Doyeun Oh

CHA University, Sŏul, Seoul, South Korea

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Publications (106)209.08 Total impact

  • British Journal of Haematology 06/2015; DOI:10.1111/bjh.13564 · 4.96 Impact Factor
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    ABSTRACT: Polymorphisms in the methylenetetrahydrofolate reductase (MTHFR) play important roles in tumor development, progression, and metastasis. Moreover, recent studies have reported that a number of 3′-UTR polymorphisms potentially bind to specific microRNAs in a variety of cancers. The aim of this study was to investigate the association of four MTHFR polymorphisms, 2572C>A [rs4846049], 4869C>G [rs1537514], 5488C>T [rs3737967], and 6685T>C [rs4846048] with colorectal cancer (CRC) in Koreans. A total of 850 participants (450 CRC patients and 400 controls) were enrolled in the study. The genotyping of MTHFR 3′-UTR polymorphisms was performed by polymerase chain reaction-restriction fragment length polymorphism analysis or TaqMan allelic discrimination assay. We found that MTHFR 2572C>A, 4869C>G, and 5488C>T genotypes were substantially associated with CRC susceptibility. Of the potentially susceptible polymorphisms, MTHFR 2572C>A was associated with increased homocysteine and decreased folate levels in the plasma based on MTHFR 677CC. Our study provides the evidences for 3′-UTR variants in MTHFR gene as potential biomarkers for use in CRC prevention.
    Scientific Reports 06/2015; 5. DOI:10.1038/srep11006 · 5.58 Impact Factor
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    Molecular and Clinical Oncology 02/2015; DOI:10.3892/mco.2015.520
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    ABSTRACT: Bortezomib (Velcade®) came into the spotlight as a target therapy for multiple myeloma. It acts through reversible inhibition of intracellular proteasomes, which triggers apoptosis, with relative selectivity for malignant cells. It has been hypothesized that the accumulation of damaged proteins in myocytes impairs cardiac function. Cardiotoxicity is a rare side effect of bortezomib treatment. We report a case of reversible systolic heart failure that probably occurred after bortezomib treatment in a patient with multiple myeloma. Patients being treated with bortezomib who have previously had cardiac comorbidities should undergo routine cardiac monitoring.
    01/2015; 88(4):459. DOI:10.3904/kjm.2015.88.4.459
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    ABSTRACT: Polymorphisms in angiogenesis-related genes and metabolic syndrome (MetS) risk factors play important roles in cancer development. Moreover, recent studies have reported associations between a number of 3[prime]-UTR polymorphisms and a variety of cancers. The aim of this study was to investigate the associations of three VEGF 3[prime]-UTR polymorphisms (1451C > T [rs3025040], 1612G > A [rs10434], and 1725G > A [rs3025053]) and MS with colorectal cancer (CRC) susceptibility in Koreans. A total of 850 participants (450 CRC patients and 400 controls) were enrolled in the study. The genotyping of VEGF polymorphisms was performed by TaqMan allelic discrimination assays. Cancer risks of genetic variations and gene-environment interactions were assessed by adjusted odds ratios (AORs) and 95% confidence intervals (CIs) of multivariate logistic regression analyses. VEGF 1451C > T was significantly associated with rectal cancer risk (Dominant model; AOR =1.58; 95% CI =1.09 - 2.28; p =0.015) whereas VEGF 1725G > A correlated with MetS risk (Dominant model; AOR =1.61; 95% CI =1.06 - 2.46; p =0.026). Of the gene-environment combined effects, the interaction of VEGF 1451C > T and MetS contributed to increased RC risk (AOR =3.15; 95% CI =1.74 - 5.70; p < .001) whereas the combination of VEGF 1725G > A and MetS was involved with elevated CC risk (AOR =2.68; 95% CI =1.30 - 1.55; p =0.008). Our results implicate that VEGF 1451C > T and 1725G > A may predispose to CRC susceptibility and the genetic contributions may be varied with the presence of MetS.
    BMC Cancer 11/2014; 14(1):881. DOI:10.1186/1471-2407-14-881 · 3.32 Impact Factor
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    ABSTRACT: To gain insight into the natural history of cytomegalovirus (CMV) infection following unrelated cord blood transplantation (UCBT) in seropositive patients, we analyzed the data of 349 seropositive patients who received UCBT in Korea between 2000 and 2011. CMV reactivation occurred in 49 % (171/349) of the CMV-seropositive transplant recipients at a median of 31 days post UCBT. One hundred sixty-four out of 171 patients (96 %) received preemptive therapy. The median duration of CMV reactivation was 29 days. In multivariate analysis, weight >22 kg, use of total body irradiation, use of pre-transplant antithymocyte globulin, graft-versus-host disease (GVHD) prophylaxis with mycophenolate mofetil, and presence of grade II-IV acute GVHD were independent predictors of CMV reactivation. CMV reactivation did not impact transplantation-related mortality (TRM), leukemia relapse, or survival. CMV disease was diagnosed in 62 patients (17.8 %) at a median 55 days after UCBT. Longer duration of CMV reactivation was the only risk factor for progression to CMV disease (p = 0.01). CMV disease resulted in higher TRM (56.0 vs. 31.4 %, p < 0.01) and lower survival (36.1 vs. 55.1 %, p = 0.02).
    Annals of Hematology 11/2014; 94(3). DOI:10.1007/s00277-014-2222-x · 2.40 Impact Factor
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    ABSTRACT: Objective The metabolic syndrome (MetS) may contribute to the pathogenesis of venous thromboembolism (VTE), but this association requires additional investigation. Approach and Results We performed a patient-level meta-analysis of case-control and cohort studies that evaluated the role of MetS and risk of unprovoked VTE. For case-control studies, odds ratios and 95% confidence intervals were calculated using logistic regression analysis to estimate the influence of individual variables on the risk of VTE; (2) tests for trend were used to investigate the effect of increasing number of components of MetS on the risk of VTE and to explore the influence of abdominal obesity on this relationship. For cohort studies, hazard ratios and 95% confidence interval were calculated using multivariable Cox regression analysis. Six case-control studies were included (908 cases with unprovoked VTE and 1794 controls): in multivariate analysis, MetS was independently associated with VTE (odds ratio, 1.91; 95% confidence interval, 1.57-2.33), and both MetS and abdominal obesity were better predictors of unprovoked VTE than obesity defined by the body mass index. Two prospective cohort studies were included (26531 subjects and 289 unprovoked VTE events): age, obesity, and abdominal obesity, but not MetS were associated with VTE. Conclusions Case-control but not prospective cohort studies support an association between MetS and VTE. Abdominal adiposity is a strong risk factor for VTE.
    Arteriosclerosis Thrombosis and Vascular Biology 09/2014; 34(11). DOI:10.1161/ATVBAHA.114.304085 · 5.53 Impact Factor
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    ABSTRACT: Hereditary protein S deficiency from a mutation in the PROS1 gene causes a genetic predisposition to develop venous thromboembolic disorders in humans. Recently, the acknowledgment of the clinical significance of large copy number mutations in protein S deficiency has increased. In this study, the authors investigated the genomic architecture of PROS1 in order to understand the microscopic sequence environment leading to large intragenic copy number mutations in the gene. The study subjects were 3 unrelated male patients with hereditary protein S deficiency from a tandem duplication mutation involving exons 5-10 of PROS1. Breakpoint analyses revealed 10-bp microhomology sequences in the intervening sequence (IVS)-4 and IVS-10 at the duplication junction without additional sequence changes, suggesting a single replication-based event as the potential molecular mechanism of rearrangement and founder effect in the mutant alleles. Further analyses on nucleotide sequences flanking the microhomology sequence revealed the presence of a repeat element (LTR-ERV1) and quadruplex-forming G-rich sequences in IVS-4. The results from genotyping multi-allelic short tandem repeats supported founder effect in the identical mutations in the 3 unrelated patients. In conclusion, we identified unique genomic architectures in the intervening sequences of PROS1 that underlie a large intragenic tandem duplication mutation leading to inherited thrombophilia.
    Gene 06/2014; DOI:10.1016/j.gene.2014.06.067 · 2.08 Impact Factor
  • 05/2014; 1(1):17-21. DOI:10.14345/ceth.14006
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    ABSTRACT: Background Data on the incidence of venous thromboembolism (VTE) following major surgery in Asian populations are limited.Methods Using the Korean Health Insurance Review and Assessment Service database, we performed a nationwide population-based epidemiologic study to estimate the incidence of VTE after major orthopaedic, cancer, and benign surgeries. VTE cases were identified from all patients undergoing major surgery between 2007 and 2011 using both diagnostic and drug codes as treatment evidence of VTE within 5 weeks of surgery. We also calculated the relative risk of VTE in major orthopaedic and cancer surgery compared to benign surgery.ResultsThe overall rates of postoperative VTE were 1.24%, 0.67%, and 0.05% for major orthopaedic, cancer, and benign surgeries, respectively. Hip fracture (1.60%) and colorectal cancer surgeries (1.67%) were associated with the highest rates of VTE, and the rates steadily increased during the study period. Advanced age, female sex, and general anaesthesia were independent risk factors for VTE. Patients undergoing surgery for colorectal, pancreatic, ovarian, and oesophageal cancer, and major orthopaedic surgery had more than a 20-fold higher risk of VTE than those undergoing benign surgery.Conclusions This is the largest epidemiologic study to investigate the incidence of VTE after major surgery in Asia, demonstrating that the rates of postoperative VTE are lower than in Caucasian populations. This study contributes to a better understanding of the differences in postoperative VTE development between Korean and Caucasian populations; the data also suggest that perioperative prophylactic strategies in Asians should be based on studies of such populations.This article is protected by copyright. All rights reserved.
    Journal of Thrombosis and Haemostasis 05/2014; 12(7). DOI:10.1111/jth.12611 · 5.55 Impact Factor
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    ABSTRACT: Silent brain infarction (SBI) is an asymptomatic cerebrovascular disorder. The aim of the present study was to investigate the association between adrenoceptor‑α2 (ADRA2) gene polymorphisms and SBI. A total of 361 patients with SBI and 467 healthy control subjects were examined. The polymerase chain reaction was performed to genotype the ADRA2A 1780G>A, ADRA2B 301‑303 insertion/deletion (I/D) and ADRA2C 322‑325I/D polymorphisms. The frequency of the ADRA2C 322‑325I/D polymorphism was significantly different between patients with SBI and control subjects. When interaction analyses were performed for vascular risk factors, the ADRA2C 322‑325ID genotype increased the risk for SBI in the presence of hypertension and elevated plasma homocysteine levels. The ADRA2C 322‑325ID genotype and plasma homocysteine levels showed a significant synergistic effect for SBI. In addition, the ADRA2A 1780AA genotype was associated with elevated plasma homocysteine levels. Although further analysis of the association between ADRA2 polymorphisms and clinical risk factors of SBI is required, the present study of a limited set of SBI risk factors with ADRA2 polymorphisms provides the first evidence of the involvement of ADRA2 gene family members in the development of SBI. Further studies using larger and more heterogeneous populations are required to validate the association of ADRA2 polymorphisms with SBI.
    Molecular Medicine Reports 03/2014; 9(6). DOI:10.3892/mmr.2014.2072 · 1.48 Impact Factor
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    ABSTRACT: Oxaliplatin is a platinum compound used in patients with gastrointestinal malignancies. It is known to evoke a drug-induced immune-mediated thrombocytopenia, which has not been reported in Korea. We describe a 53-year-old man who developed oxaliplatin-induced immune-mediated thrombocytopenia during chemotherapy for colon cancer. Oxaliplatin-dependent IgG platelet antibodies were detected in his serum on flow cytometry. He was treated with immunoglobulin and corticosteroids without any complications. Physicians should consider oxaliplatin-induced immune-mediated thrombocytopenia, when a sudden, isolated thrombocytopenia develops during chemotherapy with oxaliplatin.
    03/2014; 49(1):61-4. DOI:10.5045/br.2014.49.1.61
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    ABSTRACT: In 2010, we proposed the first Korean Guidelines for the Prevention of Venous Thromboembolism (VTE). It was applicable to Korean patients, by modifying the contents of the second edition of the Japanese guidelines for the prevention of VTE and the 8th edition of the American College of Chest Physicians (ACCP) evidence-based clinical practice guidelines. From 2007 to 2011, we conducted a nationwide study regarding the incidence of VTE after major surgery using the Health Insurance Review and Assessment Service (HIRA) database. In addition, we have considered the 9th edition of the ACCP Evidenced-Based Clinical Practice Guidelines, published in 2012. It emphasized the importance of clinically relevant events as opposed to asymptomatic outcomes with preferences for both thrombotic and bleeding outcomes. Thus, in the development of the new Korean guidelines, three major points were addressed: 1) the new guidelines stratify patients into 4 risk groups (very low, low, moderate, and high) according to the actual incidence of symptomatic VTE from the HIRA databases; 2) the recommended optimal VTE prophylaxis for each group was modified according to condition-specific thrombotic and bleeding risks; 3) guidelines are intended for general information only, are not medical advice, and do not replace professional medical care and/or physician advice. Graphical Abstract
    Journal of Korean medical science 02/2014; 29(2):164-171. DOI:10.3346/jkms.2014.29.2.164 · 1.25 Impact Factor
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    ABSTRACT: Primary autoimmune myelofibrosis, the development of which is not preceded by a well-defined autoimmune disease, has recently been defined as a distinct clinicopathologic syndrome. We report herein a case of a 68-year-old woman who was diagnosed with primary autoimmune myelofibrosis and present a review of the literature. The patient manifested peripheral pancytopenia, was positive for autoantibodies, and developed myelofibrosis with no preceding autoimmune or hematologic disorders. Her condition was dramatically improved after administration of prednisolone.
    01/2014; 86(5):632. DOI:10.3904/kjm.2014.86.5.632
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    ABSTRACT: To investigate the association between potentially functional plasminogen activator inhibitor-1 (PAI-1) genetic polymorphisms and primary ovarian insufficiency (POI). Case-control study. Urban university-based hospital. A cohort of 137 POI patients and 227 controls. None. Genotyping of five PAI-1 polymorphisms (-844G>A [rs2227631], -675 4G/5G [rs1799889], 43G>A (Ala>Thr) [rs6092], 9785G>A [rs2227694], and 11053T>G [rs7242]) was assessed by polymerase chain reaction-restriction fragment length polymorphism assay. PAI-1 polymorphisms 9785GA+AA, -844A/9785A, 4G/9785A, and 9785A/11053G were associated with POI occurrence. Moreover, -844GA+AA and 11053TG+GG were associated with lower serum E2 levels in controls. We have identified an association between five PAI-1 polymorphisms and POI occurrence. However, the mechanism underlying the function of these polymorphisms in POI remains to be determined. Further studies are needed to improve understanding of the roles of PAI-1 polymorphisms and genes in related pathways, using a larger and more heterogeneous cohort.
    Fertility and sterility 12/2013; 101(3). DOI:10.1016/j.fertnstert.2013.11.015 · 4.30 Impact Factor
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    ABSTRACT: The microRNA (miR)-34 family is a direct transcriptional target of tumor-suppressor TP53 and loss of miR-34 function may impair TP53-mediated cell cycle arrest and apoptosis. In the present study, we investigated whether the single nucleotide polymorphisms (SNPs) rs4938723 (T>C) in the promoter region of miR-34b/c and Arg72Pro (G>C) in codon 72 of TP53 are independently or complementarily associated with the risks and clinical outcomes of colorectal cancer (CRC) and whether the combined effect of these SNPs and metabolic risk factors are related to CRC. We evaluated the SNPs in 545 CRC patients and 428 healthy controls using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and DNA sequence analysis. We found that the GC and GC/CC genotypes of TP53 Arg72Pro were associated with decreased risk of CRC (adjusted OR = 0.727 for GC; OR = 0.735 for GC/CC). The combined genotypes of TT-GC and CC-GG were significantly associated with reduced CRC risk (adjusted OR = 0.628 for TT-GC; OR = 0.381 for CC-GG, respectively). The SNP rs4938723 and diabetes mellitus (DM) together were associated with an increased CRC risk, but the SNP TP53 Arg72Pro CC with DM showed a protective effect against CRC. These findings indicate that rs4938723 in the promoter region of pri-miR-34b/c and the SNP in TP53 codon 72 were related to decreased risk of CRC in the population studied and those metabolic diseases and genetic variants influence each other with regard to CRC susceptibility.
    Oncology Reports 12/2013; DOI:10.3892/or.2013.2926 · 2.19 Impact Factor
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    ABSTRACT: Vascular endothelial growth factor (VEGF) and its receptor kinase insert domain-containing receptor (KDR) play crucial roles in angiogenesis, which contributes to the development and progression of solid tumors. The aim of this study was to investigate the associations of VEGF (-2578C > A, -1154G > A, -634G > C, and 936C > T) and KDR (-604T > C and 1192G > A) polymorphisms with the development of colorectal cancer (CRC). A total of 882 participants (390 CRC patients and 492 controls) were enrolled in the study. The genotyping of VEGF and KDR polymorphisms was performed by polymerase chain reaction-restriction fragment length polymorphism assay. We found that the CT and TT genotype of the 936C > T was associated with an increased risk of CRC compared with the CC genotype as the dominant model for the T allele. In addition, we also found a increased CRC risk with TC + CC genotype of KDR -604T > C compared with TT genotype in CRC patients and control subjects. Similarly, KDR 1192G > A also showed significant association between 1192G > A variants and risk of CRC. In the haplotype analyses, haplotype -2578A/-1154A/-634G/936T of VEGF polymorphisms and haplotype -604C/1192G and -604C/1192A of KDR polymorphisms were associated with an increased susceptibility of CRC. Our results suggest that the VEGF 936C > T, KDR -604T > C, and KDR 1192G > A polymorphisms may be contribute to CRC risk in the Korean population. © 2012 Wiley Periodicals, Inc.
    Molecular Carcinogenesis 11/2013; 52(S1). DOI:10.1002/mc.21980 · 4.77 Impact Factor
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    ABSTRACT: 5-Fluorouracil (5-FU) is a cornerstone of chemotherapy for colorectal cancer (CRC), and the major targets of 5-FU are thymidylate synthase (TS), methylenetetrahydrofolate reductase (MTHFR), and reduced folate carrier 1 (RFC1). We hypothesized that polymorphisms in the genes encoding these proteins would be associated with CRC patient survival. Patients and methods We genotyped the following polymorphisms in 372 CRC patients: TS enhancer region (TSER), TS 1494del6, MTHFR 677C>T and 1298A>C, and RFC1 -43T>C, 80G>A, and 696C>T. Using Kaplan-Meier curves, log-rank tests, and Cox proportional hazard models, we evaluated associations between these polymorphisms and overall survival (OS). The combined TS 1494 0bp6bp+6bp6bp genotype was associated with reduced OS compared to the TS 1494 0bp0bp genotype. Among rectal cancer patients, the RFC1 -43CC and 80AA genotypes were associated with favorable OS. Our data suggest that TS and RFC1 polymorphisms are associated with CRC prognosis in Korean patients. Further studies are needed to verify these findings.
    Gene 10/2013; 533(2). DOI:10.1016/j.gene.2013.09.056 · 2.08 Impact Factor
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    ABSTRACT: Allogeneic umbilical cord blood (UCB) has therapeutic potential for cerebral palsy (CP). Concomitant administration of recombinant human erythropoietin (rhEPO) may boost the efficacy of UCB, as it has neurotrophic effects. The objectives of this study were to assess the safety and efficacy of allogeneic UCB potentiated with rhEPO in children with CP. Children with CP, were randomly assigned to one of three parallel groups: the pUCB group, which received allogeneic UCB potentiated with rhEPO; the EPO group, which received rhEPO and placebo UCB; and the Control group, which received placebo UCB and placebo rhEPO. All participants received rehabilitation therapy. The main outcomes were changes in scores on the following measures during the six months treatment period: the Gross Motor Performance Measure (GMPM), Gross Motor Function Measure, and Bayley Scales of Infant Development-II (BSID-II) Mental and Motor scales. (18) F-fluorodeoxyglucose positron emission tomography ((18) F-FDG-PET/CT) and diffusion tensor images (DTI) were acquired at baseline and followed up to detect changes in the brain. In total, 96 subjects completed the study. Compared with the EPO (n = 33) and Control (n = 32) groups, the pUCB (n = 31) group had significantly higher scores on the GMPM and BSID-II Mental and Motor scales at six months. DTI revealed significant correlations between the GMPM increment and changes in fractional anisotropy in the pUCB group. (18) F-FDG-PET/CT showed differential activation and deactivation patterns between the three groups. The incidence of serious adverse events did not differ between groups. In conclusion, UCB treatment ameliorated motor and cognitive dysfunction in children with CP undergoing active rehabilitation, accompanied by structural and metabolic changes in the brain.
    Stem Cells 03/2013; 31(3). DOI:10.1002/stem.1304 · 7.70 Impact Factor
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    ABSTRACT: Acquired hemophilia A (AHA) is a bleeding disorder caused by the development of an auto-antibody against endogenous factor VIII (FVIII). In this study, the epitope of the autoantibody was identified in a 67-year-old female patient with AHA. A prolonged activated partial thromboplastin time (77.4 s) that failed to correct in an incubation mixing test (68.2 s), a decreased FVIII activity, and a high FVIII inhibitor (14.6 Bethesda units/mL) were observed. Enzyme-linked immunosorbent assay demonstrated that the antibody belonged to the immunoglobulin G4 subclass. An immunoblotting assay revealed the light chain (A3/C1/C2 domain) of FVIII as the binding region of the antibody. The bleeding experienced by our patient resulted from the interference of FVIII binding to both FIX by anti-A3 antibodies and phospholipids and von Willebrand factor by anti-C2 antibodies. To the best of our knowledge, this is the first study in Korea characterizing an autoantibody in the context of AHA.
    03/2013; 48(1):58-62. DOI:10.5045/br.2013.48.1.58

Publication Stats

710 Citations
209.08 Total Impact Points

Institutions

  • 2001–2014
    • CHA University
      • • School of Medicine
      • • Department of Internal Medicine
      • • College of Medicine
      Sŏul, Seoul, South Korea
  • 1994
    • Soonchunhyang University
      Onyang, Chungcheongnam-do, South Korea