Jung Min Park

Publications (10)38.01 Total impact

• Article: Polymorphisms in the caspase-8 gene and the risk of lung cancer.

  Ji-Woong Son, Hyo-Kyung Kang, Myung Hwa Chae, Jin Eun Choi, Jung Min Park, Won Kee Lee, Chang Ho Kim, Dong Sun Kim, Sin Kam, Young Mo Kang, Jae Yong Park
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  ABSTRACT: Caspase-8 (CASP-8) is an initiator CASP in the cell death receptor-mediated apoptotic pathway, and plays an important role in the development of cancer. Polymorphisms and their haplotypes in the CASP-8 gene can result in alterations in CASP-8 expression and/or activity, thereby modulating the susceptibility to lung cancer. To test this hypothesis, we examined the association of -678_-673delAGTAAG (-678del) and IVS12-19G-->A polymorphisms and their haplotypes with the risk of lung cancer in a Korean population. The CASP-8 genotypes were determined in 432 lung cancer patients and 432 healthy age- and gender-matched control subjects. The distributions of the CASP-8 -678del and IVS12-19G-->A genotypes were not significantly different between the overall lung cancer cases and the controls. When the cases were categorized by tumor histology, however, the IVS12-19 AA genotype and the combined IVS12-19 GA + AA genotype were associated with a significantly decreased risk of small cell carcinoma (SmCC) compared with the IVS12-19 GG genotype [adjusted odds ratio (OR) = 0.14, 95% confidence interval (CI) = 0.03-0.64, P = 0.01; and adjusted OR = 0.56, 95% CI = 0.33-0.96, P = 0.03, respectively]. Consistent with the genotyping analyses, the -678del-/IVS12-19A haplotype containing 94% of the IVS12-19A allele in the study population was associated with a significantly decreased risk of SmCC compared with the -678del-/IVS12-19G (adjusted OR = 0.58, 95% CI = 0.36-0.93, P = 0.023, and Pc = 0.046). These findings suggest that the CASP-8 gene may contribute to an inherited predisposition to SmCC of the lung.
  Cancer Genetics and Cytogenetics 09/2006; 169(2):121-7. · 1.39 Impact Factor
• Article: Caspase 9 promoter polymorphisms and risk of primary lung cancer.

  Jae Yong Park, Jung Min Park, Jin Sung Jang, Jin Eun Choi, Kyung Mee Kim, Sung Ick Cha, Chang Ho Kim, Young Mo Kang, Won Kee Lee, Sin Kam, Rang Woon Park, In San Kim, Jae-Tae Lee, Tae Hoon Jung
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  ABSTRACT: Caspase-9 (CASP-9) is an initiator CASP in the apoptosome-driven apoptosis pathway and plays an important role in the development and progression of cancer. Polymorphisms in the promoter region of the CASP-9 gene may influence the promoter activity of this gene, thereby modulating susceptibility to lung cancer. To test this hypothesis, we examined the association of four polymorphisms [-1263A>G, -905T>G, -712C>T and -293_-275delCGTGAGGTCAGTGCGGGGA (-293del)] in the CASP-9 promoter with the risk of lung cancer in a Korean population. The CASP-9 genotypes were determined in 432 lung cancer patients and 432 healthy controls that were frequency-matched for age and gender. The -1263 GG genotype was associated with a significantly decreased risk of lung cancer compared with the -1263 AA genotype or combined -1263 AA+AG genotype [adjusted odds ratio (OR)=0.64, 95% confidence interval (95% CI)=0.42-0.98, P=0.04 and adjusted OR=0.67, 95% CI=0.46-0.97, P=0.01, respectively]. For the -712C>T polymorphism, individuals with at least one -712T allele were at a significantly increased risk of lung cancer compared with those harboring the -712 CC genotype (adjusted OR=1.42, 95% CI=1.06-1.89, P=0.02). Consistent with the results of genotype analyses, the -1263G/-712C (G-C) haplotype was associated with a significantly decreased risk of lung cancer [adjusted OR=0.59, 95% CI=0.47-0.75, P and Bonferroni corrected P (Pc)<0.001]. Moreover, the risk of lung cancer decreased in a dose-dependent manner as the number of the G-C haplotypes increased (adjusted OR=0.60, 95% CI=0.45-0.81, P=0.0007 and Pc=0.0014 for the G-C heterozygotes and adjusted OR=0.34, 95% CI=0.17-0.68, P=0.0023 and Pc=0.0046 for the G-C homozygotes; P(trend)<0.001). The promoter assay revealed the G-C haplotype to have a significantly higher promoter activity than the -1263G/-712T and -1263A/-712C haplotypes. These results suggest that CASP-9 promoter polymorphisms affect CASP-9 expression and contribute to genetic susceptibility to lung cancer.
  Human Molecular Genetics 07/2006; 15(12):1963-71. · 7.64 Impact Factor
• Article: Polymorphisms in TGF-beta1 gene and the risk of lung cancer.

  Hyo-Gyoung Kang, Myung Hwa Chae, Jung Min Park, Eun Jin Kim, Jae Hyung Park, Sin Kam, Sung Ick Cha, Chang Ho Kim, Rang-Woon Park, Sun Hee Park, Yong Lim Kim, In-San Kim, Tae Hoon Jung, Jae Yong Park
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  ABSTRACT: Transforming growth factor-beta1 (TGF-beta1) functions as a suppressor of tumor initiation by inhibiting cellular proliferation or by promoting cellular differentiation or apoptosis in the early phase of cancer development. Variations in the DNA sequence in the TGF-beta1 gene may lead to altered TGF-beta1 production and/or activity, and so this can modulate an individual's susceptibility to lung cancer. To test this hypothesis, we investigated the association of the TGF-beta1 -509C > T and 869T > C (L10P) polymorphisms and their haplotypes with the risk of lung cancer in a Korean population. The TGF-beta1 genotypes were determined in 432 lung cancer patients and in 432 healthy control subjects who were frequency-matched for age and gender. The TGF-beta1 haplotypes were predicted using a Bayesian algorithm in the Phase program. Individuals with at least one -509T allele were at a significantly decreased risk of adenocarcinoma (AC) and small cell carcinoma (SM), as compared with carriers with the -509CC genotype [adjusted odds ratio (OR), 0.63; 95% confidence interval (CI), 0.42-0.96; P = 0.04; and adjusted OR, 0.45; 95% CI, 0.27-0.76; P = 0.002; respectively]. For the 869T > C polymorphism, the combined TC + CC genotype was associated with a significantly decreased risk of SM compared with the TT genotype (adjusted OR, 0.52; 95% CI, 0.31-0.88; P = 0.01). Consistent with the results of the genotyping analyses, the -509T/869C haplotype was associated with a significantly decreased risk of AC and SM as compared with the -509C/869T haplotype (adjusted OR, 0.75; 95% CI, 0.57-0.98; P = 0.04; and adjusted OR, 0.67; 95% CI, 0.47-0.96; P = 0.02; respectively). The TGF-beta1 -509C > T and 869T > C polymorphisms and their haplotypes may contribute to genetic susceptibility to AC and SM of the lung.
  Lung Cancer 05/2006; 52(1):1-7. · 3.43 Impact Factor
• Article: Polymorphisms in the hMSH2 gene and the risk of primary lung cancer.

  Chi Young Jung, Jin Eun Choi, Jung Min Park, Myung Hwa Chae, Hyo-Gyoung Kang, Kyung Mee Kim, Su Jeong Lee, Won Kee Lee, Sin Kam, Seung Ick Cha, Chang Ho Kim, Sung Beom Han, Tae Hoon Jung, Su Han Jeon, Jae Yong Park
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  ABSTRACT: Polymorphisms in the DNA repair genes may be associated with differences in the capacity to repair DNA damage, and so this can influence an individual's susceptibility to lung cancer. To test this hypothesis, we investigated the association of hMSH2 -118T>C, IVS1+9G>C, IVS10+12A>G, and IVS12-6T>C genotypes and their haplotypes with the risk of lung cancer in a Korean population. The hMSH2 genotypes were determined in 432 lung cancer patients and in 432 healthy controls who were frequency matched for age and gender. The hMSH2 haplotypes were estimated based on a Bayesian algorithm using the Phase program. The presence of at least one IVS10+12G allele was associated with a significantly decreased risk of adenocarcinoma, as compared with the IVS10+12AA genotype [adjusted odds ratio (OR), 0.59; 95% confidence interval (95% CI), 0.40-0.88; P = 0.01], and the presence of at least one IVS12-6C allele was associated with a significantly increased risk of adenocarcinoma, as compared with the IVS12-6TT genotype (adjusted OR, 1.52; 95% CI, 1.02-2.27; P = 0.04). Consistent with the results of the genotyping analysis, the TGGT haplotype with no risk allele was associated with a significantly decreased risk of adenocarcinoma, as compared with the TCAC haplotype with two risk allele [i.e., IVS10+12A and IVS12-6C allele; adjusted OR, 0.49; 95% CI, 0.30-0.78; P = 0.003 and P(c) (Bonferroni corrected P value) = 0.012]. The effect of the hMSH2 haplotypes on the risk of adenocarcinoma was statistically significant in the never smokers and younger individuals (adjusted OR, 0.45; 95% CI, 0.27-0.75; P = 0.002 and P(c) = 0.004; and adjusted OR, 0.44; 95% CI, 0.23-0.85; P = 0.014 and P(c) = 0.028, respectively) but not in the ever-smokers and older individuals. These results suggest that the hMSH2 polymorphisms and their haplotypes may be an important genetic determinant of adenocarcinoma of the lung, particularly in never smokers.
  Cancer Epidemiology Biomarkers &amp Prevention 04/2006; 15(4):762-8. · 4.12 Impact Factor
• Article: O6-alkylguanine-DNA alkyltransferase gene polymorphisms and the risk of primary lung cancer.

  Myung Hwa Chae, Jin-Sung Jang, Hyo-Gyoung Kang, Jae Hyung Park, Jung Min Park, Won Kee Lee, Sin Kam, Eung Bae Lee, Ji-Woong Son, Jae Yong Park
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  ABSTRACT: O6-alkylguanine-DNA alkyltransferase (AGT) plays an important role in the repair of O6-alkylguanine adducts, which are major mutagenic lesions produced by environmental carcinogens. Polymorphisms in the AGT gene may affect the capacity to repair DNA damage and thereby have influence on individual's susceptibility to smoking-related cancer. To test this hypothesis, we investigated the potential association of AGT polymorphisms (485C > A, Leu53Leu (C > T) and Leu84Phe] with the risk of lung cancer in a Korean population. The AGT genotypes were determined in 432 lung cancer patients and in 432 healthy controls who were frequency-matched for age and gender. The 485 AA genotype was associated with a significantly increased risk for overall lung cancer as compared with the 485 CC genotype and the combined 485 CC + CA genotype, respectively (adjusted odds ratio (OR) = 1.83, 95% confidence interval (CI) = 1.12-2.99, P = 0.02, and Bonferroni corrected P-value (Pc) = 0.04; and adjusted OR = 1.67, 95% CI = 1.05-2.66, P = 0.03, respectively). When the lung cancer cases were categorized by the tumor histology, the 485 AA genotype was associated with a significantly increased risk of adenocarcinoma (AC) and small cell carcinoma (SmCC), respectively, as compared with the combined 485 CC + CA genotype (adjusted OR = 2.54, 95% CI = 1.39-4.66, P = 0.003; and adjusted OR = 2.19, 95% CI = 1.06-4.55, P = 0.04, respectively). However, the genotype distributions of the Leu53Leu and Leu84Phe polymorphisms were not significantly different between the lung cancer cases and the controls. On a promoter assay, the 485C > A polymorphism did not have an effect on the promoter activity of the AGT gene. These results suggest that the effect of the AGT 485C > A polymorphism on the risk of lung cancer may be secondary to linkage disequilibrium (LD) with either another AGT variant or with a true susceptibility gene, and that the AGT 485C > A polymorphism could be used as a marker for the genetic susceptibility to lung cancer.
  Molecular Carcinogenesis 04/2006; 45(4):239-49. · 3.16 Impact Factor
• Article: Myeloperoxidase -463G>A polymorphism and risk of primary lung cancer in a Korean population.

  Jae Hyung Park, Jung Min Park, Eun Jin Kim, Sung Ick Cha, Eung Bae Lee, Chang Ho Kim, Sin Kam, Tae Hoon Jung, Jae Yong Park
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  ABSTRACT: Myeloperoxidase (MPO) contributes to pulmonary carcinogenesis through activation of a wide range of tobacco smoke procarcinogens, including benzo[a]pyrene and aromatic amines. A -463G>A polymorphism in the promoter region of the MPO gene has been shown to reduce MPO expression and activity. It is therefore possible that carriers of the -463A allele may be at decreased risk of lung cancer. To test this hypothesis we have investigated the association between the -463G>A polymorphism of MPO gene and the risk of lung cancer in a Korean population. The MPO genotype was determined in 432 lung cancer patients and 432 healthy controls that were frequency-matched for age and gender. In the current study, the risk estimate for lung cancer of the combined -463 AA+GA genotype was not significantly different from that of the -463GG genotype (adjusted OR=1.03, 95% CI=0.72-1.47). In addition, we observed no evidence of effect modification by age, gender, smoking history or tumor histology. These results suggest that the MPO -463G>A polymorphism does not significantly affect the susceptibility to lung cancer in Koreans.
  Cancer Detection and Prevention 01/2006; 30(3):257-61. · 2.52 Impact Factor
• Source

  Available from: PubMed Central

  Article: Relationship between cyclooxygenase 8473T>C polymorphism and the risk of lung cancer: a case-control study.

  Jung Min Park, Jin Eun Choi, Myung Hwa Chae, Won Kee Lee, Sung Ick Cha, Ji-Woong Son, Chang Ho Kim, Sin Kam, Young Mo Kang, Tae Hoon Jung, Jae Yong Park
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  ABSTRACT: Cyclooxygenase-2 (COX-2) plays an important role in the development of lung cancer. DNA sequence variations in the COX-2 gene may lead to altered COX-2 production and/or activity, and so they cause inter-individual differences in the susceptibility to lung cancer. To test this hypothesis, we investigated the association between the 8473T>C polymorphism in the 3'-untranslated region of the COX-2 gene and the risk of lung cancer in a Korean population. The COX-2 genotypes were determined using PCR-based primer-introduced restriction analysis in 582 lung cancer patients and in 582 healthy controls that were frequency-matched for age and gender. The distribution of the COX-2 8473T>C genotypes was not significantly different between the overall lung cancer cases and the controls. However, when the cases were categorized by the tumor histology, the combined 8473 TC + CC genotype was associated with a significantly decreased risk of adenocarcinoma as compared with the 8473 TT genotype (adjusted OR = 0.64; 95% CI = 0.46-0.90, P = 0.01). On the stratification analysis, the protective effect of the combined 8473 TC + CC genotype against adenocarcinoma was statistically significant in the males, older individuals and ever-smokers (adjusted OR = 0.59; 95% CI = 0.39-0.91, P = 0.02; adjusted OR = 0.55; 95% CI = 0.33-0.93, P = 0.03; and adjusted OR = 0.57; 95% CI = 0.37-0.87, P = 0.01, respectively). These findings suggest that the COX-2 8473T>C polymorphism could be used as a marker for the genetic susceptibility to adenocarcinoma of the lung.
  BMC Cancer 01/2006; 6:70. · 3.01 Impact Factor
• Article: O6‐alkylguanine‐DNA alkyltransferase gene polymorphisms and the risk of primary lung cancer

  Myung Hwa Chae, Jin-Sung Jang, Hyo-Gyoung Kang, Jae Hyung Park, Jung Min Park, Won Kee Lee, Sin Kam, Eung Bae Lee, Ji-Woong Son, Jae Yong Park
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  ABSTRACT: O6-alkylguanine-DNA alkyltransferase (AGT) plays an important role in the repair of O6-alkylguanine adducts, which are major mutagenic lesions produced by environmental carcinogens. Polymorphisms in the AGT gene may affect the capacity to repair DNA damage and thereby have influence on individual's susceptibility to smoking-related cancer. To test this hypothesis, we investigated the potential association of AGT polymorphisms (485C > A, Leu53Leu (C > T) and Leu84Phe] with the risk of lung cancer in a Korean population. The AGT genotypes were determined in 432 lung cancer patients and in 432 healthy controls who were frequency-matched for age and gender. The 485 AA genotype was associated with a significantly increased risk for overall lung cancer as compared with the 485 CC genotype and the combined 485 CC + CA genotype, respectively (adjusted odds ratio (OR) = 1.83, 95% confidence interval (CI) = 1.12–2.99, P = 0.02, and Bonferroni corrected P-value (Pc) = 0.04; and adjusted OR = 1.67, 95% CI = 1.05–2.66, P = 0.03, respectively). When the lung cancer cases were categorized by the tumor histology, the 485 AA genotype was associated with a significantly increased risk of adenocarcinoma (AC) and small cell carcinoma (SmCC), respectively, as compared with the combined 485 CC + CA genotype (adjusted OR = 2.54, 95% CI = 1.39–4.66, P = 0.003; and adjusted OR = 2.19, 95% CI = 1.06–4.55, P = 0.04, respectively). However, the genotype distributions of the Leu53Leu and Leu84Phe polymorphisms were not significantly different between the lung cancer cases and the controls. On a promoter assay, the 485C > A polymorphism did not have an effect on the promoter activity of the AGT gene. These results suggest that the effect of the AGT 485C > A polymorphism on the risk of lung cancer may be secondary to linkage disequilibrium (LD) with either another AGT variant or with a true susceptibility gene, and that the AGT 485C > A polymorphism could be used as a marker for the genetic susceptibility to lung cancer. © 2005 Wiley-Liss, Inc.
  Molecular Carcinogenesis 12/2005; 45(4):239 - 249. · 3.16 Impact Factor
• Article: XPC polymorphisms and lung cancer risk.

  Ga Young Lee, Jin-Sung Jang, Sin Yeob Lee, Hyo-Sung Jeon, Kyung Mee Kim, Jin Eun Choi, Jung Min Park, Myung Hwa Chae, Won Kee Lee, Sin Kam, In-San Kim, Jae-Tae Lee, Tae Hoon Jung, Jae Yong Park
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  ABSTRACT: Polymorphisms in DNA repair genes may be associated with differences in the capacity to repair DNA damage and thereby influence an individual's susceptibility to smoking-related cancer. To test this hypothesis, we investigated the potential association of 7 XPC polymorphisms (-449G-->C, -371G-->A, -27G-->C, Val499Arg, PAT-/+, IVS11-5C-->A and Lys939Gln) and their haplotypes with lung cancer risk in a Korean population. XPC genotypes were determined in 432 lung cancer patients and 432 healthy controls frequency-matched for age and sex. XPC haplotypes were predicted using a Bayesian algorithm in the Phase program. The combined -27CG+CC genotype was associated with a significantly increased risk for overall lung cancer compared to the -27GG genotype (adjusted OR = 1.97, 95% CI 1.22-3.17, p = 0.005). The other 6 polymorphisms were not significantly associated with overall risk of lung cancer. When lung cancer cases were categorized by tumor histology, the -371AA genotype was associated with a significantly increased risk of squamous cell carcinoma compared to the combined -371GG and GA genotype (adjusted OR = 2.08, 95% CI 1.09-4.00, p = 0.03). The PAT-/+, IVS11-5C-->A and Lys939Gln polymorphisms were associated with a significantly decreased risk of small cell carcinoma (SM) under a dominant model for the polymorphic allele (adjusted OR = 0.49, 95% CI 0.29-0.82, p = 0.006; adjusted OR = 0.60, 95% CI 0.36-1.00, p = 0.05; and adjusted OR = 0.58, 95% CI 0.35-0.97, p = 0.04, respectively). Consistent with genotyping analyses, haplotype 4 (1112222) containing the PAT+/IVS11-5A/939Gln alleles was associated with a significantly decreased risk of SM (adjusted OR = 0.56, 95% CI 0.37-0.85, p = 0.007 and Bonferroni-corrected p = 0.049), whereas haplotype 5 (1122111) containing the -27C allele was associated with a significantly increased risk of SM (adjusted OR = 2.88, 95% CI 1.41-5.87, p = 0.004 and Bonferroni-corrected p = 0.028). These results suggest that XPC polymorphisms/haplotypes may contribute to genetic susceptibility for lung cancer.
  International Journal of Cancer 08/2005; 115(5):807-13. · 5.44 Impact Factor
• Article: No association between polymorphisms in the histone deacetylase genes and the risk of lung cancer.

  Jung Min Park, Ga Young Lee, Jin Eun Choi, Hyo Gyoung Kang, Jin Sung Jang, Sung Ick Cha, Eung Bae Lee, Sang Geol Kim, Chang Ho Kim, Won Kee Lee, Sin Kam, Dong Sun Kim, Tae Hoon Jung, Jae Yong Park
  Cancer Epidemiology Biomarkers &amp Prevention 08/2005; 14(7):1841-3. · 4.12 Impact Factor