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이신엽,김광,최의영,전효성,유승수,이재희,이응배,차승익,김창호,박재용 대한결핵 및 호흡기학회 2012 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.114 No.-
Fusion oncogene has been identified as one of driver mutations in NSCLC. We searched for EML4-ALK and CCDC6-RET fusion genes in NSCLC and analyzed their relationship with clinicopathologic features. Fusion oncogenes EML4-ALK and CCDC6-RET were identified by reverse transcriptase-polymerase chain reaction (RT-PCR) in 156 surgically resected NSCLCs - 52 squamous cell carcinomas (SCCs) and 104 adenocarcinomas (ACs). In addition, mutations of EGFR, ERBB2, KRAS, NRAS, BRAF, PIK3CA, PTEN, and LKB1 were determined by PCR and direct sequencing. The EML4-ALK was found in 4 (2.6%) of 156 NSCLCs; 3 (2.8%) of 107 ACs. For EML4-ALK, all four cases were detected in younger patients (≤ 64 years old), three in males, three in ever smokers. The CCDC6-RET were found in 4 (2.6%) of 156 NSCLCs; 4 (3.8%) of 107 ACs. For CCDC6-RET, all four cases were found in never-smoker ACs, two in younger patients, and two in females. One of the four EML4-ALK positive cases also had a KRAS mutation. However, none of four CCDC6-RET positive cases harbored any other mutation. Overall, among the 156 NSCLCs, a total of 55 genetic alterations were detected in 51 (32.7%) tumors - 7 (14.3%) in SCCs and 44 (41.1%) in ACs. Genetic alterations were significantly more frequent in women, never smokers and ACs than in men, ever smokers and SCCs (p=0.001, p=0.003 and p=0.001, respectively). The mutations occurred in a mutually exclusive pattern. Here we report the frequency of EML4-ALK and CCDC6-RET fusion oncogenes in Korean NSCLC.
이신엽,강효경,최의영,최진은,전효성,신경민,유승수,이재희,차승익,김창호,박재용 대한결핵 및 호흡기학회 2012 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.114 No.-
This study was conducted to analyze a comprehensive panel of single nucleotide polymorphisms (SNPs) in genes in DNA repair and apoptosis pathways to determine the relationship between polymorphisms and treatment outcomes of patients with non-small cell lung cancer (NSCLC) treated with first line paclitaxel-cisplatin chemotherapy. Three hundred eighty two patients with NSCLC were enrolled. Seventy-four SNPs in 48 genes (42 SNPs in 27 DNA repair pathway genes and 32 SNPs in 21 apoptotic pathway genes) were genotyped and their associations with response to chemotherapy and overall survival (OS) were analyzed. Results: Among SNPs in DNA repair genes, BRCA1 rs799917 was significantly associated with both response to chemotherapy and OS. XRCC1 rs25487 exhibited significant association with response to chemotherapy and XPD/ERCC2 rs1052555 with OS. Four SNPs in apoptotic genes (TNFRSF1B rs1061624, BCL2 rs2279115, BIRC5 rs9904341, and CASP8 rs3769818) were significantly associated with OS, but not with response to chemotherapy. When the six SNPs which were associated with OS in individual analysis were combined, OS w decreased as the number of bad genotypes increased (Ptrend=2×10-6). Patients with 3, and 4-6 bad genotypes had a significantly worse OS compared with those carrying 0-2 bad genotypes (aHR=1.54, 95% CI=1.14-2.08, P=0.005; aHR=2.10, 95% CI=1.55-2.85, P=2×10-6, respectively). These findings suggest that the SNPs identified can be used as biomarkers predicting chemotherapy response and survival for NSCLC patients treated with first line paclitaxel-cisplatin.
한국인에서 DNMT3b의 39179G>T 다형성과 원발성 폐암의 위험도
이신엽,이재희,박재형,김은진,이수정,전효성,손지웅,차승익,김창호,정태훈,박재용 대한내과학회 2004 대한내과학회지 Vol.66 No.6
목적 : DNA 메틸화는 후생유전적인 변형의주요 기전이며 암 발생에서 중요한 역할을 한다. 유전자 촉진자의 메틸화는 유전자 발현의 중요한 조절기전으로 종양억제유전자 촉진자의 과메틸화는 종양억제유전자의 불활성화를 초래한다. 저자들은 한국인에서 de novo 메틸화에 관여하는 유전자인 DNMT3b의 39179G>T 다형성에 따른 폐암의 위험도를 조사하였다. 방법 : 경북대학교병원 호흡기내과에서 병리학적으로 폐암으로 진단된 392에(편평상피암 194예, 선암 128예, 대세포암 16예, 소세포암 54예)를 대상으로 하였으며 대조군은 경북대학교병원 건강검진센타를 방문한 건강인 가운데 환자군과 연령 및 성을 match하여 무작위로 선택한 391명을 대상으로 하였다. 시료는 전혈 5cc에서 DNA를 추출하고 PCR-RELP법을 통해 DNMT3b 유전자 다형성을 조사하였다. 결과 : DNMT3b 39179G>T의 유전자형은 환자군은 GG형, GT형, TT형이 각각 0.8%, 19.9%, 79.3%였고, 대조군은 각각 1.5%, 25.1%, 73.4%로 유의한 차이는 없었다. TT형에 대한 GT+GG형의 폐암 대응비(OR)는 0.71(95% CI\0.51∼1.00, p=0.05)이었다. 폐암을 조직형에 따라 구분한 경우 TT형에 대한 GT+GG형의 선암 대응비는 0.46 (95% CI=0.26∼0.80, p=0.006)으로 통계적으로 유의하게 낮았다. 선암 환자군과 대조군을 연령, 성, 흡연력 및 흡연양(흡연 갑-년)으로 구분하여 TT형에 대한 GT+GG형의 선암 대응비를 구하였을 때 61세 이상 (OR=0.23, 95% CI=0.09∼0.58, p=0.02), 35갑-년 이상(OR=0.34, 95% CI=0.13∼0.88, p=0.028)의 경우에서 유의하게 낮았다. 결론 : DNMT3b 유전자의 39179G>T 다형성은 한국인에서 선암의 위험도를 결정하는 유전적 인자 가운데 하나로 생각된다. Background : DNA methylation is the main mechanism of epigenetic modification of genes and plays an important role in carcinogenesis. The methylation of promoter can inactivate the tumor suppressor gene by repression of transcription. We investigated the relationship between the 39179G>T (-579bp from exon 1B) polymorphism in DNMT3b gene, which is involved in de novo methylation, and the risk of primary lung cancer in Koreans. Methods : The DNMT3b 39179G>T genotypes were determined using PCR-RFLP method in 392 primary lung cancer patients and 391 healthy controls who were frequency (1:1) matched based on age and sex. Results : although the frequencies of GG, GT, TT genotypes among cases (0.8%, 19.9%, 79.3%, respectively) were not significantly different from those among controls (1.5%, 25.1%, 73.4%, respectively) the frequency of wild-type G allele among cases was significantly different from that of controls (14.1% vs 10.7%, p=0.05). The combined GT and GG genotype was associated with a significantly decreased risk of lung cancer [adjusted odds ratio (OR)=0.71, 95% confidence interval (CI)=0.51∼1.00, p=0.05] when TT genotype was used as reference. When the lung cancers were categorized by tumor higtology, the combined GT and GG genotype was associated with a significantly decreased risk of adenocarcinoma (adjusted OR=0.46, 95% CI=0.26∼0.80, p=0.006). In adenocarcinoma, the decreased risk of the combined GT and GG genotype was statistically significant in older patients (≥61 years, adjusted OR=0.23, 95% CI=0.09∼0.58, p=0.002) and in heavier smokers(≥35 pack years, adjusted OR=0.34, 95% CI=0.13∼0.88, p=0.028) in stratification analyses. Conclusion : DNMT3b 39179G>T polymorphism may be a genetic determinant of lung cancer, especially adenocarcinoma in Koreans.
Chemical Composition, Saccharification Yield, and the Potential of the Green Seaweed Ulva pertusa
이신엽,장진화,이선복 한국생물공학회 2014 Biotechnology and Bioprocess Engineering Vol.19 No.6
Recently, seaweeds have gained attention aspossible renewable sources for biofuel and bioproductproduction. To investigate the possibility of using greenseaweeds as biomass feedstocks, the chemical compositionand saccharification yield of the green seaweed Ulva pertusawere investigated. In this study, we evaluated U. pertusathat was harvested from the seashore in Jeju Island, Korea. By proximate composition analysis, dried U. pertusa wasfound to contain 52.3% carbohydrate, 25.1% protein, 0.1%lipid, and 22.5% ash. The elemental analysis of U. pertusaindicated the content of carbon to be 34.9%, hydrogen5.3%, oxygen 46.5%, nitrogen 3.8%, sulfur 3.1%, andphosphorous 0.12%. The optimal conditions for the acidhydrolysis and saccharification of U. pertusa were investigatedby varying the types of catalysts, catalyst concentration,reaction time, reaction temperature, and seaweed concentration. Under optimized acid hydrolysis condition,32.9% of seaweed was recovered as monosaccharides andthe monosaccharide composition was 11.5% D-glucuronicacid and D-glucuronic acid lactone, 11.1% L-rhamnose, 6.7%D-glucose, and 3.7% D-xylose. The concept of degree ofreductance was introduced to assess the potential of U. pertusaas an industrial feedstock. It was found that the degree ofreductance of U. pertusa was lowest among the biomassconsidered in this study. Based on the comparison of chemicalcomposition and reductance degree of various biomassresources, the competitiveness of U. pertusa as a biomassfeedstock for biofuel and bioproduct production was discussed.
이신엽,이수만,김동선,손지웅,유승수,이재희,차승익,김창호,박재용 대한결핵 및 호흡기학회 2012 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.114 No.-
MicroRNA (miR)-34 and miR-124 have been demonstrated as a potential tumor suppressor in several types of cancers. Each family includes three processed miRNAs (miR-34a, miR-34b, miR-34c, miR-124-1, miR-124-2, and miR-124-3). The tran-scriptional silencing of tumor suppressor genes by CpG island promoter hypermethylation has emerged as a common hallmark. To understand the role of miR-34 and miR-124 in non-small cell lung cancer (NSCLC) and to develop a promising candidate biomarker for diagnosis and prognosis of NSCLC, we determined the methylation status of 6 miR genes in primary lung tissues using a methylation-specific PCR (MSP) and evaluated their relationship with clinicopatholgial features and survival in patients with NSCLC. The methylation frequencies of 6 miR genes were 15.1% for miR-34a, 55.9% for miR-34b/c, 25.6% for miR-124-1, 52.9% for miR-124-3 in malignant tissues. The methylation frequencies of miR-34b/c and miR-124-3 were significantly higher in squamous cell carcinomas than in adenocarcinomas. In addition, miR-34b/c methylation was frequently observed in EGFR mutation-negative adenocarcinomas compared to EGFR mutation-positive ones. However, there was no significant difference in overall survival of the total patients according to six miR genes.