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LEE, SUN MI,LEE, EUI JIN,KO, YOUNG-HYEH,LEE, SUG HYUNG,MAENG, LEESO,KIM, KYOUNG-MEE Blackwell Publishing Ltd 2009 APMIS Vol.117 No.2
<P>To evaluate whether promoter methylation is related to responsiveness for chemotherapy or clinical outcome, we performed an association analysis between methylation and clinical outcomes. Patients with nodal diffuse large B-cell lymphomas (DLBCL) at a single institute (n=44) were studied for methylation of tumor-related genes, <I>MGMT, p15</I><SUP><I>INK4B</I></SUP>, <I>p16</I><SUP><I>INK4A</I></SUP>, <I>p16</I><SUP><I>INK4A</I></SUP>, <I>Mad2, TMS1/ASC, CASP8</I>, and <I>GSTP1</I>. The clinical behavior of DLBCL after chemotherapy was followed up and analyzed. Hypermethylation of promoters of <I>MGMT, p15</I><SUP><I>INK4B</I></SUP>, <I>p16</I><SUP><I>INK4A</I></SUP>, <I>p16</I><SUP><I>INK4A</I></SUP>, <I>Mad2</I>, and <I>TMS1/ASC</I> genes was observed in 52.3%, 31.8%, 54.5%, 47.7%, 50%, and 2.3% of the cases, respectively. Methylation of <I>CASP8</I> and <I>GSTP1</I> genes was not observed. Promoter methylation was not related to chemo-responsiveness, disease-free survival, and progress of disease after chemotherapy. However, in overall survival analyses, <I>MGMT</I> methylation (p<0.05) and responsiveness to chemotherapy (p<0.01) were significant prognostic factors in patients with DLBCL. In the low-risk group, patients with <I>p57</I> methylation showed longer overall survival than patients without <I>p57</I> methylation (p=0.02) and all patients with <I>p57</I> methylation were alive during follow-up. Our results demonstrate that aberrant promoter methylation of <I>MGMT</I> and <I>p57</I> is an additional biological marker for predicting increased overall survival in patients with DLBCL.</P>
혈연간 부분 간이식후 생긴 간동맥 협착에 대한 풍선 확장술 1예
이영호,김영훈,김정태,김상순,최홍조,김형호,나서희,정갑중,진영준,박한석,구봉식,이형두,이수일,이용언 대한혈관외과학회 1997 Vascular Specialist International Vol.13 No.1
Liver transplantation is an accepted and successful mode of treatment for pediatric end-stage liver disease. Living related liver transplatation(LRLT) in child has certain potential advantages, such as short cold ischemic time, accurate graft size and vessel diameter match based on elective preoperative preparations. Recently, introduction of microvasular surgery technique to hepatic artery reconstruction has been used, but still remained the possibility of hepatic artery thrombosis. Herein, We report a LRLT case, which showed hepatic artery stenosis postoperatively, successfully dilated by ballon angioplasty technique.
<i>ERBB2</i> kinase domain mutation in a gastric cancer metastasis
LEE, JONG WOO,SOUNG, YOUNG HWA,KIM, SU YOUNG,PARK, WON SANG,NAM, SUK WOO,KIM, SANG HO,LEE, JUNG YOUNG,YOO, NAM JIN,LEE, SUG HYUNG Munksgaard International Publishers 2005 APMIS Vol.113 No.10
<P>ERBB2 is a member of the epidermal growth factor receptor (EGFR) family. Recent studies revealed that the kinase domain of the <I>ERBB2</I> gene was mutated in human cancers, including gastric cancer. Despite the importance of cancer metastasis in the pathogenesis of cancers, data on the <I>ERBB2</I> kinase domain mutation in cancer metastasis are lacking. In this study, to explore the possibility that <I>ERBB2</I> mutation is involved in the metastasis mechanism, we analyzed the kinase domain of <I>ERBB2</I> for the detection of somatic mutations in 58 gastric adenocarcinomas with lymph node metastasis. We found one <I>ERBB2</I> mutation, which was detected in the lymph node metastasis, but not in the primary tumor of the same patient. The <I>ERBB2</I> mutation was a missense mutation which substituted an amino acid in exon 21 (V832I). We simultaneously analyzed the somatic mutations of <I>EGFR</I>, <I>K-RAS</I>, <I>PIK3CA</I> and <I>BRAF</I> genes in the sample with the <I>ERBB2</I> mutation, and found that this metastatic carcinoma did not harbor any of the mutations. Our data suggest that <I>ERBB2</I> kinase domain mutation occasionally occurs in metastatic gastric carcinoma and might play a role in the metastatic process of some gastric carcinomas.</P>
Mutational analysis of the <i>CASP6</i> gene in colorectal and gastric carcinomas
LEE, JONG WOO,KIM, MEE RAN,SOUNG, YOUNG HWA,NAM, SUK WOO,KIM, SANG HO,LEE, JUNG YOUNG,YOO, NAM JIN,LEE, SUG HYUNG Blackwell Publishing Ltd 2006 APMIS Vol.114 No.9
<P>Failure of apoptosis is one of the hallmarks of cancer. As an execution-phase caspase, caspase-6 plays a crucial role during apoptosis. To explore the possibility that the genetic alterations of <I>CASP</I>, which encodes caspase-6, might be involved in the development of human cancers, we analyzed the entire coding region and all splice sites of the human <I>CASP6</I> gene for the detection of somatic mutations in 100 colorectal carcinomas and 50 gastric carcinomas. Overall, we detected three somatic mutations of the <I>CASP6</I> gene, including two missense mutations and one splice-site mutation. The mutations were observed in two of the 100 colorectal carcinomas (2.0%) and one of the 50 gastric carcinomas (2.0%). Of note, one colorectal carcinoma with the <I>CASP6</I> mutation harbored <I>CASP3</I> and <I>CASP8</I> gene mutations as well. We also analyzed caspase-6 expression by immunohistochemistry, and found that caspase-6 was expressed in 60% of the gastric cancers and 90% of the colorectal cancers. This is the first report on <I>CASP6</I> gene mutations in human cancers, and these data indicate that the <I>CASP6</I> gene is occasionally mutated in gastric and colorectal carcinomas. Also, the data suggest the possibility that deficiency of caspase-6 expression might contribute to the pathogenesis of gastric cancers.</P>
PIK3CA gene is frequently mutated in breast carcinomas and hepatocellular carcinomas
Lee, Jong Woo,Soung, Young Hwa,Kim, Su Young,Lee, Hae Woo,Park, Won Sang,Nam, Suk Woo,Kim, Sang Ho,Lee, Jung Young,Yoo, Nam Jin,Lee, Sug Hyung Nature Publishing Group 2005 Oncogene Vol.24 No.8
A recent report revealed that phosphoinositide-3-kinase, catalytic, alpha (PIK3CA) gene is somatically mutated in several types of human cancer, suggesting the mutated PIK3CA gene as an oncogene in human cancers. However, because the previous report focused the mutational search primarily on colon cancers, the data on PIK3CA mutations in other types of human cancers have been largely unknown. Here, we performed mutational analysis of the PIK3CA gene by polymerase chain reaction-single-strand conformation polymorphism assay in 668 cases of common human cancers, including hepatocellular carcinomas, acute leukemias, gastric carcinomas, breast carcinomas, and non-small-cell lung cancers. We detected PIK3CA somatic mutations in 26 of 73 hepatocellular carcinomas (35.6%), 25 of 93 breast carcinomas (26.9%), 12 of 185 gastric carcinomas (6.5%), one of 88 acute leukemias (1.1%), and three of 229 non-small-cell lung cancers (1.3%). Some of the PIK3CA mutations were detected in the early lesions of breast cancer carcinoma, hepatocellular carcinoma, and gastric carcinomas, suggesting that PIK3CA mutation may occur independent of stage of the tumors. The high incidence and wide distribution of PIK3CA gene mutation in the common human cancers suggest that alterations of lipid kinase pathway by PIK3CA mutations contribute to the development of human cancers.Oncogene (2005) 24, 1477–1480. doi:10.1038/sj.onc.1208304 Published online 20 December 2004
Lee Hyung-Woo,Han Chang-Soo,Lee Eung-Sug,Chul Youm,Kim Jae Ho,Kim Soo-Hyun,Kwak Yoon-Keun Korean Society for Precision Engineering 2005 International Journal of Precision Engineering and Vol.6 No.2
We report a simple, low cost, and reliable method for assembling a multi-walled nanotube (MWNT) to the end of a metal coated scanning probe microscopy (SPM) tip. By dropping the MWNT solution and applying an electric field between an SPM tip and an electrode, MWNTs which were dispersed into a dielectric solution were directly assembled onto the apex of the SPM tip due to the attraction by the dielectrophoretic force. The effective measurement of a MWNT -attached SPM tip was demonstrated by direct comparison with AFM images of a standard sample with a bare AFM tip.
Somatic mutations of <i>BECN1</i>, an autophagy-related gene, in human cancers
LEE, JONG WOO,JEONG, EUN GOO,LEE, SUNG HAK,YOO, NAM JIN,LEE, SUG HYUNG Wiley-Blackwell Munksgaard 2007 APMIS Vol. No.
<P>Evasion of programmed cell death (PCD) is one of the hallmarks of human cancers. It is well known that not only apoptosis, but also autophagy, acts as an action mechanism of PCD. BECN1 protein is a key regulator of autophagic PCD. The <I>BECN1</I> gene that encodes BECN1 protein acts as a haploinsufficient tumor-suppressor gene. However, to date, data on <I>BECN1</I> mutation in human cancer tissues are lacking. To explore the possibility that somatic mutation of the <I>BECN1</I> gene might contribute to the development of human cancers, we analyzed the entire coding region and all splice sites of the human <I>BECN1</I> gene for detection of somatic mutations in 180 gastric carcinomas, 94 breast carcinomas, 50 acute leukemias, 50 colorectal carcinomas, 50 hepatocellular carcinomas, and 124 non-small cell lung cancers by single-strand conformation polymorphism (SSCP) and DNA sequencing. Overall, we detected 11 somatic mutations of the <I>BECN1</I> gene, including 3 missense mutations (N8K, P350R and R389C) in coding sequences and 8 mutations in introns. The mutations were observed in five gastric, three colorectal, one lung and one breast carcinoma (s). We expressed the three mutations (N8K, P350R and R389C) in HT1080 cells, and found that two (P350R and R389C) of them showed only slightly decreased cell death activities compared to the wild-type BECN1. This is the first report on <I>BECN1 </I>gene mutations in human cancer tissues, and the data suggest that point mutations are a rare event in common human cancers and probably do not play a major role in cancer pathogenesis.</P>