kn-copyright=
en-aut-name=UenoTsuyoshi
en-aut-sei=Ueno
en-aut-mei=Tsuyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=ToyookaShinichi
en-aut-sei=Toyooka
en-aut-mei=Shinichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=FukazawaTakuya
en-aut-sei=Fukazawa
en-aut-mei=Takuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=KuboTakafumi
en-aut-sei=Kubo
en-aut-mei=Takafumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=SohJunichi
en-aut-sei=Soh
en-aut-mei=Junichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=AsanoHiroaki
en-aut-sei=Asano
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
en-aut-name=MuraokaTakayuki
en-aut-sei=Muraoka
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=
en-aut-name=TanakaNorimitsu
en-aut-sei=Tanaka
en-aut-mei=Norimitsu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
en-aut-name=MakiYuho
en-aut-sei=Maki
en-aut-mei=Yuho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=
en-aut-name=ShienKazuhiko
en-aut-sei=Shien
en-aut-mei=Kazuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=
en-aut-name=FurukawaMasashi
en-aut-sei=Furukawa
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=
en-aut-name=SakaguchiMasakiyo
en-aut-sei=Sakaguchi
en-aut-mei=Masakiyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=
en-aut-name=YamamotoHiromasa
en-aut-sei=Yamamoto
en-aut-mei=Hiromasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=
en-aut-name=TsukudaKazunori
en-aut-sei=Tsukuda
en-aut-mei=Kazunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=
en-aut-name=MiyoshiShinichiro
en-aut-sei=Miyoshi
en-aut-mei=Shinichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=
affil-num=1
en-affil=
kn-affil=Department of Thoracic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
affil-num=2
en-affil=
kn-affil=Department of Thoracic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
affil-num=3
en-affil=
kn-affil=Department of General Surgery, Kawasaki Medical School
affil-num=4
en-affil=
kn-affil=Department of Thoracic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
affil-num=5
en-affil=
kn-affil=Department of Thoracic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
affil-num=6
en-affil=
kn-affil=Department of Thoracic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
affil-num=7
en-affil=
kn-affil=Department of Thoracic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
affil-num=8
en-affil=
kn-affil=Department of Thoracic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
affil-num=9
en-affil=
kn-affil=Department of Thoracic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
affil-num=10
en-affil=
kn-affil=Department of Thoracic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
affil-num=11
en-affil=
kn-affil=Department of Thoracic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
affil-num=12
en-affil=
kn-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
affil-num=13
en-affil=
kn-affil=Department of Thoracic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
affil-num=14
en-affil=
kn-affil=Department of Thoracic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
affil-num=15
en-affil=
kn-affil=Department of Thoracic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
en-keyword=mesothelioma
kn-keyword=mesothelioma
en-keyword=microRNA
kn-keyword=microRNA
en-keyword=microRNA-34b/c
kn-keyword=microRNA-34b/c
en-keyword=p53
kn-keyword=p53
END
start-ver=1.4
cd-journal=joma
no-vol=82
cd-vols=
no-issue=3
article-no=
start-page=485
end-page=490
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2013
dt-pub=201312
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The degree of microRNA-34b/c methylation in serum-circulating DNA is associated with malignant pleural mesothelioma
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Objectives: Malignant pleural mesothelioma (MPM) is an aggressive tumor with a poor prognosis. microRNA-34b/c (miR-34b/c), which plays an important role in the pathogenesis of MPM, is frequently downregulated by DNA methylation in approximately 90% of MPM cases. In this study, we estimated the degree of miR-34b/c methylation in serum-circulating DNA using a digital methylation specific PCR assay (MSP).
Materials and methods: A real-time MSP assay was performed using the SYBR Green method. The melting temperature (Tm) of each PCR product was examined using a melting curve analysis. For a digital MSP assay, 40 wells were analyzed per sample. A total of 110 serum samples from 48 MPM cases, 21 benign asbestos pleurisy (BAP) cases, and 41 healthy volunteers (HVs) were examined.
Results: Positive range of Tm value for miR-34b/c methylation was defined as 77.71-78.79 degrees C which was the mean 3 standard deviations of 40 wells of a positive control. The number of miR-34b/c methylated wells was counted per sample according to this criterion. The number of miR-34b/c methylated wells in MPM cases was significantly higher than that in BAP cases (P = 0.03) or HVs (P < 0.001). Advanced MPM cases tended to have higher number of miR-34b/c methylated wells than early MPM cases. Receiver-operating characteristic (ROC) curve analysis revealed that three number of miR-34b/c methylated wells per sample was the best cut-off of positivity of MPM with a 67% of sensitivity and a 77% specificity for prediction. The area under the ROC curve was 0.77.
Conclusions: Our digital MSP assay can quantify miR-34b/c methylation in serum-circulating DNA. The degree of miR-34b/c methylation in serum-circulating DNA is associated with MPM, suggesting that this approach might be useful for the establishment of a new detection system for MPM.
en-copyright=
kn-copyright=
en-aut-name=MuraokaTakayuki
en-aut-sei=Muraoka
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=SohJunichi
en-aut-sei=Soh
en-aut-mei=Junichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=ToyookaShinichi
en-aut-sei=Toyooka
en-aut-mei=Shinichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=AoeKeisuke
en-aut-sei=Aoe
en-aut-mei=Keisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=FujimotoNobukazu
en-aut-sei=Fujimoto
en-aut-mei=Nobukazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=HashidaShinsuke
en-aut-sei=Hashida
en-aut-mei=Shinsuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
en-aut-name=MakiYuho
en-aut-sei=Maki
en-aut-mei=Yuho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=
en-aut-name=TanakaNorimitsu
en-aut-sei=Tanaka
en-aut-mei=Norimitsu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
en-aut-name=ShienKazuhiko
en-aut-sei=Shien
en-aut-mei=Kazuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=
en-aut-name=FurukawaMasashi
en-aut-sei=Furukawa
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=
en-aut-name=YamamotoHiromasa
en-aut-sei=Yamamoto
en-aut-mei=Hiromasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=
en-aut-name=AsanoHiroaki
en-aut-sei=Asano
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=
en-aut-name=TsukudaKazunori
en-aut-sei=Tsukuda
en-aut-mei=Kazunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=
en-aut-name=KishimotoTakumi
en-aut-sei=Kishimoto
en-aut-mei=Takumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=
en-aut-name=OtsukiTakemi
en-aut-sei=Otsuki
en-aut-mei=Takemi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=
en-aut-name=MiyoshiShinichiro
en-aut-sei=Miyoshi
en-aut-mei=Shinichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=
affil-num=1
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Thorac Surg
affil-num=2
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Thorac Surg
affil-num=3
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Thorac SurgPathol
affil-num=4
en-affil=
kn-affil=Yamaguchi Ube Med Ctr, Natl Hosp Org, Dept Med Oncol & Clin Res
affil-num=5
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Canc & Thorac Surg
affil-num=6
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Thorac Surg
affil-num=7
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Thorac Surg
affil-num=8
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Thorac Surg
affil-num=9
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Thorac Surg
affil-num=10
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Thorac Surg
affil-num=11
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Thorac Surg
affil-num=12
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Thorac Surg
affil-num=13
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Thorac Surg
affil-num=14
en-affil=
kn-affil=Okayama Rosai Hosp, Dept Resp Med
affil-num=15
en-affil=
kn-affil=Kawasaki Med Univ, Dept Hyg
affil-num=16
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Thorac Surg
en-keyword=Digital PCR
kn-keyword=Digital PCR
en-keyword=Malignant pleural mesothelioma
kn-keyword=Malignant pleural mesothelioma
en-keyword=microRNA
kn-keyword=microRNA
en-keyword=miR-34b/c
kn-keyword=miR-34b/c
en-keyword=Methylation
kn-keyword=Methylation
en-keyword=Circulating DNA
kn-keyword=Circulating DNA
END
start-ver=1.4
cd-journal=joma
no-vol=29
cd-vols=
no-issue=1
article-no=
start-page=133
end-page=140
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2013
dt-pub=201301
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Impact of GLUT1 and Ki-67 expression on early-stage lung adenocarcinoma diagnosed according to a new international multidisciplinary classification
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=High expression levels of glucose transporter isoform 1 (GLUT1) and Ki-67 are reportedly associated with malignancy-related clinicopathological factors in malignant tumors. Recently, a new histological IASLC/ATS/ERS classification for lung adenocarcinoma was proposed. In this study, we investigated the clinicopathological impact of GLUT1 and Ki-67 expression on early-stage lung adenocarcinoma classified according to the IASLC/ATS/ERS classification. One hundred and five patients with completely resected stage IA lung adenocarcinoma were retrospectively classified into two groups, a 'non-invasive type' (n=31) or an 'invasive type' (n=74), based on the IASLC/ATS/ERS classification. GLUT1 and Ki-67 expression status was evaluated using immunohistochemistry. The epidermal growth factor receptor (EGFR) and KRAS mutation status was determined using PCR-based assays. Positive GLUT1 and Ki-67 expression and EGFR and KRAS mutations were detected in 28 (27%), 33 (31%), 51 (49%) and 5 (8%) cases, respectively. Positive GLUT1 expression was significantly associated with a wild-type EGFR and mutant KRAS status. A multivariate analysis revealed that positive GLUT1 expression was independently associated with the 'invasive type'. In multivariate analyses for overall survival (OS) and disease-free survival (DFS), positive Ki-67 and GLUT1 expression was the only independent factor for a poor OS (P=0.012) and DFS (P=0.040), respectively. In addition, when stratified according to the GLUT1 and Ki-67 status, double-positive cases had the poorest DFS and OS times, compared with the other categories. Positive GLUT1 expression is associated with the invasive character of early-stage lung adenocarcinoma and with early disease relapse. Our results strongly suggest that GLUT1 and Ki-67 play important roles in acquiring biological malignant potential in early-stage lung adenocarcinoma.
en-copyright=
kn-copyright=
en-aut-name=MakiYuho
en-aut-sei=Maki
en-aut-mei=Yuho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=SohJunichi
en-aut-sei=Soh
en-aut-mei=Junichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=IchimuraKouichi
en-aut-sei=Ichimura
en-aut-mei=Kouichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=ShienKazuhiko
en-aut-sei=Shien
en-aut-mei=Kazuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=FurukawaMasashi
en-aut-sei=Furukawa
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=MuraokaTakayuki
en-aut-sei=Muraoka
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
en-aut-name=TanakaNorimitsu
en-aut-sei=Tanaka
en-aut-mei=Norimitsu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=
en-aut-name=UenoTsuyoshi
en-aut-sei=Ueno
en-aut-mei=Tsuyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
en-aut-name=YamamotoHiromasa
en-aut-sei=Yamamoto
en-aut-mei=Hiromasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=
en-aut-name=AsanoHiroaki
en-aut-sei=Asano
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=
en-aut-name=TsukudaKazunori
en-aut-sei=Tsukuda
en-aut-mei=Kazunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=
en-aut-name=ToyookaShinichi
en-aut-sei=Toyooka
en-aut-mei=Shinichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=
en-aut-name=MiyoshiShinichiro
en-aut-sei=Miyoshi
en-aut-mei=Shinichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=
affil-num=1
en-affil=
kn-affil=Okayama Univ Hosp, Dept Thorac Surg
affil-num=2
en-affil=
kn-affil=Okayama Univ Hosp, Dept Thorac Surg
affil-num=3
en-affil=
kn-affil=Okayama Univ Hosp, Dept Pathol
affil-num=4
en-affil=
kn-affil=Okayama Univ Hosp, Dept Thorac Surg
affil-num=5
en-affil=
kn-affil=Okayama Univ Hosp, Dept Thorac Surg
affil-num=6
en-affil=
kn-affil=Okayama Univ Hosp, Dept Thorac Surg
affil-num=7
en-affil=
kn-affil=Okayama Univ Hosp, Dept Thorac Surg
affil-num=8
en-affil=
kn-affil=Okayama Univ Hosp, Dept Thorac Surg
affil-num=9
en-affil=
kn-affil=Okayama Univ Hosp, Dept Thorac Surg
affil-num=10
en-affil=
kn-affil=Okayama Univ Hosp, Dept Thorac Surg
affil-num=11
en-affil=
kn-affil=Okayama Univ Hosp, Dept Thorac Surg
affil-num=12
en-affil=
kn-affil=Okayama Univ Hosp, Dept Thorac Surg
affil-num=13
en-affil=
kn-affil=Okayama Univ Hosp, Dept Thorac Surg
en-keyword=early-stage lung adenocarcinoma
kn-keyword=early-stage lung adenocarcinoma
en-keyword=glucose transporter isoform 1
kn-keyword=glucose transporter isoform 1
en-keyword=Ki-67
kn-keyword=Ki-67
END
start-ver=1.4
cd-journal=joma
no-vol=76
cd-vols=
no-issue=1
article-no=
start-page=26
end-page=31
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2012
dt-pub=201204
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Strong anti-tumor effect of NVP-AUY922, a novel Hsp90 inhibitor, on non-small cell lung cancer
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The anti-tumor activity of a newly developed Hsp90 inhibitor, NVP-AUY922 (AUY922), against non-small cell lung cancer (NSCLC) was examined. Twenty-one NSCLC cell lines were used, the somatic alterations of which were characterized. Cell proliferation was analyzed using a modified MTS assay. Expression of the client proteins was assessed using Western blotting. The cell cycle was analyzed using flow cytometry. The IC50 value of AUY922 for the NSCLC cell lines ranged from 5.2 to 860 nM (median, 20.4 nM). Based on previous data, cells with an IC50 of less than 50 nM were classified as sensitive cells and 19 of the 21 NSCLC cell lines were judged to be sensitive. The IC50 of five malignant pleural mesothelioma (MPM) cell lines revealed that the MPM cells had a significantly higher IC50 value (median, 89.2 nM; range, 22.2-24, 100 nM) than the NSCLC cells (p = 0.015). There was significant depletion of both the total and phosphorylated client proteins - EGFR, MET, HERZ and ART - at low drug concentrations (50-100 nM) in drug-sensitive cell lines. Cell-cycle analysis was performed for two sensitive cell lines, H1975 and H838. Following AUY922 treatment, an increase in the sub-G(0)-G(1) cell population, as well as appearance of cleaved PARP expression, indicated the induction of apoptosis. In conclusion, AUY922 was effective against most NSCLC cell lines, independent of the type of known molecular alteration, and appears to be a promising new drug for the treatment of NSCLC. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
en-copyright=
kn-copyright=
en-aut-name=UenoTsuyoshi
en-aut-sei=Ueno
en-aut-mei=Tsuyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=TsukudaKazunori
en-aut-sei=Tsukuda
en-aut-mei=Kazunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=ToyookaShinichi
en-aut-sei=Toyooka
en-aut-mei=Shinichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=AndoMidori
en-aut-sei=Ando
en-aut-mei=Midori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=TakaokaMunenori
en-aut-sei=Takaoka
en-aut-mei=Munenori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=SohJunichi
en-aut-sei=Soh
en-aut-mei=Junichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
en-aut-name=AsanoHiroaki
en-aut-sei=Asano
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=
en-aut-name=MakiYuho
en-aut-sei=Maki
en-aut-mei=Yuho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
en-aut-name=MuraokaTakayuki
en-aut-sei=Muraoka
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=
en-aut-name=TanakaNorimitsu
en-aut-sei=Tanaka
en-aut-mei=Norimitsu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=
en-aut-name=ShienKazuhiko
en-aut-sei=Shien
en-aut-mei=Kazuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=
en-aut-name=FurukawaMasashi
en-aut-sei=Furukawa
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=
en-aut-name=YamatsujiTomoki
en-aut-sei=Yamatsuji
en-aut-mei=Tomoki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=
en-aut-name=KiuraKatsuyuki
en-aut-sei=Kiura
en-aut-mei=Katsuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=
en-aut-name=NaomotoYoshio
en-aut-sei=Naomoto
en-aut-mei=Yoshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=
en-aut-name=MiyoshiShinichiro
en-aut-sei=Miyoshi
en-aut-mei=Shinichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=
affil-num=1
en-affil=
kn-affil=Okayama Univ, Dept Gen Thorac Surg, Grad Sch Med Dent & Pharmaceut Sci
affil-num=2
en-affil=
kn-affil=Okayama Univ, Dept Gen Thorac Surg, Grad Sch Med Dent & Pharmaceut Sci
affil-num=3
en-affil=
kn-affil=Okayama Univ, Dept Gen Thorac Surg, Grad Sch Med Dent & Pharmaceut Sci
affil-num=4
en-affil=
kn-affil=Okayama Univ, Dept Gen Thorac Surg, Grad Sch Med Dent & Pharmaceut Sci
affil-num=5
en-affil=
kn-affil=Kawasaki Med Univ, Dept Gen Surg
affil-num=6
en-affil=
kn-affil=Okayama Univ, Dept Gen Thorac Surg, Grad Sch Med Dent & Pharmaceut Sci
affil-num=7
en-affil=
kn-affil=Okayama Univ, Dept Gen Thorac Surg, Grad Sch Med Dent & Pharmaceut Sci
affil-num=8
en-affil=
kn-affil=Okayama Univ, Dept Gen Thorac Surg, Grad Sch Med Dent & Pharmaceut Sci
affil-num=9
en-affil=
kn-affil=Okayama Univ, Dept Gen Thorac Surg, Grad Sch Med Dent & Pharmaceut Sci
affil-num=10
en-affil=
kn-affil=Okayama Univ, Dept Gen Thorac Surg, Grad Sch Med Dent & Pharmaceut Sci
affil-num=11
en-affil=
kn-affil=Okayama Univ, Dept Gen Thorac Surg, Grad Sch Med Dent & Pharmaceut Sci
affil-num=12
en-affil=
kn-affil=Okayama Univ, Dept Gen Thorac Surg, Grad Sch Med Dent & Pharmaceut Sci
affil-num=13
en-affil=
kn-affil=Kawasaki Med Univ, Dept Gen Surg
affil-num=14
en-affil=
kn-affil=Okayama Univ, Dept Hematol Oncol & Resp Med, Grad Sch Med Dent & Pharmaceut Sci
affil-num=15
en-affil=
kn-affil=Kawasaki Med Univ, Dept Gen Surg
affil-num=16
en-affil=
kn-affil=Okayama Univ, Dept Gen Thorac Surg, Grad Sch Med Dent & Pharmaceut Sci
en-keyword=NSCLC
kn-keyword=NSCLC
en-keyword=Hsp90
kn-keyword=Hsp90
en-keyword=AUY922
kn-keyword=AUY922
en-keyword=EGFR
kn-keyword=EGFR
en-keyword=EGFR-TKI
kn-keyword=EGFR-TKI
en-keyword=Mesothelioma
kn-keyword=Mesothelioma
END
start-ver=1.4
cd-journal=joma
no-vol=76
cd-vols=
no-issue=1
article-no=
start-page=32
end-page=38
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2012
dt-pub=201204
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Frequent methylation and oncogenic role of microRNA-34b/c in small-cell lung cancer
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Small-cell lung cancer (SCLC) is an aggressive tumor with a dismal prognosis among primary lung cancers. MicroRNAs (miRNAs) can act as oncogenes or tumor-suppressor genes in human malignancy. The miR-34 family is comprised of tumor-suppressive miRNAs, and its reduced expression by methylation has been reported in various cancers, including non-small cell lung cancer (NSCLC). In this study, we investigated the alteration and tumor-suppressive impact of miR-34s in SCLC. The methylation of miR-34a and miR-34b/c was observed in 4 (36%) and 7 (64%) of 11 SCLC cell lines, respectively. Among the 27 SCLC clinical specimens, miR-34a and miR-34b/c were methylated in 4(15%) and 18 (67%), respectively. In contrast, 13 (28%) miR-34a methylated cases and 12 (26%) miR-34b/c methylated cases were found in 47 NSCLC primary tumors. The frequency of miR-34b/c methylation was significantly higher in SCLC than in NSCLC (p < 0.001). The expressions of miR-34s were reduced in methylated cell lines and tumors and restored after 5-aza-2'-deoxycytidine treatment, indicating that methylation was responsible for the reduced expression of miR-34s. Because the frequency of methylation was higher in miR-34b/c, we focused on miR-34b/c for a functional analysis. We examined the effect of miR-34b/c introduction on cell proliferation, migration and invasion. The transfection of miR-34b/c to two SCLC cell lines (H1048 and SBC5) resulted in the significant inhibition of cell growth, migration, and invasion, compared with control transfectants. Our results indicate that the aberrant methylation of miR-34b/c plays an important role in the pathogenesis of SCLC, implying that miR-34b/c may be a useful therapeutic target for SCLC.
en-copyright=
kn-copyright=
en-aut-name=TanakaNorimitsu
en-aut-sei=Tanaka
en-aut-mei=Norimitsu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=ToyookaShinichi
en-aut-sei=Toyooka
en-aut-mei=Shinichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=SohJunichi
en-aut-sei=Soh
en-aut-mei=Junichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=KuboTakafumi
en-aut-sei=Kubo
en-aut-mei=Takafumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=YamamotoHiromasa
en-aut-sei=Yamamoto
en-aut-mei=Hiromasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=MakiYuho
en-aut-sei=Maki
en-aut-mei=Yuho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
en-aut-name=MuraokaTakayuki
en-aut-sei=Muraoka
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=
en-aut-name=ShienKazuhiko
en-aut-sei=Shien
en-aut-mei=Kazuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
en-aut-name=FurukawaMasashi
en-aut-sei=Furukawa
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=
en-aut-name=UenoTsuyoshi
en-aut-sei=Ueno
en-aut-mei=Tsuyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=
en-aut-name=AsanoHiroaki
en-aut-sei=Asano
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=
en-aut-name=TsukudaKazunori
en-aut-sei=Tsukuda
en-aut-mei=Kazunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=
en-aut-name=AoeKeisuke
en-aut-sei=Aoe
en-aut-mei=Keisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=
en-aut-name=MiyoshiShinichiro
en-aut-sei=Miyoshi
en-aut-mei=Shinichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=
affil-num=1
en-affil=
kn-affil=Okayama Univ, Dept Canc & Thorac Surg, Grad Sch Med Dent & Pharmaceut Sci
affil-num=2
en-affil=
kn-affil=Okayama Univ, Dept Canc & Thorac Surg, Grad Sch Med Dent & Pharmaceut Sci
affil-num=3
en-affil=
kn-affil=Okayama Univ, Dept Canc & Thorac Surg, Grad Sch Med Dent & Pharmaceut Sci
affil-num=4
en-affil=
kn-affil=Okayama Univ, Dept Canc & Thorac Surg, Grad Sch Med Dent & Pharmaceut Sci
affil-num=5
en-affil=
kn-affil=Okayama Univ, Dept Canc & Thorac Surg, Grad Sch Med Dent & Pharmaceut Sci
affil-num=6
en-affil=
kn-affil=Okayama Univ, Dept Canc & Thorac Surg, Grad Sch Med Dent & Pharmaceut Sci
affil-num=7
en-affil=
kn-affil=Okayama Univ, Dept Canc & Thorac Surg, Grad Sch Med Dent & Pharmaceut Sci
affil-num=8
en-affil=
kn-affil=Okayama Univ, Dept Canc & Thorac Surg, Grad Sch Med Dent & Pharmaceut Sci
affil-num=9
en-affil=
kn-affil=Okayama Univ, Dept Canc & Thorac Surg, Grad Sch Med Dent & Pharmaceut Sci
affil-num=10
en-affil=
kn-affil=Okayama Univ, Dept Canc & Thorac Surg, Grad Sch Med Dent & Pharmaceut Sci
affil-num=11
en-affil=
kn-affil=Okayama Univ, Dept Canc & Thorac Surg, Grad Sch Med Dent & Pharmaceut Sci
affil-num=12
en-affil=
kn-affil=Okayama Univ, Dept Canc & Thorac Surg, Grad Sch Med Dent & Pharmaceut Sci
affil-num=13
en-affil=
kn-affil=Natl Hosp Org Yamaguchi Ube Med Ctr, Dept Med Oncol
affil-num=14
en-affil=
kn-affil=Okayama Univ, Dept Canc & Thorac Surg, Grad Sch Med Dent & Pharmaceut Sci
en-keyword=Methylation
kn-keyword=Methylation
en-keyword=MicroRNA
kn-keyword=MicroRNA
en-keyword=MicroRNA-34b/c
kn-keyword=MicroRNA-34b/c
en-keyword=Small cell lung cancer
kn-keyword=Small cell lung cancer
en-keyword=Non-small cell lung cancer
kn-keyword=Non-small cell lung cancer
en-keyword=p53
kn-keyword=p53
END
start-ver=1.4
cd-journal=joma
no-vol=77
cd-vols=
no-issue=1
article-no=
start-page=162
end-page=167
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2012
dt-pub=201207
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Prognostic impact of cancer stem cell-related markers in non-small cell lung cancer patients treated with induction chemoradiotherapy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The expression of several cancer stem cell (CSC)-related markers has been confirmed in non-small cell lung cancer (NSCLC). The aim of this study was to clarify the clinical role of CSC-related markers in patients with NSCLC undergoing induction chemoradiotherapy (CRT). Fifty patients with clinically diagnosed N2 or N3 NSCLC who underwent induction CRT with docetaxel and cisplatin concurrently with thoracic radiation followed by surgery were examined in this study. The expressions of CSC related markers (CD133, ALDH1, ABCG2, and Bmi-1) were examined using immunohistochemical staining in surgically resected specimens. Among the 50 patients, 20 patients had no residual tumor cells in the resected specimen when examined pathologically; CSC-related marker expressions and their correlation to survival were evaluated in the other 30 patients. After a median follow-up period of 72 months, the 5-year overall survival rate of the patients with CD133-positive or ALDH1-positive specimens was significantly worse than that of the patients with both CD133-negative and ALDH1-negative expressions (449% vs. 90.0%, respectively; P=0.042). In a multivariate analysis. CD133 and ALDH1 negativity (P=0.047) and cN2-3 single station metastasis (P=0.03) were significant independent prognostic factors for prolonged survival. The expressions of CSC-related markers after CRT were significantly correlated with a poor prognosis in patients with NSCLC. The development of therapeutic strategies including adjuvant therapy that take CSC-related marker positivity into consideration is likely to be a key factor in further improvements of the prognosis of patients undergoing trimodality therapy.
en-copyright=
kn-copyright=
en-aut-name=ShienKazuhiko
en-aut-sei=Shien
en-aut-mei=Kazuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=ToyookaShinichi
en-aut-sei=Toyooka
en-aut-mei=Shinichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=IchimuraKouichi
en-aut-sei=Ichimura
en-aut-mei=Kouichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=SohJunichi
en-aut-sei=Soh
en-aut-mei=Junichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=FurukawaMasashi
en-aut-sei=Furukawa
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=MakiYuho
en-aut-sei=Maki
en-aut-mei=Yuho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
en-aut-name=MuraokaTakayuki
en-aut-sei=Muraoka
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=
en-aut-name=TanakaNorimitsu
en-aut-sei=Tanaka
en-aut-mei=Norimitsu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
en-aut-name=UenoTsuyoshi
en-aut-sei=Ueno
en-aut-mei=Tsuyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=
en-aut-name=AsanoHiroaki
en-aut-sei=Asano
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=
en-aut-name=TsukudaKazunori
en-aut-sei=Tsukuda
en-aut-mei=Kazunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=
en-aut-name=YamaneMasaomi
en-aut-sei=Yamane
en-aut-mei=Masaomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=
en-aut-name=OtoTakahiro
en-aut-sei=Oto
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=
en-aut-name=KiuraKatsuyuki
en-aut-sei=Kiura
en-aut-mei=Katsuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=
en-aut-name=MiyoshiShinichiro
en-aut-sei=Miyoshi
en-aut-mei=Shinichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=
affil-num=1
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Canc & Thorac Surg
affil-num=2
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Canc & Thorac Surg
affil-num=3
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Pathol
affil-num=4
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Canc & Thorac Surg
affil-num=5
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Canc & Thorac Surg
affil-num=6
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Canc & Thorac Surg
affil-num=7
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Canc & Thorac Surg
affil-num=8
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Canc & Thorac Surg
affil-num=9
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Canc & Thorac Surg
affil-num=10
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Canc & Thorac Surg
affil-num=11
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Canc & Thorac Surg
affil-num=12
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Canc & Thorac Surg
affil-num=13
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Canc & Thorac Surg
affil-num=14
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Resp Med
affil-num=15
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Canc & Thorac Surg
en-keyword=NSCLC
kn-keyword=NSCLC
en-keyword=Cancer stem cell
kn-keyword=Cancer stem cell
en-keyword=CD133
kn-keyword=CD133
en-keyword=ALDH1
kn-keyword=ALDH1
en-keyword=Chemoradiotherapy
kn-keyword=Chemoradiotherapy
en-keyword=Induction therapy
kn-keyword=Induction therapy
END
start-ver=1.4
cd-journal=joma
no-vol=67
cd-vols=
no-issue=1
article-no=
start-page=19
end-page=24
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2013
dt-pub=201302
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Silenced Expression of NFKBIA in Lung Adenocarcinoma Patients with a Never-smoking History
en-subtitle=
kn-subtitle=
en-abstract=
kn-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.
en-copyright=
kn-copyright=
en-aut-name=FurukawaMasashi
en-aut-sei=Furukawa
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=SohJunichi
en-aut-sei=Soh
en-aut-mei=Junichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=YamamotoHiromasa
en-aut-sei=Yamamoto
en-aut-mei=Hiromasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=IchimuraKouichi
en-aut-sei=Ichimura
en-aut-mei=Kouichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=ShienKazuhiko
en-aut-sei=Shien
en-aut-mei=Kazuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=MakiYuho
en-aut-sei=Maki
en-aut-mei=Yuho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
en-aut-name=MuraokaTakayuki
en-aut-sei=Muraoka
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=
en-aut-name=TanakaNorimitsu
en-aut-sei=Tanaka
en-aut-mei=Norimitsu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
en-aut-name=UenoTsuyoshi
en-aut-sei=Ueno
en-aut-mei=Tsuyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=
en-aut-name=AsanoHiroaki
en-aut-sei=Asano
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=
en-aut-name=TsukudaKazunori
en-aut-sei=Tsukuda
en-aut-mei=Kazunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=
en-aut-name=ToyookaShinichi
en-aut-sei=Toyooka
en-aut-mei=Shinichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=
en-aut-name=MiyoshiShinichiro
en-aut-sei=Miyoshi
en-aut-mei=Shinichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=
affil-num=1
en-affil=
kn-affil=Department of Thoracic Surgery, Okayama University Hospital
affil-num=2
en-affil=
kn-affil=Department of Thoracic Surgery, Okayama University Hospital
affil-num=3
en-affil=
kn-affil=Department of Thoracic Surgery, Okayama University Hospital
affil-num=4
en-affil=
kn-affil=Department of Pathology, Okayama University Hospital
affil-num=5
en-affil=
kn-affil=Department of Thoracic Surgery, Okayama University Hospital
affil-num=6
en-affil=
kn-affil=Department of Thoracic Surgery, Okayama University Hospital
affil-num=7
en-affil=
kn-affil=Department of Thoracic Surgery, Okayama University Hospital
affil-num=8
en-affil=
kn-affil=Department of Thoracic Surgery, Okayama University Hospital
affil-num=9
en-affil=
kn-affil=Department of Thoracic Surgery, Okayama University Hospital
affil-num=10
en-affil=
kn-affil=Department of Thoracic Surgery, Okayama University Hospital
affil-num=11
en-affil=
kn-affil=Department of Thoracic Surgery, Okayama University Hospital
affil-num=12
en-affil=
kn-affil=Department of Thoracic Surgery, Okayama University Hospital
affil-num=13
en-affil=
kn-affil=Department of Thoracic Surgery, Okayama University Hospital
en-keyword=never-smoker
kn-keyword=never-smoker
en-keyword=lung cancer
kn-keyword=lung cancer
en-keyword=adenocarcinoma
kn-keyword=adenocarcinoma
en-keyword=nuclear factor of κ-light polypeptide gene enhancer in B cells inhibitor α
kn-keyword=nuclear factor of κ-light polypeptide gene enhancer in B cells inhibitor α
en-keyword=epidermal growth factor receptor
kn-keyword=epidermal growth factor receptor
END
start-ver=1.4
cd-journal=joma
no-vol=66
cd-vols=
no-issue=5
article-no=
start-page=423
end-page=427
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2012
dt-pub=201210
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Duodenal Carcinoma from a Duodenal Diverticulum Mimicking Pancreatic Carcinoma
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=An 81-year-old man was found to have a pancreatic head tumor on abdominal computed tomography (CT) performed during a follow-up visit for sigmoid colon cancer. The tumor had a diameter of 35mm on the CT scan and was diagnosed as pancreatic head carcinoma T3N0M0. The patient was treated with pylorus-preserving pancreaticoduodenectomy. Histopathological examination showed that the tumor had grown within a hollow structure, was contiguous with a duodenal diverticulum, and had partially invaded the pancreas. Immunohistochemistry results were as follows:CK7 negative, CK20 positive, CD10 negative, CDX2 positive, MUC1 negative, MUC2 positive, MUC5AC negative, and MUC6 negative. The tumor was diagnosed as duodenal carcinoma from the duodenal diverticulum. Preoperative imaging showed that the tumor was located in the head of the pancreas and was compressing the common bile duct, thus making it appear like pancreatic cancer. To the best of our knowledge, this is the second report of a case of duodenal carcinoma from a duodenal diverticulum mimicking pancreatic carcinoma.
en-copyright=
kn-copyright=
en-aut-name=FurukawaMasashi
en-aut-sei=Furukawa
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=IzumiSadanobu
en-aut-sei=Izumi
en-aut-mei=Sadanobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=TsukudaKazunori
en-aut-sei=Tsukuda
en-aut-mei=Kazunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=TokumoMasaki
en-aut-sei=Tokumo
en-aut-mei=Masaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=SakuraiJun
en-aut-sei=Sakurai
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=ManoShohey
en-aut-sei=Mano
en-aut-mei=Shohey
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
affil-num=1
en-affil=
kn-affil=Department of Thoracic Surgery, Okayama University Hospital
affil-num=2
en-affil=
kn-affil=Department of Surgery, Kagawa Prefectural Central Hospital
affil-num=3
en-affil=
kn-affil=Department of Thoracic Surgery, Okayama University Hospital
affil-num=4
en-affil=
kn-affil=Department of Surgery, National Hospital Organization Minami-Okayama Medical Center
affil-num=5
en-affil=
kn-affil=Department of Diagnostic Radiology, Kagawa Prefectural Central Hospital
affil-num=6
en-affil=
kn-affil=Department of Pathology, Kagawa Prefectural Central Hospital
en-keyword=duodenal carcinoma
kn-keyword=duodenal carcinoma
en-keyword=duodenal diverticulum
kn-keyword=duodenal diverticulum
en-keyword=pancreatic carcinoma
kn-keyword=pancreatic carcinoma
END
start-ver=1.4
cd-journal=joma
no-vol=65
cd-vols=
no-issue=3
article-no=
start-page=179
end-page=184
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2011
dt-pub=201106
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Aberrant Methylation of p21 Gene in Lung Cancer and Malignant Pleural Mesothelioma
en-subtitle=
kn-subtitle=
en-abstract=
kn-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.
en-copyright=
kn-copyright=
en-aut-name=TeramenHirotake
en-aut-sei=Teramen
en-aut-mei=Hirotake
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=TsukudaKazunori
en-aut-sei=Tsukuda
en-aut-mei=Kazunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=TanakaNorimitsu
en-aut-sei=Tanaka
en-aut-mei=Norimitsu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=UenoTsuyoshi
en-aut-sei=Ueno
en-aut-mei=Tsuyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=KuboTakafumi
en-aut-sei=Kubo
en-aut-mei=Takafumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=AndoMidori
en-aut-sei=Ando
en-aut-mei=Midori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
en-aut-name=SohJunichi
en-aut-sei=Soh
en-aut-mei=Junichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=
en-aut-name=AsanoHiroaki
en-aut-sei=Asano
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
en-aut-name=PassHarvery I.
en-aut-sei=Pass
en-aut-mei=Harvery I.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=
en-aut-name=ToyookaShinichi
en-aut-sei=Toyooka
en-aut-mei=Shinichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=
en-aut-name=MiyoshiShinichiro
en-aut-sei=Miyoshi
en-aut-mei=Shinichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=
affil-num=1
en-affil=
kn-affil=Department of Cancer and Thoracic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
affil-num=2
en-affil=
kn-affil=Department of Cancer and Thoracic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
affil-num=3
en-affil=
kn-affil=Department of Cancer and Thoracic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
affil-num=4
en-affil=
kn-affil=Department of Cancer and Thoracic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
affil-num=5
en-affil=
kn-affil=Department of Cancer and Thoracic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
affil-num=6
en-affil=
kn-affil=Department of Cancer and Thoracic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
affil-num=7
en-affil=
kn-affil=Department of Cancer and Thoracic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
affil-num=8
en-affil=
kn-affil=Department of Cancer and Thoracic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
affil-num=9
en-affil=
kn-affil=Department of Thoracic Surgery, NYU Langone Medical Center
affil-num=10
en-affil=
kn-affil=Department of Cancer and Thoracic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
affil-num=11
en-affil=
kn-affil=Department of Cancer and Thoracic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
en-keyword=p21
kn-keyword=p21
en-keyword=methylation
kn-keyword=methylation
en-keyword=lung cancer
kn-keyword=lung cancer
en-keyword=mesothelioma
kn-keyword=mesothelioma
END
start-ver=1.4
cd-journal=joma
no-vol=112
cd-vols=
no-issue=1
article-no=
start-page=8
end-page=13
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2004
dt-pub=20041020
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Tumor-specific exon creation of the HELLS/SMARCA6 gene in non-small cell lung cancer
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=In an attempt to identify tumor suppressor genes on chromosome 10 in non-small cell lung
cancers, we isolated 10 types of splicing variants of the HELLS/ SMARCA6 gene transcripts.
HELLS/SMARCA6 is a novel member of SNF2 family, which is implicated in cellular function like chromatin remodeling. Variant 1 was an alternatively spliced isoform containing
an insertion of a 44-ntd intronic sequence between exons 3 and 4, giving rise to a premature
termination of translation. The expression of the variant 1 was detected exclusively in the
lung cancer specimens (11 of 43 cases, 26%), but was not detected in corresponding normal tissues. D10S520 marker in the proximity of the HELLS/SMARCA6 gene showed prevalent allelic loss (41%) as compared with flanking markers (25-31%). These results suggest that loss of function of HELLS/SMARCA6 by allelic loss and aberrant proteins by tumor-specific exon creation may result in epigenetic deregulation, leading the lung cells to malignancy or its progression.
en-copyright=
kn-copyright=
en-aut-name=YanoMasaaki
en-aut-sei=Yano
en-aut-mei=Masaaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=OuchidaMamoru
en-aut-sei=Ouchida
en-aut-mei=Mamoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=ShigematsuHisayuki
en-aut-sei=Shigematsu
en-aut-mei=Hisayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=TanakaNoriyoshi
en-aut-sei=Tanaka
en-aut-mei=Noriyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=IchimuraKoichi
en-aut-sei=Ichimura
en-aut-mei=Koichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=KobayashiKazuyasu
en-aut-sei=Kobayashi
en-aut-mei=Kazuyasu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
en-aut-name=InakiYasuhiko
en-aut-sei=Inaki
en-aut-mei=Yasuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=
en-aut-name=ToyookaShinichi
en-aut-sei=Toyooka
en-aut-mei=Shinichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
en-aut-name=TsukudaKazunori
en-aut-sei=Tsukuda
en-aut-mei=Kazunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=
en-aut-name=ShimizuNobuyoshi
en-aut-sei=Shimizu
en-aut-mei=Nobuyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=
en-aut-name=ShimizuKenji
en-aut-sei=Shimizu
en-aut-mei=Kenji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=
affil-num=1
en-affil=
kn-affil=Department of Surgical Oncology and Thoracic Surgery, Graduate School of Medicine and Dentistry, Okayama University
affil-num=2
en-affil=
kn-affil=Department of Molecular Genetics, Graduate School of Medicine and Dentistry, Okayama University
affil-num=3
en-affil=
kn-affil=Department of Surgical Oncology and Thoracic Surgery, Graduate School of Medicine and Dentistry, Okayama University
affil-num=4
en-affil=
kn-affil=Department of Surgical Oncology and Thoracic Surgery, Graduate School of Medicine and Dentistry, Okayama University
affil-num=5
en-affil=
kn-affil=Department of Pathology, Graduate School of Medicine and Dentistry, Okayama University
affil-num=6
en-affil=
kn-affil=Department of Surgical Oncology and Thoracic Surgery, Graduate School of Medicine and Dentistry, Okayama University
affil-num=7
en-affil=
kn-affil=Department of Surgical Oncology and Thoracic Surgery, Graduate School of Medicine and Dentistry, Okayama University
affil-num=8
en-affil=
kn-affil=Department of Surgical Oncology and Thoracic Surgery, Graduate School of Medicine and Dentistry, Okayama University
affil-num=9
en-affil=
kn-affil=Department of Surgical Oncology and Thoracic Surgery, Graduate School of Medicine and Dentistry, Okayama University
affil-num=10
en-affil=
kn-affil=Department of Surgical Oncology and Thoracic Surgery, Graduate School of Medicine and Dentistry, Okayama University
affil-num=11
en-affil=
kn-affil=Department of Molecular Genetics, Graduate School of Medicine and Dentistry, Okayama University
en-keyword=alternative splicing
kn-keyword=alternative splicing
en-keyword=HELLS
kn-keyword=HELLS
en-keyword=loss of heterozygosity
kn-keyword=loss of heterozygosity
en-keyword=lung cancer
kn-keyword=lung cancer
en-keyword=SMARCA6
kn-keyword=SMARCA6
END
start-ver=1.4
cd-journal=joma
no-vol=61
cd-vols=
no-issue=1
article-no=
start-page=47
end-page=50
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2007
dt-pub=200702
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Multiple gastrointestinal stromal tumors in neurofi bromatosis type 1 treated with laparoscopic surgery
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Gastrointestinal stromal tumors (GISTs) have been reported to occasionally occur in patients with
neurofi bromatosis type 1 (NF-1), and many cases have had multiple lesions predominantly involving
the small intestine. We report herein a case of multiple GISTs associated with NF-1 from whom laparoscopic
surgery was benefi cial. In a 79-year-old female admitted with anemia and melena, the
abdominal computed tomography revealed a tumor arising from the small intestine. Laparoscopic
surgery was performed, and another small tumor was revealed during laparoscopic observation.
Extracorporeal partial and wedge resection of the small intestine were undertaken. Both lesions
were diagnosed as typical GISTs of low risk. Laparoscopic surgery would be useful for examination
and a minimally invasive approach to tumors of the small intestine, especially on cases with the possibility
of multiple tumors.
en-copyright=
kn-copyright=
en-aut-name=TsukudaKazunori
en-aut-sei=Tsukuda
en-aut-mei=Kazunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=IkedaEiji
en-aut-sei=Ikeda
en-aut-mei=Eiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=TakagiShoji
en-aut-sei=Takagi
en-aut-mei=Shoji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=MiyakeTakayoshi
en-aut-sei=Miyake
en-aut-mei=Takayoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=MuraokaTakayuki
en-aut-sei=Muraoka
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=WatanabeKeitaro
en-aut-sei=Watanabe
en-aut-mei=Keitaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
en-aut-name=HiraiRyuji
en-aut-sei=Hirai
en-aut-mei=Ryuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=
en-aut-name=MoriyamaShigeharu
en-aut-sei=Moriyama
en-aut-mei=Shigeharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
en-aut-name=NawaSugato
en-aut-sei=Nawa
en-aut-mei=Sugato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=
en-aut-name=KunitomoTadayoshi
en-aut-sei=Kunitomo
en-aut-mei=Tadayoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=
en-aut-name=TsujiHisashi
en-aut-sei=Tsuji
en-aut-mei=Hisashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=
affil-num=1
en-affil=
kn-affil=Okayama Red Cross General Hospital
affil-num=2
en-affil=
kn-affil=Okayama Red Cross General Hospital
affil-num=3
en-affil=
kn-affil=Okayama Red Cross General Hospital
affil-num=4
en-affil=
kn-affil=Okayama Red Cross General Hospital
affil-num=5
en-affil=
kn-affil=Okayama Red Cross General Hospital
affil-num=6
en-affil=
kn-affil=Okayama Red Cross General Hospital
affil-num=7
en-affil=
kn-affil=Okayama Red Cross General Hospital
affil-num=8
en-affil=
kn-affil=Okayama Red Cross General Hospital
affil-num=9
en-affil=
kn-affil=Okayama Red Cross General Hospital
affil-num=10
en-affil=
kn-affil=Okayama Red Cross General Hospital
affil-num=11
en-affil=
kn-affil=Okayama Red Cross General Hospital
en-keyword=gastrointestinal stromal tumor
kn-keyword=gastrointestinal stromal tumor
en-keyword=neurofi bromatosis type 1
kn-keyword=neurofi bromatosis type 1
en-keyword=laparoscopic surgery
kn-keyword=laparoscopic surgery
END
start-ver=1.4
cd-journal=joma
no-vol=61
cd-vols=
no-issue=2
article-no=
start-page=81
end-page=88
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2007
dt-pub=200704
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Effects of adenoviral-mediated hepatocyte growth factor on liver regeneration after massive hepatectomy in rats
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Resection is the only curative treatment for liver metastasis of colorectal cancers. Despite the supreme regenerative potential of the liver, major hepatectomy sometimes leads to liver failure, and the limitation of resectable liver volumes makes advanced tumors inoperable. This study was attempted to promote liver regeneration using hepatocyte growth factor (HGF) gene transfection by venous-administered adenovirus and to improve the survival of rats after massive hepatectomy. The adenovirus that encodes HGF was administered to rats before 85%-hepatectomy. The administration of HGF gene improved the survival of rats after massive hepatectomy, while the administration of control adenovirus deteriorated their survival. Gene transfection of HGF showed up-regulation of serum HGF, stimulation of hepatocellular proliferation and rapid liver regeneration. Moreover, HGF administration reduced apoptosis of hepatocytes. The administration of HGF gene prevented liver dysfunction after major hepatectomy and may be a new assist for surgery.
en-copyright=
kn-copyright=
en-aut-name=YuasaIchiro
en-aut-sei=Yuasa
en-aut-mei=Ichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=TsukudaKazunori
en-aut-sei=Tsukuda
en-aut-mei=Kazunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=HiraiRyuji
en-aut-sei=Hirai
en-aut-mei=Ryuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=OtaTetsuya
en-aut-sei=Ota
en-aut-mei=Tetsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=MurakamiMasakazu
en-aut-sei=Murakami
en-aut-mei=Masakazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=NaitoMinoru
en-aut-sei=Naito
en-aut-mei=Minoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
en-aut-name=DoiharaHiroyoshi
en-aut-sei=Doihara
en-aut-mei=Hiroyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=
en-aut-name=DateHiroshi
en-aut-sei=Date
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
en-aut-name=ShimizuNobuyoshi
en-aut-sei=Shimizu
en-aut-mei=Nobuyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=
affil-num=1
en-affil=
kn-affil=Okayama University
affil-num=2
en-affil=
kn-affil=Okayama University
affil-num=3
en-affil=
kn-affil=Okayama University
affil-num=4
en-affil=
kn-affil=Okayama University
affil-num=5
en-affil=
kn-affil=Okayama University
affil-num=6
en-affil=
kn-affil=Okayama University
affil-num=7
en-affil=
kn-affil=Okayama University
affil-num=8
en-affil=
kn-affil=Okayama University
affil-num=9
en-affil=
kn-affil=Okayama University
en-keyword=gene therapy
kn-keyword=gene therapy
en-keyword=hepatectomy
kn-keyword=hepatectomy
en-keyword=HGF
kn-keyword=HGF
en-keyword=adenoviral vector
kn-keyword=adenoviral vector
END
start-ver=1.4
cd-journal=joma
no-vol=58
cd-vols=
no-issue=3
article-no=
start-page=163
end-page=167
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2004
dt-pub=200406
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Biliary reconstruction with right hepatic lobectomy due to delayed management of laparoscopic bile duct injuries: a case report.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=We report a case requiring biliary reconstruction with right hepatic lobectomy due to biliary strictures caused by continuous cholangitis after laparoscopic bile duct injury. The patient, a 55-year-old woman, underwent laparoscopic cholecystectomy for cholelithiasis at another hospital. Although a bile leakage from the intraabdominal drain was observed several days after the operation, the patient was not given adequate treatment to stop the leakage. Two months after the initial laparoscopic cholecystectomy, she was referred to our hospital. Endoscopic retrograde cholangiopancreatography (ERCP) showed complete obstruction of the common hepatic duct, which was caused by clipping during laparoscopic cholecystectomy. Cholangiography from percutaneous transhepatic biliary drainage (PTBD) catheters revealed that sections of the secondary branches of the right intrahepatic bile duct had become constricted due to persistent cholangitis. Fortunately, the left hepatic duct was judged to be normal by imaging. Therefore, we elected to perform a right hepatic lobectomy and left hepaticojejunostomy, because we felt that performing a hepaticojejunostomy without hepatic resection would put the patient at risk of continuing to suffer from cholangitis. The patient was discharged on the 55 th postoperative day, and, 5 years after reconstructive surgery, is healthy and has remained free from biliary strictures in the remnant liver. Appropriate decision-making is essential in the treatment of biliary injury after laparoscopic cholecystectomy. Surgeons should not hesitate to perform biliary reconstruction with hepatic resection to reduce the risk of cholangitis or biliary strictures of the remnant liver. More importantly, preoperative clear imaging of the biliary tree and suitable management of any biliary injury which might occur are necessary to avoid having to perform reconstructive surgery.
en-copyright=
kn-copyright=
en-aut-name=OtaTetsuya
en-aut-sei=Ota
en-aut-mei=Tetsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=HiraiRyuji
en-aut-sei=Hirai
en-aut-mei=Ryuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=TsukudaKazunori
en-aut-sei=Tsukuda
en-aut-mei=Kazunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=MurakamiMasakazu
en-aut-sei=Murakami
en-aut-mei=Masakazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=NaitouMinoru
en-aut-sei=Naitou
en-aut-mei=Minoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=ShimizuNobuyoshi
en-aut-sei=Shimizu
en-aut-mei=Nobuyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
affil-num=1
en-affil=
kn-affil=Okayama University
affil-num=2
en-affil=
kn-affil=Okayama Red Cross Hospital
affil-num=3
en-affil=
kn-affil=Okayama University
affil-num=4
en-affil=
kn-affil=Okayama University
affil-num=5
en-affil=
kn-affil=Okayama University
affil-num=6
en-affil=
kn-affil=Okayama University
en-keyword=?biliary injury
kn-keyword=?biliary injury
en-keyword=laparoscopic cholecystectomy
kn-keyword=laparoscopic cholecystectomy
en-keyword=hepatic resection
kn-keyword=hepatic resection
END
start-ver=1.4
cd-journal=joma
no-vol=63
cd-vols=
no-issue=6
article-no=
start-page=367
end-page=371
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2009
dt-pub=200912
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Breast Cancer with Cartilaginous and/or Osseous Metaplasia Diagnosed by Lymph Nodal Metastasis:A Case Report
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Breast cancer with cartilaginous and/or osseous metaplasia is a type of metaplastic carcinomas and is a rare disease. We report the case of a 49 year-old female who underwent right mastectomy for a large breast tumor. Histological examinations revealed a mixed tumor with both stromal and epithelial elements;the stroma showed poor differentiated spindle-shape and multiform cells with a massive osseous matrix, and atypical epithelial cells, which mainly existed on the surface of the cysts, showed nucleic atypia. The tumor was diagnosed as a malignant phyllodes tumor with osteosarcomatous differentiation;it was not identified as a metaplastic carcinoma because of the lack of proof of a cancerous component. Two years after a mastectomy, swelling of the axillary lymph nodes was found and a biopsy was performed. Histological findings for the lymph node indicated a metastasis of the invasive ductal carcinoma. The primary tumor was re-examined and was considered to be the origin of the lymph nodal metastasis. Lymph nodal metastasis of cancer proved that the primary tumor had cancerous potential, and the pathological diagnosis was altered to a breast cancer with cartilaginous and/or osseous metaplasia.
en-copyright=
kn-copyright=
en-aut-name=TsukudaKazunori
en-aut-sei=Tsukuda
en-aut-mei=Kazunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=TsujiHisashi
en-aut-sei=Tsuji
en-aut-mei=Hisashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=KunitomoTadayoshi
en-aut-sei=Kunitomo
en-aut-mei=Tadayoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=AokageKeiju
en-aut-sei=Aokage
en-aut-mei=Keiju
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=MiyakeTakayoshi
en-aut-sei=Miyake
en-aut-mei=Takayoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=NakaharaSaki
en-aut-sei=Nakahara
en-aut-mei=Saki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
en-aut-name=MasudaHiroko
en-aut-sei=Masuda
en-aut-mei=Hiroko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=
affil-num=1
en-affil=
kn-affil=Department of Surgery, Okayama Red Cross General Hospital
affil-num=2
en-affil=
kn-affil=Department of Surgery, Okayama Red Cross General Hospital
affil-num=3
en-affil=
kn-affil=Department of Pathology, Okayama Red Cross General Hospital
affil-num=4
en-affil=
kn-affil=Department of Surgery, Okayama Red Cross General Hospital
affil-num=5
en-affil=
kn-affil=Department of Pathology, Okayama Red Cross General Hospital
affil-num=6
en-affil=
kn-affil=Department of Surgery, Okayama Red Cross General Hospital
affil-num=7
en-affil=
kn-affil=Department of Surgery, Okayama Red Cross General Hospital
en-keyword=breast cancer
kn-keyword=breast cancer
en-keyword=metaplastic cancer
kn-keyword=metaplastic cancer
en-keyword=phyllodes tumor
kn-keyword=phyllodes tumor
END
start-ver=1.4
cd-journal=joma
no-vol=62
cd-vols=
no-issue=6
article-no=
start-page=411
end-page=413
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2008
dt-pub=200812
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Abscess Formation of the Round Ligament of the Liver: Report of a Case
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Abscess formation of the round ligament of the liver is very rare. We report a case of a 70-year-old female with abscess of the round ligament after an endoscopic papillotomy for choledocholithiasis. On the 21st day following papillotomy, abscess formation of the round ligament was found by ultrasonographic
examination. Surgical treatment was performed because conservative therapy was not effective. The purulent fluid and necrotic tissue at the round ligament were completely removed. Cultures obtained from the abscess grew Staphylococcus epidermidis, but the mechanism of abscess formation in this case remains unclear.
en-copyright=
kn-copyright=
en-aut-name=TsukudaKazunori
en-aut-sei=Tsukuda
en-aut-mei=Kazunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=FurutaniShiro
en-aut-sei=Furutani
en-aut-mei=Shiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=NakaharaSaki
en-aut-sei=Nakahara
en-aut-mei=Saki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=TadaAkihiro
en-aut-sei=Tada
en-aut-mei=Akihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=WatanabeKeitaro
en-aut-sei=Watanabe
en-aut-mei=Keitaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=TakagiShoji
en-aut-sei=Takagi
en-aut-mei=Shoji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
en-aut-name=IkedaEiji
en-aut-sei=Ikeda
en-aut-mei=Eiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=
en-aut-name=HiraiRyuji
en-aut-sei=Hirai
en-aut-mei=Ryuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
en-aut-name=TsujiHisashi
en-aut-sei=Tsuji
en-aut-mei=Hisashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=
affil-num=1
en-affil=
kn-affil=Department of Surgery, Okayama Red Cross General Hospital
affil-num=2
en-affil=
kn-affil=Department of Surgery, Okayama Red Cross General Hospital
affil-num=3
en-affil=
kn-affil=Department of Surgery, Okayama Red Cross General Hospital
affil-num=4
en-affil=
kn-affil=Department of Surgery, Okayama Red Cross General Hospita
affil-num=5
en-affil=
kn-affil=Department of Surgery, Okayama Red Cross General Hospital
affil-num=6
en-affil=
kn-affil=Department of Surgery, Okayama Red Cross General Hospital
affil-num=7
en-affil=
kn-affil=Department of Surgery, Okayama Red Cross General Hospital
affil-num=8
en-affil=
kn-affil=Department of Surgery, Okayama Red Cross General Hospital
affil-num=9
en-affil=
kn-affil=Department of Surgery, Okayama Red Cross General Hospital
en-keyword=round ligament of the liver
kn-keyword=round ligament of the liver
en-keyword=abscess
kn-keyword=abscess
END
start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2001
dt-pub=20010325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=原発性大腸癌で発見されたK-ras遺伝子の新しい活性型突然変異
kn-title=A novel activating mutation of the K-ras gene in human primary colon adenocarcinoma
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=
en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=佃和憲
kn-aut-sei=佃
kn-aut-mei=和憲
aut-affil-num=1
ORCID=
affil-num=1
en-affil=
kn-affil=岡山大学
END