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  <Article>
    <Journal>
      <PublisherName>Okayama University Medical School</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0386-300X</Issn>
      <Volume>75</Volume>
      <Issue>4</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2021</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>The Cell Cycle Checkpoint Gene, RAD17 rs1045051, Is Associated with Prostate Cancer Risk</ArticleTitle>
    <FirstPage LZero="delete">415</FirstPage>
    <LastPage>421</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Jingkai</FirstName>
        <LastName>Sun</LastName>
        <Affiliation>Department of Urology, Zhujiang Hospital, Southern Medical University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Wenfeng</FirstName>
        <LastName>Lin</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Qixu</FirstName>
        <LastName>Wang</LastName>
        <Affiliation>Department of Urology, Zhujiang Hospital, Southern Medical University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Akiko</FirstName>
        <LastName>Sakai</LastName>
        <Affiliation>Department of Molecular Genetics,  Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Ruizhi</FirstName>
        <LastName>Xue</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Masami</FirstName>
        <LastName>Watanabe</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Chunxiao</FirstName>
        <LastName>Liu</LastName>
        <Affiliation>Department of Urology, Zhujiang Hospital, Southern Medical University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takuya</FirstName>
        <LastName>Sadahira</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yasutomo</FirstName>
        <LastName>Nasu</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Abai</FirstName>
        <LastName>Xu</LastName>
        <Affiliation>Department of Urology, Zhujiang Hospital, Southern Medical University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Peng</FirstName>
        <LastName>Huang</LastName>
        <Affiliation>Department of Urology, Zhujiang Hospital, Southern Medical University</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType>Original Article</PublicationType>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/AMO/62379</ArticleId>
    </ArticleIdList>
    <Abstract>Human RAD17, as an agonist of checkpoint signaling, plays an essential role in mediating DNA damage. This hospital-based case-control study aimed to explore the association between RAD17 rs1045051, a missense sin-gle nucleotide polymorphism (SNP), and prostate cancer risk. Subjects were 358 prostate cancer patients and 314 cancer-free urology patients undergoing treatment at the Zhujiang Hospital of Southern Medical University in China. RAD17 gene polymorphism rs1045051 was evaluated by the SNaPshot method. Compared with the RAD17 gene polymorphism rs1045051 AA genotype, there was a higher risk of prostate cancer for the CC gen-otype (adjusted odds ratio [AOR] = 1.731, 95% confidence interval [95%CI] = 1.031|2.908, p = 0.038). Compared with the A allele, the C allele was significantly associated with the disease status (AOR = 1.302, 95%CI = 1.037|1.634, p = 0.023). All these findings indicate that in the SNP rs1045051, both the CC genotype and C allele may have a substantial influence on the prostate cancer risk.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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        <Param Name="value">cell cycle checkpoint</Param>
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  </Article>
  <Article>
    <Journal>
      <PublisherName>Spandidos Publications</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>2049-9434</Issn>
      <Volume>13</Volume>
      <Issue>5</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2020</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Human NINEIN polymorphism at codon 1111 is associated with the risk of colorectal cancer</ArticleTitle>
    <FirstPage LZero="delete">45</FirstPage>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Yukiko</FirstName>
        <LastName>Yasuda</LastName>
        <Affiliation>Department of Molecular Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Akiko</FirstName>
        <LastName>Sakai</LastName>
        <Affiliation>Department of Molecular Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Sachio</FirstName>
        <LastName>Ito</LastName>
        <Affiliation>Department of Molecular Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kaori</FirstName>
        <LastName>Sasai</LastName>
        <Affiliation>Department of Molecular Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Akisada</FirstName>
        <LastName>Ishizaki</LastName>
        <Affiliation>Department of Molecular Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshiya</FirstName>
        <LastName>Okano</LastName>
        <Affiliation>Department of Molecular Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Seito</FirstName>
        <LastName>Kawahara</LastName>
        <Affiliation>Department of Molecular Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshimi</FirstName>
        <LastName>Jitsumori</LastName>
        <Affiliation>Department of Molecular Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiromasa</FirstName>
        <LastName>Yamamoto</LastName>
        <Affiliation>Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Nagahide</FirstName>
        <LastName>Matsubara</LastName>
        <Affiliation>Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kenji</FirstName>
        <LastName>Shimizu</LastName>
        <Affiliation>Department of Molecular Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroshi</FirstName>
        <LastName>Katayama</LastName>
        <Affiliation>Department of Molecular Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
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      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <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&#8209;free control participants were assessed in a case&#8209;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 (&lt;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.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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      </Object>
      <Object Type="keyword">
        <Param Name="value">centrosome</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">single nucleotide polymorphism</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">colon cancer</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">tumor susceptibility</Param>
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  </Article>
  <Article>
    <Journal>
      <PublisherName>Okayama University Medical School</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0386-300X</Issn>
      <Volume>71</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2017</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Human RAD 17 Polymorphism at Codon 546 Is Associated with the Risk of Colorectal Cancer</ArticleTitle>
    <FirstPage LZero="delete">59</FirstPage>
    <LastPage>68</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Yukiko</FirstName>
        <LastName>Yasuda</LastName>
        <Affiliation>Department of Molecular Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Akiko</FirstName>
        <LastName>Sakai</LastName>
        <Affiliation>Department of Molecular Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Sachio</FirstName>
        <LastName>Ito</LastName>
        <Affiliation>Department of Molecular Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kaori</FirstName>
        <LastName>Sasai</LastName>
        <Affiliation>Department of Molecular Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiromasa</FirstName>
        <LastName>Yamamoto</LastName>
        <Affiliation>Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Nagahide</FirstName>
        <LastName>Matsubara</LastName>
        <Affiliation>Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Mamoru</FirstName>
        <LastName>Ouchida</LastName>
        <Affiliation>Department of Molecular Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroshi</FirstName>
        <LastName>Katayama</LastName>
        <Affiliation>Department of Molecular Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kenji</FirstName>
        <LastName>Shimizu</LastName>
        <Affiliation>Department of Molecular Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType>Original Article</PublicationType>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/AMO/54826</ArticleId>
    </ArticleIdList>
    <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 (&lt; 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 (&#8805; 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.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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        <Param Name="value">colorectal cancer</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">single nucleotide polymorphism</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">human RAD17</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">DNA damage</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Okayama University Medical School</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0386-300X</Issn>
      <Volume>65</Volume>
      <Issue>5</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2011</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Single Nucleotide Polymorphism WRN Leu1074Phe Is Associated with Prostate Cancer Susceptibility in Chinese Subjects</ArticleTitle>
    <FirstPage LZero="delete">315</FirstPage>
    <LastPage>323</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Lei</FirstName>
        <LastName>Wang</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Haruki</FirstName>
        <LastName>Kaku</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Peng</FirstName>
        <LastName>Huang</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kexin</FirstName>
        <LastName>Xu</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kai</FirstName>
        <LastName>Yang</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Jiheng</FirstName>
        <LastName>Zhang</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Ming</FirstName>
        <LastName>Li</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Liping</FirstName>
        <LastName>Xie</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Xiaofeng</FirstName>
        <LastName>Wang</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Akiko</FirstName>
        <LastName>Sakai</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Masami</FirstName>
        <LastName>Watanabe</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yasutomo</FirstName>
        <LastName>Nasu</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kenji</FirstName>
        <LastName>Shimizu</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiromi</FirstName>
        <LastName>Kumon</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yanqun</FirstName>
        <LastName>Na</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType>Original Article</PublicationType>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/AMO/47013</ArticleId>
    </ArticleIdList>
    <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 &lt;_ 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.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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        <Param Name="value">WRN</Param>
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  </Article>
  <Article>
    <Journal>
      <PublisherName>Okayama University Medical School</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0386-300X</Issn>
      <Volume>42</Volume>
      <Issue>4</Issue>
      <PubDate PubStatus="ppublish">
        <Year>1988</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Two human papillomavirus DNAs molecularly cloned from a patient with epidermodysplasia verruciformis: restriction maps.</ArticleTitle>
    <FirstPage LZero="delete">243</FirstPage>
    <LastPage>245</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Yoshiro</FirstName>
        <LastName>Yabe</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Akiko</FirstName>
        <LastName>Sakai</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshie</FirstName>
        <LastName>Tanimura</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Masae</FirstName>
        <LastName>Kuramitsu</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takako</FirstName>
        <LastName>Hitsumoto</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kanji</FirstName>
        <LastName>Ishii</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroaki</FirstName>
        <LastName>Ueki</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType>Article</PublicationType>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/AMO/30999</ArticleId>
    </ArticleIdList>
    <Abstract>&lt;p&gt;Two distinct human papillomavirus (HPV) DNAs (MY-1 and MY-2) were molecularly cloned from the benign skin lesions of a patient with epidermodysplasia verruciformis. The restriction map of MY-1 was the same as that of HPV 3a. The map of MY-2 appeared to be different from those of any HPVs reported in the literature. MY-2 did not cross-hybridize with MY-1 or the DNAs of HPV types 1, 2 and 4 under stringent conditions.&lt;/p&gt;
</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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        <Param Name="value">molecular cloning</Param>
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        <Param Name="value">epidermodysplasia verruciformis</Param>
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  </Article>
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