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=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=75
cd-vols=
no-issue=4
article-no=
start-page=415
end-page=421
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=202108
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The Cell Cycle Checkpoint Gene, RAD17 rs1045051, Is Associated with Prostate Cancer Risk
en-subtitle=
kn-subtitle=
en-abstract=
kn-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.
en-copyright=
kn-copyright=

en-aut-name=SunJingkai
en-aut-sei=Sun
en-aut-mei=Jingkai
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=LinWenfeng
en-aut-sei=Lin
en-aut-mei=Wenfeng
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=WangQixu
en-aut-sei=Wang
en-aut-mei=Qixu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
ORCID=

en-aut-name=XueRuizhi
en-aut-sei=Xue
en-aut-mei=Ruizhi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
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=6
ORCID=

en-aut-name=LiuChunxiao
en-aut-sei=Liu
en-aut-mei=Chunxiao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=SadahiraTakuya
en-aut-sei=Sadahira
en-aut-mei=Takuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
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=9
ORCID=

en-aut-name=XuAbai
en-aut-sei=Xu
en-aut-mei=Abai
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
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=11
ORCID=

affil-num=1
en-affil=Department of Urology, Zhujiang Hospital, Southern Medical University
kn-affil=

affil-num=2
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Urology, Zhujiang Hospital, Southern Medical University
kn-affil=

affil-num=4
en-affil=Department of Molecular Genetics,  Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Urology, Zhujiang Hospital, Southern Medical University
kn-affil=

affil-num=8
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of Urology, Zhujiang Hospital, Southern Medical University
kn-affil=

affil-num=11
en-affil=Department of Urology, Zhujiang Hospital, Southern Medical University
kn-affil=
en-keyword=prostate cancer
kn-keyword=prostate cancer
en-keyword=single-nucleotide polymorphisms
kn-keyword=single-nucleotide polymorphisms
en-keyword=cell cycle checkpoint
kn-keyword=cell cycle checkpoint
en-keyword=rs1045051
kn-keyword=rs1045051
en-keyword=RAD17
kn-keyword=RAD17
END

start-ver=1.4
cd-journal=joma
no-vol=42
cd-vols=
no-issue=4
article-no=
start-page=243
end-page=245
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1988
dt-pub=198808
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Two human papillomavirus DNAs molecularly cloned from a patient with epidermodysplasia verruciformis: restriction maps.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>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.</p>

en-copyright=
kn-copyright=

en-aut-name=YabeYoshiro
en-aut-sei=Yabe
en-aut-mei=Yoshiro
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=TanimuraYoshie
en-aut-sei=Tanimura
en-aut-mei=Yoshie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KuramitsuMasae
en-aut-sei=Kuramitsu
en-aut-mei=Masae
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HitsumotoTakako
en-aut-sei=Hitsumoto
en-aut-mei=Takako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=IshiiKanji
en-aut-sei=Ishii
en-aut-mei=Kanji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=UekiHiroaki
en-aut-sei=Ueki
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
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
en-keyword=papillomavirus
kn-keyword=papillomavirus
en-keyword=viral DNA
kn-keyword=viral DNA
en-keyword=molecular cloning
kn-keyword=molecular cloning
en-keyword=restriction map
kn-keyword=restriction map
en-keyword=epidermodysplasia verruciformis
kn-keyword=epidermodysplasia verruciformis
END