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Jun, Ikhyun,Rim, John Hoon,Kim, Mee Kum,Yoon, Kyung-Chul,Joo, Choun-Ki,Kinoshita, Shigeru,Seo, Kyoung Yul,Ueta, Mayumi British Medical Association 2019 British journal of ophthalmology Vol.103 No.4
<P><B>Background/aims</B></P><P>Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are a spectrum of diseases that cause an acute vesiculobullous reaction in the skin and mucous membranes. The occurrence of these diseases is associated with various drugs, a large proportion of which is comprised cold medicines (CM). We try to investigate the association between human leucocyte antigen (HLA) class I genes and CM-related SJS/TEN (CM-SJS/TEN) with severe ocular complications (SOC) in the Korean population.</P><P><B>Methods</B></P><P>This multicentre case-control study enrolled 40 Korean patients with CM-SJS/TEN with SOC and 120 age-matched and sex-matched Korean healthy volunteers between January 2012 and May 2014. HLA genotyping was performed using PCR followed by hybridisation with sequence-specific oligonucleotide probes.</P><P><B>Results </B></P><P>The carrier frequency and gene frequency of HLA-A*02:06 were 37.5 % and 20.0 %, respectively, in patients, and 16.7 % and 9.6 %, respectively, in controls (p=0.018). The carrier frequency of HLA-C*03:04 was 30 % in patients and 10.8 % in controls, and gene frequency of HLA-C*03:04 was 15 % in patients and 5.4 % in controls (p=0.003). The carrier frequency and gene frequency of HLA-C*03:03 were 2.5 % and 1.3 %, respectively, in patients, and 20 % and 10.4 %, respectively, in controls (p=0.006).</P><P><B>Conclusions </B></P><P>As per our results, we suggest that HLA-A*02:06 and HLA-C*03:04 might be positive markers for CM-SJS/TEN with SOC, and HLA-C*03:03 might be an indicator of protection against CM-SJS/TEN with SOC in the Korean population.</P>
Hu, Nan,Wang, Zhaoming,Song, Xin,Wei, Lixuan,Kim, Byung Sik,Freedman, Neal D,Baek, Jiwon,Burdette, Laurie,Chang, Jiang,Chung, Charles,Dawsey, Sanford M,Ding, Ti,Gao, Yu-Tang,Giffen, Carol,Han, Yaling British Medical Association 2016 Gut Vol.65 No.10
<P>Objective Genome-wide association studies (GWAS) of gastric cancer have reported differences in single-nucleotide polymorphism (SNP) associations for tumour subtypes, particularly when divided by location into the gastric cardia versus the non-cardia. Design Here we present results for a GWAS using 2350 East Asian gastric cancer cases divided as 1189 gastric cardia and 1027 gastric non-cardia cases and 2708 controls. We also included up to 3042 cardia cases, 4359 non-cardia cases and 7548 controls for replication from two Chinese studies and one Korean study. From the GWAS, we selected 12 top SNPs for each gastric cancer subtype, 4 top SNPs for total gastric cancer and 1 SNP in MUC1 for replication testing. Results We observed genome-wide significant associations for rs10074991 in PRKAA1 at 5p13.1 for cardia (p=7.36x10(-12)) and non-cardia cancers (p=2.42x10(-23)) with per allele OR (95% CI) for the combined endpoint of 0.80 (0.77 to 0.83). At 6p21.1, rs2294693 near UNC5CL was significantly associated with gastric non-cardia cancer risk (p=2.50x10(-8)), with OR (95% CI) of 1.18 (1.12 to 1.26), but there was only a nominal association for cardia cancer (p=1.47x10(-2)). We also confirmed a previously reported association for rs4072037 in MUC1 with p=6.59x10(-8) for total gastric cancer and similar estimates for cardia and non-cardia cancers. Three SNPs in PSCA previously reported to be associated with gastric non-cardia cancer showed no apparent association for cardia cancer. Conclusions Our results suggest that associations for SNPs with gastric cancer show some different results by tumour location in the stomach.</P>
Yoo, So Young,Kim, Tae-Im,Lee, Sang Yup,Kim, Eung Kweon,Keum, Ki Chang,Yoo, Nae Choon,Yoo, Won Min British Medical Association 2007 British journal of ophthalmology Vol.91 No.6
<P>AIM: To develop a diagnostic DNA chip to detect mutations in the betaigh3 gene causing the most common corneal dystrophies (CDs). METHODS: Samples from 98 people, including patients with betaigh3-associated CDs (beta-aCDs), were examined. Specific primer and probe sets were designed to examine exons 4 and 12 of the betaigh3 gene, in order to identify mutant and wild-type alleles. Mutations were then identified by hybridisation signals of sequence-specific probes immobilised on the slide glass. RESULTS: Direct sequencing of exons 4 and 12 of the betaigh3 gene in the patients' genome showed that beta-aCDs could be mainly classified into five types: homozygotic Avellino corneal dystrophy (ACD), heterozygotic ACD, heterozygotic lattice CD I, heterozygotic Reis-Bucklers CD and heterozygotic granular CD. Blind tests were performed by applying the target DNA amplified from the genomic DNA isolated from the peripheral blood of the participants onto a DNA chip. The results obtained by DNA chip hybridisation matched well with the direct DNA sequencing results. CONCLUSIONS: The DNA chip developed in this study allowed successful detection of beta-aCDs with a sensitivity of 100%. Mutational analysis of exons 4 and 12 of the betaigh3 gene, which are the mutational hot spots causing beta-aCDs, can be successfully performed with the DNA chip. Thus, this DNA chip-based method should allow a convenient, yet highly accurate, diagnosis of beta-aCDs, and can be further applied to diagnose other types of CDs.</P>
Lee, Ji Hee,Bae, Jeong A,Lee, Jae Hyuk,Seo, Young-Woo,Kho, Dhong Hyo,Sun, Eun Gene,Lee, Song Eun,Cho, Sang Hee,Joo, Young Eun,Ahn, Kyu Youn,Chung, Ik Joo,Kim, Kyung Keun British Medical Association 2010 Gut Vol.59 No.7
<P>BACKGROUND AND AIMS: 90K, a tumour-associated glycoprotein, interacts with galectins and has roles in host defence by augmenting the immune response, but the serum 90K level was suggested to indicate poor prognosis in several cancers. The cellular mechanisms of 90K action on colorectal cancer (CRC) cell motility and its effect on CRC progression were investigated. METHODS: The impact of 90K was analysed by combining cell cultures, in vitro assays, and immunohistochemistry. RESULTS: Secreted 90K suppresses CRC cell invasion, but this action of 90K is masked through binding with extracellular galectins. A novel pathway is identified comprising a secretory 90K and a CD9/CD82 tetraspanin web; in this pathway, 90K interacts with CD9/CD82, suppresses the Wnt/beta-catenin signal via a novel proteasomal-ubiquitination mechanism of beta-catenin that is dependent on ISG15 (interferon-stimulated gene-15) modification (ISGylation) but not on glycogen synthase kinase 3beta (GSK-3beta) and Siah/Adenomatous polyposis coli (APC). In a syngeneic mouse colon tumour model, tumour growth and lung metastasis were increased with 90K knockdown. In colon tissues from stage IV human CRC and invading cancer cells of corresponding metastatic liver tissues, in which beta-catenin and galectin expression was higher, immunostained 90K and CD9/CD82 were lower than in adjacent hepatic tissues or colon tissues from stage I. CONCLUSIONS: 90K itself has antitumour activity in CRC cells via suppression of Wnt signalling with a novel mechanism of ISGylation-dependent ubiquitination of beta-catenin when it interacts with CD9/CD82, but is downregulated in advanced CRC tissues. The data suggest a strategy of strengthening this novel pathway with concomitant knockdown of galectins as a potential therapeutic approach to CRC progression.</P>