• Proceedings of the Korean Information Science Society Conference
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• 2005.11b
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• pp.799-801
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• 2005

현재 마이크로어레이 기술은 대량의 유전자 발현 데이터 특히 종양과 관련한 데이터들을 쏟아내고 있다. 이 데이터를 기반으로 종양의 종류에 따른 유전자들의 차별적 발현 양상을 분석하고 발현량의 변화가 두드러지는 유전자들에 기반하여 종양을 분별할 수 있는 분류 모델을 구축한 후, 이것을 종양을 진단하거나 예측하는데 이용할 수 있다. 대부분의 종양은 생성 매커니즘에 따라 세부 부류로 나눌 수 있고 세부 부류에 따라 치료 방법이나 예후가 달라지므로, 정확하게 종양의 세부 부류를 진단하는 것이 매우 중요하다. 본 논문에서는 종양의 종류에 따라 발현량이 민감하게 변화하는 유전자들을 뽑아내기 위한 특징 추출 방법들과 추출된 특징들에 기반해서 종양의 종류를 분별할 수 있는 기계학습 알고리즘들의 조합들의 성능을 비교분석 하였다.

• Journal of Veterinary Clinics
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• v.19 no.2
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• pp.195-198
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• 2002

To identify mutations in exons 5 to 8 of the p53 tumor suppressor gene, we have analysed in 12 spontaneous canine tumors. In a malignant mast cell tumor, a 1 base pair alteration AGT $\longrightarrow$AGC (silent point mutation, serine) in codon 249 in exon 8 was detected. And the mammary gland adenocarcinoma was found to have a mis-sense point mutation (CCT $\longrightarrow$ TCT) in codon 285 in exon 8.

• Journal of the Korea Institute of Information and Communication Engineering
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• v.11 no.10
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• pp.1924-1929
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• 2007

Nowadays, a lot of related data obtained from these research could be given a new present meaning to accomplish the original purpose of the whole research as a human project. The method of tumor classification based on microarray could contribute to being accurate tumor classification by finding differently expressing gene pattern statistically according to a tumor type. Therefore, the process to select a closely related informative gene with a particular tumor classification to classify tumor using present microarray technology with effect is essential. In this thesis, we used cDNA microarrays of 3840 genes obtained from neuronal differentiation experiment of cortical stem cells on white mouse with cancer, constructed accurate tumor classification model by extracting informative gene list through normalization separately and then did performance estimation by analyzing and comparing each of the experiment results. Result classifying Multi-Perceptron classifier for selected genes using Pearson correlation coefficient represented the accuracy of 95.6%.

• The Journal of the Korean bone and joint tumor society
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• v.6 no.4
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• pp.143-151
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• 2000

Purpose : The p53 tumor suppressor gene is one of the most frequently altered genes in human malignancies. We try to explore the implication of p53 alteration in Ewing's sarcoma. Materials and Methods : We analyzed 35 paraffin blocks to explore the deletion and sequence alterations of p53. Results : Quantitative PCR analysis showed that 2 tumors showed a homozygous deletion of the gene. Mutational analysis of exons 4 to 9 of p53 by PCR-SSCP revealed that 3 tumors carry sequence alterations in exons 5 or 8, and DNA sequencing analysis identified missense point mutations. Conclusion : Taken together, our data demonstrate that p53 is genetically altered in a small fraction of Ewing's sarcoma.

• 대한두경부종양학회:학술대회논문집
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• 1998.05a
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• pp.115-117
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• 1998

• Journal of Chest Surgery
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• v.37 no.3
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• pp.261-266
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• 2004

Although significant progress has been made in the surgical treatment of esophageal carcinoma as well as in the detection of early stage esophageal carcinoma by diagnostic techniques, the prognosis of the esophageal carcinoma patients remain poor. The p53 gene product is known to regulate cell growth and proliferation. And the nm23 gene was identified originally as an anti-metastatic influence whose expression was correlated inversely with tumor metastatic potential in murine melanoma cell lines. This experiment was intended to know the relationship among the p53 and nm23 gene expression versus clinicopahologic characteristics of the esophageal cancer. Total 40 cases were collected from patients who had undergone esophagectomy at St. Mary's Hospital, Catholic university of Korea. Immunohistochemical stain for p53 mutant-type protein and nm23 protein was graded as <10% positive tumor cells: negative; 10∼30% positive tumor cells: ＋ ; 30∼50% positive tumor cells: ＋＋, and >50% positive tumor cells: ＋＋＋. The tumor invasion was grades as none:－ ; mild:＋ ; moderate:＋＋ ; severe: ＋＋＋. Overexpression of p53 protein and nm23 was not associated with the survival and cliniocopathologic characteristics of the esophageal cancer. Moreover, the combination analysis of p53 and nm23 revealed that there was no relationship between the gene expression and the clinicopatholic characteristics of the esophageal cancer.

• Proceedings of the Korea Information Processing Society Conference
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• 2007.11a
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• pp.713-716
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• 2007

오늘날 인간 프로젝트와 같은 종합적인 연구의 궁극적 목적을 달성하기 위해서는 이들 연구로부터 획득한 대량의 관련 데이터에 대해 새로운 현실적 의미를 부여할 수 있어야 한다. 따라서 현재의 마이크로어레이 기술을 이용해서 효과적으로 종양을 분류하기 위해서는 특정 종양 분류와 밀접하게 관련이 있는 정보력 있는 유전자를 선택하는 과정이 필수적이다. 본 논문에서는 암에 걸린 흰쥐 외피 기간 세포 분화 실험에서 얻어진 3840 유전자의 마이크로어레이 cDNA를 이용해 데이터의 정규화를 거쳐 유사성 척도 방법으로 정보력 있는 유전자들을 추출한 후, DT, NB, SVM, MLP 알고리즘을 이용하여 클래스 분류 모델을 구축하고, 성능을 비교분석하였다. 피어슨 적률 상관 계수를 이용하여 선택된 50 유전자들을 멀티퍼셉트론 분류기로 분류한 결과 94.8%의 정확도를 보여 가장 최적의 조합을 보였다.

• Nuclear Medicine and Molecular Imaging
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• v.42 no.3
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• pp.235-245
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• 2008

Purpose: The HSV1-tk gene has been extensively studied as a type of reporter gene. In hepatocellular carcinoma (HCC), only a small proportion of patients are eligible for surgical resection and there is limitation in palliative options. Therefore, there is a need for the development of new treatment modalities and gene therapy is a leading candidate. In the present study, we investigated the usefulness of substrate, 2'-fluoro-2'-deoxy-1-${\beta}$-D-arabino-furanosyi-5-[$^{124/125}I$]iodo- uracil ([$I^{124/125}I$]FIAU) as a non-invasive imaging agent for HSV1-tk gene therapy in hepatoma model using small animal PET. Material and Methods: With the Morris hepatoma MCA cell line and MCA-tk cell line which was transduced with the HSV1-tk gene, in vitro uptake and correlation study between [$^{125}I$]FIAU uptake according to increasing numeric count of percentage of MCA-tk cell were performed. The biodistribution data and small animal PET images with [$^{124}I$]FIAU were obtained with Balb/c-nude mice bearing both MCA and MCA-tk tumors. Results:, Specific accumulation of [[$^{125}I$]FIAU was observed in MCA-tk cells but uptake was low in MCA cells. Uptake in MCA-tk cells was 15 times higher than that of MCA cells at 480 min. [$^{125}I$]FIAU uptake was linearly correlated (R2 =0.964, p =0.01) with increasing percentage of MCA-tk numeric cell count. Biodistribution results showed that [$^{125}I$]FIAU was mainly excreted via the renal system in the early phase. Ratios of MCA-tk tumor to blood acting were 10, 41, and 641 at 1 h, 4 h, and 24 h post-injection, respectively. The maximum ratio of MCA-tk to MCA tumor was 192.7 at 24 h. Ratios of MCA-tk tumor to liver were 13.8, 66.8, and 588.3 at 1 h, 4 h, and 24 h, respectively. On small animal PET, [$^{124}I$]FIAU accumulated in substantial higher levels in MCA-tk tumor and liver than MCA tumor. Conclusion: FIAU shows selective accumulation to HSV1-tk expressing hepatoma cell tumors with minimal uptake in normal liver. Therefore, radiolabelled FIAU is expected to be a useful substrate for non-invasive imaging of HSV1-tk gene therapy and therapeutic response monitoring of HCC.

• Journal of Chest Surgery
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• v.42 no.2
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• pp.141-147
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• 2009

Background: We performed this study to identify the tumor suppressor genes located in the long arm of chromosome 21 in non-small cell lung cancer. Material and Method: The genes of USP25 in 21q11.2, NCAM2, ADAMTS1 in 21q21.2, and Claudin-8 (CLDN8), Claudin-17 (CLDN17) and TIAM1 in 21q22.1 were investigated for their gene expressions, genetic alterations and promoter methylation. Result: The expressions of CLDN8 and CLDN17 were significantly decreased in 7 (L132, H157, H358, H522, H1299, H1703 and HCC2108) of 13 cell lines, and the expression of ADAMTS1 was also significantly reduced in 6 cell lines (A549, SW900, H1299, H1373, H1703 and H1793). There were no genetic alterations by PCR-SSCP and cDNA cloning in the cell lines with a decreased gene. In the cell lines with a decreased gene expression, the mRNA expression was increased significantly with treatment of 5-Aza-CdR. Conclusion: These results suggest that the ADMTS1, CLDN8 and CLDN17 may act as tumor suppressor genes.

• The Journal of the Korean bone and joint tumor society
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• v.8 no.3
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• pp.69-75
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• 2002

Werner's syndrome is a rare autosomal recessive disorder manifesting as premature aging. It is also known to be characterized by a high frequency of malignant tumors, especially sarcomas. However, Werner's syndrome may be not only a premature aging disease but also a cancer syndrome, because the malignant tumors in these patients are different from those of normal population with respect to involved site, histological type, and age of onset. Recent studies found Werner's syndrome was caused by a mutation of Werner helicase suggesting that WRN helicase may participate in metabolism and repair of DNA. And a dysfunction of WRN helicase may induce the genomic instability causing somatic mutations. Further studies of Werner's syndrome associated with sarcoma might give much informations about the normal aging process and the pathogenesis of sarcomas.