start-ver=1.4 cd-journal=joma no-vol=13 cd-vols= no-issue=5 article-no= start-page=45 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2020 dt-pub=2020827 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Human NINEIN polymorphism at codon 1111 is associated with the risk of colorectal cancer en-subtitle= kn-subtitle= en-abstract= kn-abstract=NINEIN serves an essential role in centrosome function as a microtubule organizing center, and in the reformation of the interphase centrosome architecture following mitosis. In the present study, the association between NINEIN Pro1111Ala (rs2236316), a missense single nucleotide polymorphism, and the risk of colorectal cancer (CRC), related to smoking and alcohol consumption habits in 200 patients with CRC and 1,141 cancer‑free control participants were assessed in a case‑control study performed in Japan. The results showed that the NINEIN Ala/Ala genotype compared with the Pro/Pro genotype was significantly more associated with an increased risk of CRC, and the males with the Ala/Ala genotype exhibited a significantly increased risk of CRC compared with those with Pro/Pro and Pro/Ala genotypes. Stratified analyses of the Ala/Ala genotype with CRC risk further showed an increased association in never/light drinkers (<23 g of ethanol/day), in male never/light drinkers and in male patients with rectal cancer. These findings suggest that the genetic variant of the NINEIN Pro1111Ala polymorphism has a significant effect on CRC susceptibility in the Japanese population. en-copyright= kn-copyright= en-aut-name=YasudaYukiko en-aut-sei=Yasuda en-aut-mei=Yukiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=SakaiAkiko en-aut-sei=Sakai en-aut-mei=Akiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=ItoSachio en-aut-sei=Ito en-aut-mei=Sachio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=SasaiKaori en-aut-sei=Sasai en-aut-mei=Kaori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=IshizakiAkisada en-aut-sei=Ishizaki en-aut-mei=Akisada kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=OkanoYoshiya en-aut-sei=Okano en-aut-mei=Yoshiya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=KawaharaSeito en-aut-sei=Kawahara en-aut-mei=Seito kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=JitsumoriYoshimi en-aut-sei=Jitsumori en-aut-mei=Yoshimi 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=MatsubaraNagahide en-aut-sei=Matsubara en-aut-mei=Nagahide 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= en-aut-name=KatayamaHiroshi en-aut-sei=Katayama en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= affil-num=1 en-affil=Department of Molecular Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=2 en-affil=Department of Molecular Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=3 en-affil=Department of Molecular Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=4 en-affil=Department of Molecular Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=5 en-affil=Department of Molecular Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=6 en-affil=Department of Molecular Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=7 en-affil=Department of Molecular Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=8 en-affil=Department of Molecular Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=9 en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=10 en-affil=Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=11 en-affil=Department of Molecular Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=12 en-affil=Department of Molecular Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= en-keyword=NINEIN kn-keyword=NINEIN en-keyword=centrosome kn-keyword=centrosome en-keyword=single nucleotide polymorphism kn-keyword=single nucleotide polymorphism en-keyword=colon cancer kn-keyword=colon cancer en-keyword=tumor susceptibility kn-keyword=tumor susceptibility END start-ver=1.4 cd-journal=joma no-vol=49 cd-vols= no-issue=3 article-no= start-page=521 end-page=526 dt-received= dt-revised= dt-accepted= dt-pub-year=2007 dt-pub=20071121 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Rasmussen encephalitis associated with SCN1A mutation en-subtitle= kn-subtitle= en-abstract= kn-abstract= Mutations in the SCN 1 A gene, encoding the neuronal voltage-gated sodium channel alpha1 subunit, cause SMEI, GEFS+, and related epileptic syndromes. We herein report the R1575C-SCN 1 A mutation identified in a patient with Rasmussen encephalitis. R1575C were constructed in a recombinant human SCN 1 A and then heterologously expressed in HEK293 cells along with the human beta1 and beta2 sodium channel accessory subunits. Whole-cell patch-clamp recording was used to define biophysical properties. The R1575C channels exhibited increased channel availability and an increased persistent sodium current in comparison to the wild-type. These defects of electrophysiological properties can result in neuronal hyperexitability. The seizure susceptibility allele may influence the pathogenesis of Rasmussen encephalitis in this case. en-copyright= kn-copyright= en-aut-name=OhmoriIori en-aut-sei=Ohmori en-aut-mei=Iori 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=KobayashiKatsuhiro en-aut-sei=Kobayashi en-aut-mei=Katsuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=JitsumoriYoshimi en-aut-sei=Jitsumori en-aut-mei=Yoshimi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=InoueTakushi en-aut-sei=Inoue en-aut-mei=Takushi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 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=6 ORCID= en-aut-name=MatsuiHideki en-aut-sei=Matsui en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=OhtsukaYoko en-aut-sei=Ohtsuka en-aut-mei=Yoko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=MaegakiYoshihiro en-aut-sei=Maegaki en-aut-mei=Yoshihiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= affil-num=1 en-affil=Departments of Cellular Physiology, Graduate School of Medicine,Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=2 en-affil=Departments of Molecular Genetics, Graduate School of Medicine,Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=3 en-affil=Departments of Child Neurology, Graduate School of Medicine,Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=4 en-affil= kn-affil= affil-num=5 en-affil=Departments of Child Neurology, Graduate School of Medicine,Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=6 en-affil=Departments of Molecular Genetics, Graduate School of Medicine,Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=7 en-affil=Departments of Cellular Physiology, Graduate School of Medicine,Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=8 en-affil=Departments of Child Neurology, Graduate School of Medicine,Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=9 en-affil=Division of Child Neurology, Institute of Neurological Sciences, Faculty of Medicine, Tottori University kn-affil= en-keyword=Rasmussen encephalitis kn-keyword=Rasmussen encephalitis en-keyword=SCN1A kn-keyword=SCN1A en-keyword=genetic-environmental interaction kn-keyword=genetic-environmental interaction END start-ver=1.4 cd-journal=joma no-vol=71 cd-vols= no-issue=1 article-no= start-page=59 end-page=68 dt-received= dt-revised= dt-accepted= dt-pub-year=2017 dt-pub=201702 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Human RAD 17 Polymorphism at Codon 546 Is Associated with the Risk of Colorectal Cancer en-subtitle= kn-subtitle= en-abstract= kn-abstract=Human RAD17 acts as an activator of checkpoint signals in response to DNA damage. Here we evaluated the association of hRAD17 Leu546Arg (rs1045051), a missense single nucleotide polymorphism, with the risk of colorectal cancer (CRC) in relation to smoking and alcohol consumption habits in 212 CRC patients and 1,142 cancer-free controls in a case-control study conducted in Japan. The results showed that the hRAD17 Leu/Arg genotype compared to the Leu/Leu genotypes was significantly associated with the protective effect on CRC risk with the adjusted odds ratio (OR) of 0.68 [95% confidence interval (CI): 0.49−0.95, p=0.024], and the males with the Arg/Arg genotype had a greater risk of CRC compared to those with the Leu/Leu and Leu/Arg genotypes (OR=1.87, 95%CI 1.03−3.40, p=0.04). In stratified studies, the protective effect of the Leu/Arg genotype on CRC risk was markedly higher in the light smokers (< 20 pack years) (OR=0.61, 95%CI 0.40−0.94, p=0.024) and the rectal cancer patients (OR=0.49, 95%CI 0.31−0.78, p=0.003). The risk of the Arg/Arg genotype was associated with heavy smoking (≥ 20 pack-years) (OR=2.24, 95%CI 1.09−4.61, p=0.03). These findings suggest that the genetic variant of hRAD17 Leu546Arg polymorphism has a significant effect on CRC susceptibility in Japanese. en-copyright= kn-copyright= en-aut-name=YasudaYukiko en-aut-sei=Yasuda en-aut-mei=Yukiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=SakaiAkiko en-aut-sei=Sakai en-aut-mei=Akiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=ItoSachio en-aut-sei=Ito en-aut-mei=Sachio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=SasaiKaori en-aut-sei=Sasai en-aut-mei=Kaori 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=MatsubaraNagahide en-aut-sei=Matsubara en-aut-mei=Nagahide kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 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=7 ORCID= en-aut-name=KatayamaHiroshi en-aut-sei=Katayama en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 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=9 ORCID= affil-num=1 en-affil=Department of Molecular Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=2 en-affil=Department of Molecular Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=3 en-affil=Department of Molecular Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=4 en-affil=Department of Molecular Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=5 en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=6 en-affil=Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=7 en-affil=Department of Molecular Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=8 en-affil=Department of Molecular Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=9 en-affil=Department of Molecular Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= en-keyword=colorectal cancer kn-keyword=colorectal cancer en-keyword=single nucleotide polymorphism kn-keyword=single nucleotide polymorphism en-keyword=human RAD17 kn-keyword=human RAD17 en-keyword=DNA damage kn-keyword=DNA damage END start-ver=1.4 cd-journal=joma no-vol=65 cd-vols= no-issue=5 article-no= start-page=315 end-page=323 dt-received= dt-revised= dt-accepted= dt-pub-year=2011 dt-pub=201110 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Single Nucleotide Polymorphism WRN Leu1074Phe Is Associated with Prostate Cancer Susceptibility in Chinese Subjects en-subtitle= kn-subtitle= en-abstract= kn-abstract=Deficiencies in the human DNA repair gene WRN are the cause of Werner syndrome, a rare autosomal recessive disorder characterized by premature aging and a predisposition to cancer. This study evaluated the association of WRN Leu1074Phe (rs1801195), a common missense single nucleotide polymorphism in WRN, with prostate cancer susceptibility in Chinese subjects. One hundred and forty-seven prostate cancer patients and 111 male cancer-free control subjects from 3 university hospitals in China were included. Blood samples were obtained from each subject, and the single nucleotide polymorphism WRN Leu1074Phe was genotyped by using a Snapshot assay. The results showed that WRN Leu1074Phe was associated with the risk of prostate cancer in Chinese men and that the TG/GG genotype displayed a decreased prevalence of prostate cancer compared with the TT genotype (OR＝0.58, 95%CI:0.35-0.97, p＝0.039). Through stratified analysis, more significant associations were revealed for the TG/GG genotype in the subgroup with diagnosis age <_ 72 yr (OR＝0.27, 95%CI:0.12-0.61, p＝0.002) and in patients with localized diseases (OR＝0.36, 95%CI:0.19-0.70, p＝0.003). However, no statistically significant difference was found in the subgroup with age ＞72 yr or in patients with advanced diseases. We concluded that the genetic variant Leu1074Phe in the DNA repair gene WRN might play a role in the risk of prostate cancer in Chinese subjects. en-copyright= kn-copyright= en-aut-name=WangLei en-aut-sei=Wang en-aut-mei=Lei kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=KakuHaruki en-aut-sei=Kaku en-aut-mei=Haruki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=HuangPeng en-aut-sei=Huang en-aut-mei=Peng kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=XuKexin en-aut-sei=Xu en-aut-mei=Kexin kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=YangKai en-aut-sei=Yang en-aut-mei=Kai kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=ZhangJiheng en-aut-sei=Zhang en-aut-mei=Jiheng kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=LiMing en-aut-sei=Li en-aut-mei=Ming kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=XieLiping en-aut-sei=Xie en-aut-mei=Liping kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=WangXiaofeng en-aut-sei=Wang en-aut-mei=Xiaofeng kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=SakaiAkiko en-aut-sei=Sakai en-aut-mei=Akiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=WatanabeMasami en-aut-sei=Watanabe en-aut-mei=Masami kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 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=12 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=13 ORCID= en-aut-name=KumonHiromi en-aut-sei=Kumon en-aut-mei=Hiromi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=14 ORCID= en-aut-name=NaYanqun en-aut-sei=Na en-aut-mei=Yanqun kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=15 ORCID= affil-num=1 en-affil= kn-affil=Department of Urology, Peking University People's Hospital affil-num=2 en-affil= kn-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=3 en-affil= kn-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=4 en-affil= kn-affil=Department of Urology, Peking University People's Hospital affil-num=5 en-affil= kn-affil=Department of Urology, the First Affiliated Hospital, School of Medicine, Zhejiang University affil-num=6 en-affil= kn-affil=Department of Urology, Peking University School of Oncology, Beijing Cancer Hospital & Institute affil-num=7 en-affil= kn-affil=Department of Urology, Peking University School of Oncology, Beijing Cancer Hospital & Institute affil-num=8 en-affil= kn-affil=Department of Urology, the First Affiliated Hospital, School of Medicine, Zhejiang University affil-num=9 en-affil= kn-affil=Department of Urology, Peking University People's Hospital affil-num=10 en-affil= kn-affil=Department of Molecular Genetics, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=11 en-affil= kn-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=12 en-affil= kn-affil=Research and Develop Center for Advanced Clinical Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=13 en-affil= kn-affil=Department of Molecular Genetics, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=14 en-affil= kn-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=15 en-affil= kn-affil=Department of Urology, Peking University People's Hospital en-keyword=polymorphism kn-keyword=polymorphism en-keyword=prostatic neoplasms kn-keyword=prostatic neoplasms en-keyword=single nucleotide kn-keyword=single nucleotide en-keyword=susceptibility kn-keyword=susceptibility en-keyword=WRN kn-keyword=WRN 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=224 cd-vols= no-issue=2 article-no= start-page=311 end-page=319 dt-received= dt-revised= dt-accepted= dt-pub-year=2005 dt-pub=20050628 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Significant growth suppression of synovial sarcomas by the histone deacetylase inhibitor FK228 in vitro and in vivo en-subtitle= kn-subtitle= en-abstract= kn-abstract=About 97% of synovial sarcomas harbor the SYT-SSX fusion gene by chromosomal translocation. We found that the histone deacetylase (HDAC) inhibitor FK228 significantly suppressed the growth of synovial sarcoma cells as compared with that of osteosarcoma. The 50% growth inhibition IC50 value we obtained for FK228 was 0.02-0.2 nM, and it indicates that its suppression effect on synovial sarcoma cells is the highest of any of the HDAC inhibitors yet reported. It was not likely that the growth suppression of FK228 depends on the doubling time of these cells. Introduction of SYT-SSX cDNA into HEK293 cells enhanced the sensitivity of the cells for FK228. Immunostaining of the FK228-treated cells using an anti-acetyl-histone H3 antibody showed that FK228 inhibits deacetylation of histone. In a mice assay, the growth of synovial sarcoma cells was markedly inhibited by FK228 treatment, and the invasion of tumors into surrounding tissues was suppressed. These results suggest that FK228 may be useful in developing therapeutic strategies to treat synovial sarcoma. en-copyright= kn-copyright= en-aut-name=ItoTatsuo en-aut-sei=Ito en-aut-mei=Tatsuo 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=MorimotoYuki en-aut-sei=Morimoto en-aut-mei=Yuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=YoshidaAki en-aut-sei=Yoshida en-aut-mei=Aki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=JitsumoriYoshimi en-aut-sei=Jitsumori en-aut-mei=Yoshimi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=OzakiToshifumi en-aut-sei=Ozaki en-aut-mei=Toshifumi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=SonobeHiroshi en-aut-sei=Sonobe en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=InoueHajime en-aut-sei=Inoue en-aut-mei=Hajime kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 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=9 ORCID= affil-num=1 en-affil= kn-affil=Science of Functional Recovery and Reconstruction, 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=Science of Functional Recovery and Reconstruction, Graduate School of Medicine and Dentistry, Okayama University affil-num=4 en-affil= kn-affil=Science of Functional Recovery and Reconstruction, Graduate School of Medicine and Dentistry, Okayama University affil-num=5 en-affil= kn-affil=Department of Molecular Genetics, Graduate School of Medicine and Dentistry, Okayama University affil-num=6 en-affil= kn-affil=Science of Functional Recovery and Reconstruction, Graduate School of Medicine and Dentistry, Okayama University affil-num=7 en-affil= kn-affil=Department of Laboratory Medicine and Pathology, National Fukuyama Hospital affil-num=8 en-affil= kn-affil=Science of Functional Recovery and Reconstruction, Graduate School of Medicine and Dentistry, Okayama University affil-num=9 en-affil= kn-affil=Department of Molecular Genetics, Graduate School of Medicine and Dentistry, Okayama University en-keyword=histone deacetylase inhibitor kn-keyword=histone deacetylase inhibitor en-keyword=synovial sarcoma kn-keyword=synovial sarcoma en-keyword=growth inhibition kn-keyword=growth inhibition en-keyword=in vivo kn-keyword=in vivo END start-ver=1.4 cd-journal=joma no-vol=13 cd-vols= no-issue= article-no= start-page=11 end-page=18 dt-received= dt-revised= dt-accepted= dt-pub-year=1996 dt-pub=199609 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=細胞癌化の機構 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=ShimizuKenji en-aut-sei=Shimizu en-aut-mei=Kenji kn-aut-name=清水憲二 kn-aut-sei=清水 kn-aut-mei=憲二 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部病態遺伝子解析部門 END start-ver=1.4 cd-journal=joma no-vol=114 cd-vols= no-issue=3 article-no= start-page=309 end-page=323 dt-received= dt-revised= dt-accepted= dt-pub-year=2003 dt-pub=20030131 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=ヒト癌における遺伝子異常の検索と遺伝子診断 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=清水憲二 kn-aut-sei=清水 kn-aut-mei=憲二 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学大学院医歯学総合研究科　腫瘍制御学講座・分子遺伝学分野 en-keyword=癌遺伝子 kn-keyword=癌遺伝子 en-keyword=癌抑制遺伝子 kn-keyword=癌抑制遺伝子 en-keyword=遺伝子異常 kn-keyword=遺伝子異常 en-keyword=遺伝子診断 kn-keyword=遺伝子診断 en-keyword=早期発見 kn-keyword=早期発見 END start-ver=1.4 cd-journal=joma no-vol=119 cd-vols= no-issue=2 article-no= start-page=113 end-page=117 dt-received= dt-revised= dt-accepted= dt-pub-year=2007 dt-pub=20070903 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Accumulating DNA methylation in background mucosa plays a role in esophageal squamous cell carcinogenesis kn-title=食道扁平上皮癌の発癌過程におけるDNAメチル化の役割 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=IshiiTatsuhiro en-aut-sei=Ishii en-aut-mei=Tatsuhiro kn-aut-name=石井龍宏 kn-aut-sei=石井 kn-aut-mei=龍宏 aut-affil-num=1 ORCID= en-aut-name=MurakamiJun en-aut-sei=Murakami en-aut-mei=Jun kn-aut-name=村上純 kn-aut-sei=村上 kn-aut-mei=純 aut-affil-num=2 ORCID= en-aut-name=NotoharaKenji en-aut-sei=Notohara en-aut-mei=Kenji kn-aut-name=能登原憲司 kn-aut-sei=能登原 kn-aut-mei=憲司 aut-affil-num=3 ORCID= en-aut-name=SasamotoHiromi en-aut-sei=Sasamoto en-aut-mei=Hiromi kn-aut-name=笹本博美 kn-aut-sei=笹本 kn-aut-mei=博美 aut-affil-num=4 ORCID= en-aut-name=KambaraTakeshi en-aut-sei=Kambara en-aut-mei=Takeshi kn-aut-name=神原健 kn-aut-sei=神原 kn-aut-mei=健 aut-affil-num=5 ORCID= en-aut-name=ShirakawaYasuhiro en-aut-sei=Shirakawa en-aut-mei=Yasuhiro kn-aut-name=白川靖博 kn-aut-sei=白川 kn-aut-mei=靖博 aut-affil-num=6 ORCID= en-aut-name=NaomotoYoshio en-aut-sei=Naomoto en-aut-mei=Yoshio kn-aut-name=猶本良夫 kn-aut-sei=猶本 kn-aut-mei=良夫 aut-affil-num=7 ORCID= en-aut-name=OuchidaMamoru en-aut-sei=Ouchida en-aut-mei=Mamoru kn-aut-name=大内田守 kn-aut-sei=大内田 kn-aut-mei=守 aut-affil-num=8 ORCID= en-aut-name=ShimizuKenji en-aut-sei=Shimizu en-aut-mei=Kenji kn-aut-name=清水憲二 kn-aut-sei=清水 kn-aut-mei=憲二 aut-affil-num=9 ORCID= en-aut-name=JeremyR. Jass en-aut-sei=Jeremy en-aut-mei=R. Jass kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=MatsubaraNagahide en-aut-sei=Matsubara en-aut-mei=Nagahide kn-aut-name=松原長秀 kn-aut-sei=松原 kn-aut-mei=長秀 aut-affil-num=11 ORCID= en-aut-name=TanakaNoriaki en-aut-sei=Tanaka en-aut-mei=Noriaki kn-aut-name=田中紀章 kn-aut-sei=田中 kn-aut-mei=紀章 aut-affil-num=12 ORCID= affil-num=1 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 消化器・腫瘍外科学 affil-num=2 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 歯科口腔放射線学 affil-num=3 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 病態探究医学 affil-num=4 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 消化器・腫瘍外科学 affil-num=5 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 消化器・腫瘍外科学 affil-num=6 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 消化器・腫瘍外科学 affil-num=7 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 消化器・腫瘍外科学 affil-num=8 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 分子遺伝学 affil-num=9 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 分子遺伝学 affil-num=10 en-affil= kn-affil=Department of Pathology, McGill University affil-num=11 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 消化器・腫瘍外科学 affil-num=12 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 消化器・腫瘍外科学 en-keyword=食道扁平上皮癌 kn-keyword=食道扁平上皮癌 en-keyword=プロモーターメチル化 kn-keyword=プロモーターメチル化 en-keyword=p53遺伝子変異 kn-keyword=p53遺伝子変異 END