• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• 제26권6호
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• pp.581-590
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• 2000

Alterations in the cellular genome affecting the expression or function of genes controlling cell growth and differentiation are considered to be the main cause of cancer. Over 30 oncogenes can be activated by insertional mutagenesis, single point mutations, chromosomal translocations and gene amplification. The ras oncogenes have been detected in $15{\sim}20%$ of human tumors that include some of the most common forms of human neoplasia and are known to acquire their transforming properties by single point mutations in two domains of their coding sequences, most commonly in codons 12 and 61. The ras gene family consists of three functional genes, N-ras, K-ras and H-ras which encode highly similar proteins of 188 or 189 amino acid residues generically known as P21. ras proteins have been shown to bind GTP and GTP, and possess intrinsic GTPase activity. Experimental study was performed to observe the mutational change of the ras gene family and apply the results to the clinical activity. 36 Golden Syrian Hamster each weighing $60{\sim}80g$ were used and painted with 0.5% DMBA by 3 times weekly on the right buccal cheek(experimental side) for 6, 8, 10, 12, 14 and 16 weeks. Left buccal cheek (control side) was treated with mineral oil as the same manner of the right side. The hamsters were sacrificed on the 6, 8, 10, 12, 14 & 16 weeks. Normal and tumor tissues from paraffin block were completely dissected by microdissection and DNA from both tissue were isolated by proteinase K/phenol/chloroform extraction. Segments of the K-ras and H-ras gene were amplified by PCR using the oligonucleotide primers corresponding to the homologous region (codon 12 and 61) of the hamster gene, and then confirmational change of ras genes was observed by SSCP and autosequencing analysis. The results were as follows : 1. Malignant lesion could be found in the experimental side from the experimental six weeks. 2. One hamster among six showed point mutation of the H-ras codon 12($G{\rightarrow}A$ transition) at the experimental 10 and 14 weeks. 3. One of six at 6 weeks, two of six at 8 weeks and one of six at 12 weeks revealed the confirmational change of the H-ras codon 61($A{\rightarrow}T$ transversion). 4. The incidence of point mutation of H-ras codon 12 and 61 were 5.5%(2 of 36) and 11%(4 of 36) respectively. 5. Point mutation of the K-ras could not be seen during the whole experimental period. Form the above results, these findings strongly support the concept that H-ras oncogenes may have the influence of the DMBA induced carcinoma of hamster buccal pouch.

• Journal of Gastric Cancer
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• 제3권1호
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• pp.38-43
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• 2003

Purpose: Caspase 2, a member of the family of ICE-like proteases, is activated by the Fas pathway and induces apoptosis by triggering the caspase cascade. The purpose of this study was to determine whether the expression pattern of caspase 2 might be associated with gastric cancer development and if so, to determine to which pathologic parameter it is linked. Materials and Methods: For the construction of the gastric cancer tissue microarray, 78 paraffin-embedded tissues containing gastric cancer areas were cored 3 times and transferred to the recipient master block. The expression pattern of caspase 2 was examined on tissue microarray slides by using immunohistochemistry and was compared with pathologic parameters, including histologic type, depth of invasion, lymph node metastasis, and peritoneal dissemination. Results: Caspase 2 was expressed on superficial and foveolar epithelial cells and lymphocytes in the gastric mucosa, mainly in cytoplasm. We found loss of caspase 2 expression in 41 ($52.6\%$) of the 78 gastric cancer tissues. Statistically, histologic type and other pathologic parameters were not related with loss of caspase 2 expression Conclusion: Our findings provide enough evidence that loss of caspase 2 expression may contribute to the development of Korean gastric cancer and that it might be one of the possible escape mechanisms from apoptosis in gastric cancer.

• Asian Pacific Journal of Cancer Prevention
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• 제15권14호
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• pp.5867-5872
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• 2014

Background: Cervical cancer is listed as one of high-incidence endemic diseases in Xinjiang. Our study aimed to evaluate the expression of TLR9 in uterine cervical tissues of Uyghur women and examine associations with clinicopathological variables. We further characterized the direct effects of TLR9 upon the selective silencing of human papillomavirus (HPV) E6 and E7 oncoprotein expression in HPV 16-positive human cervical carcinoma cells treated with siRNA in vitro. Materials and Methods: Immunohistochemistry was applied to evaluate TLR9 expression in 97 formalin-fixed paraffin-embedded cervical samples from Uyghur women; 32 diagnosed with cervical squamous cell carcinomas (CSCC), 14 with low-grade cervical intraepithelial neoplasias (CINI), 10 medium-grade (CINII), 24 high-grade (CINIII), and 17 chronic cervicitis. $BLOCK-iT^{TM}$ U6 RNAi Entry Vector $pENTR^{TM}$/U6-E6 and E7 was constructed and transfected the entry clone directly into the mammalian cell line 293FT. Then the HPV 16-positive SiHa human cervical carcinoma cell line was infected with RNAi recombinant lentivirus. RT-PCR and Western blotting were used to determine the expression of TLR9 in both SiHa and HPV 16 E6 and E7 silenced SiHa cells. Results: Immunohistochemical staining showed that TLR9 expression was undetectable (88.2%) or weak (11.8%) in chronic cervicitis tissues. However, variable staining was observed in the basal layer of all normal endocervical glands. TLR9 expression, which was mainly observed as cytoplasmic staining, gradually increased in accordance with the histopathological grade in the following order: chronic cervicitis (2/17, 11.8%)

• Journal of Gastric Cancer
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• 제5권1호
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• pp.34-39
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• 2005

목적: KLF6는 모든 조직에서 발현되고 있는 zinc finger를 가진 종양억제유전자로 인체 여러 암에서 불활성화되어 있다. 연구자들은 KLF6 단백의 발현 변화가 위암의 발생에 관여하는 지를 알아보고자 하였다. 대상 및 방법: 85예의 파라핀 포매된 위암조직에서 암세포들으 각각 3군데에서 펀치하여 새로운 파라핀 블록으로 옮겨 위암의 tissue microarray를 제작하였다. Tissue microarray 절편에서 KLF6 단백에 대한 항체로 면역화학염색을 실시한 후 발현 양상을 병리 지표들인 조직학적 소견, 침습 정도, 림프절 전이 및 복막파종 등과의 연관성을 조사하였다. 결과: KLF6 단백은 위점막의 표면과 소와 상피세포에서 주로 발현되고 있었고 85예 중 28예($28.9\%$)에서 발현 소실이 관찰되었다. 흥미롭게도 KLF6 단백의 발현 소실은 림프절 전이와 통계적으로 연관성이 있었으나 조직학적 소견, 침습 정도와 복막파종과는 연관성이 없었다. 결론: 이러한 소견들은 KLF6 단백의 발현 소실이 위장관 상피세포의 비정상적인 성장과 분화를 유도하고 위암의 발생 및 진행에 관여한다는 것을 의미한다.

• Journal of Gastric Cancer
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• 제6권1호
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• pp.25-30
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• 2006

목적: EphB2 수용체는 티로신 키나제 수용체 군에 속하면서 Wnt 신호 전달계의 대상 유전자로 세포의 성장 및 이동을 조절함으로써 종양의 발생과 진행을 억제한다. 연구자들은 한국인 위암에서 EphB2 단백의 발현 변화가 위암의 발생 및 진행에 관여하는지와 위암의 병리 지표들과의 연관성을 알아보고자 하였다. 대상 및 방법: 83예의 파라핀 포매된 위암조직에서 암세포들을 각각 3군데에서 펀치하여 새로운 파라핀 블록으로 옳겨 위암의 고집적 tissue microarray를 제작하였다. Tissue microarray 절편에서 EphB2 단백에 대한 항체로 면역조직화 학염색을 실시한 후 그 발현 양상을 병리 지표들인 조직학적 분류, 침습 정도, 림프절 전이 및 복막 파종과의 연관성을 조사하였다. 결과: EphB2 단백은 정상 위 점막 상피세포의 세포막과 세포질에서 발현되고 있었고 조사된 83예의 위암 중 30예 (36.1%)에서 발현이 소실되었다. 흥미롭게도 EphB2 단백의 발현 소실은 위암의 림프절 전이와 통계적으로 연관성이 있었으나 조직학적 분류, 침습 정도 및 복막 파종과는 연관성이 없었다. 결론: 이러한 소견들은 EphB2 수용체 단백의 발현 소실이 위암의 발생 및 진행에 있어 중요한 과정 중의 하나임을 의미한다.

• Restorative Dentistry and Endodontics
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• 제25권1호
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• pp.1-16
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• 2000

It is difficult to treat the endodontic apical perforation successfully. In this study, we hypothesized that the application of PDGF-BB and IGF-I into periapical perforation site may accelerate periapical healing and lead to bone deposition. And the specificity of osteonectin in periapical healing was investigated. The experiments were performed on the upper and lower 51 premolar teeth of 4 beagle dogs. The pulp chamber of each tooth was opened and the dental plaque was inserted into the canal for developing the periapical lesion for 5 weeks. Then, the roots were artificially perforated at the apex with the number 4 profile of .06 taper. In each step, standard periapical radiographs were taken to compare the size of lesion each other. The radiographs were scanned and analyzed by image analysis system. The mean and standard deviation of periradicular radiolucency ratios were calculated in each group. ANOVA was used for comparison. 51 premolars were grouped into 3 groups; control group, calcium hydroxide-treated group and calcium hydroxide plus growth factors-treated group. In the control group, the apical perforations were not sealed and obturated with gutta-percha and ZOE sealer by lateral condensation technique. In the experimental groups, the apical perforation were sealed with calcium hydroxide and with/without $4{\mu}g$ of PDGF-BB & IGF-I in cellulose gel and obturated by lateral condensation technique. Fluorescent bone markers were used to measure new bone formation. Following 2, 4, 12 weeks after experiment the dogs were sacrificed and histologic sections were prepared. Each tooth block including periapical lesion was sectioned mesiodistally. One half of the sections were decalcified with 6% nitric acid and processed by standard paraffin embedding technique. The sections were stained by hematoxylin and eosin, and immunostained for osteonectin. Histomorphometrical measurement of neoformed bone was performed using a light microscope. And the other half of the sections were prepared by undecalcified preparation, and confocal laser scanning microscopic investigations were done.

• Tuberculosis and Respiratory Diseases
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• 제47권2호
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• pp.150-160
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• 1999

연구배경: CREST 증후군은 전신성 경화증의 이형으로 전신성 경화증에 비교하여 병의 진행이 늦은 것으로 알려져 있다. 하지만 CREST 증후군 환자의 약 50%에서 폐나 심장질환의 증거 없이 폐고혈압이 발생하며, 이러한 환자들의 이년 생존률은 40%로 폐고혈압이 없는 환자에 비해 예후가 매우 나쁘다. 그러나 CREST 증후군에 동반되는 폐고혈압의 원인과 병리기전에 대해서는 전혀 알려진 바 없으며 막연히 원발성 폐고혈압의 이형(variant form) 또는 이차성 폐고혈압으로 분류되고 있다. 총상병변(plexiform lesion) 내 증식된 내피세포의 클론성 검증은 폐고혈압을 원발성과 이차성으로 나누는 기준이 되고 있다. 이에 저자들은 CREST 증후군이 동반된 폐고혈압 환자의 총상병변 내피세포의 클론성을 분석함으로써 CREST 동반된 폐고혈압이 원발성인지 이차성인지를 알아보고자 하였다. 방법: 폐고혈압을 동반한 CREST 증후군 여자환자에서 얻은 폐조직의 파라핀 block을 사용하여 microdissection 방법으로 총상병변내에 증식된 내피세포를 분리한후 X-염색체의 methylation pattern을 이용하여 클론성 분석을 시행하였다. 같은 방법으로 중막 비후를 보이는 혈관의 혈관 평활근과 폐실질의 클론성도 분석하였다. 결과: 14개 총상병변의 '증식된 내피세포'의 클론성 모두 다클론성 이었다. 또한 중막비후가 현저한 5개 폐동맥의 평활근세포 클론성도 모두 다클론성 이었다. 결론: 이상의 결과는 CREST 증후군에 동반되는 폐고혈압이 원발성 폐고혈압과는 다른 병리 기전을 갖는 이차성 폐고혈압임을 시사한다.

• 한국건설순환자원학회논문집
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• 제1권1호
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• pp.17-25
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• 2013

축열재 이용 기술은 실내 냉난방을 위하여 사용된 에너지를 장시간 일정온도로 유지할 수 있도록 하여 에너지 사용 효율을 높이는 장점이 있다. 이 중 상변화 물질을 이용한 잠열 축열재는 물질의 잠열성질을 이용하는 것으로서 심물질로서 일정온도에서 녹는점을 갖는 물질을 캡슐화 하여 이를 건축자재에 적용하여 실내 및 외기의 온도에 따라서 심물질이 녹거나 어는 과정에서 축열과 방열로 인한 에너지 절감 및 차단 효과를 갖는다. 상변화 물질을 이용해 축열재를 만드는 방법은 마이크로 캡슐화의 방법이 있다. 이 방법은 크게 분류하면 화학적 방법, 물리 화학적 방법 및 물리적 기계적 방법의 3가지로 나눌 수 있다. 물리 화학적 방법으로 습식공정에 의한 마이크로 캡슐화 공정을 이용했으며 이 공정은 심물질을 용매에서 에멀젼화한 다음 고분자모노머를 심물질인 에멀젼의 벽면에 코팅하여 경화 시키는 공정이다. 이 경우에 심물질의 에멀젼이나 벽재 모노머의 코팅 성능을 좋게 하기 위하여 계면활성제가 사용된다. 또한 계면활성제의 특성에 따라서 마이크로 캡슐화의 성능이 좌우되고 특히 벽재물질의 코팅 두께 및 코팅의 균일성에 크게 좌우된다. 본 연구에서는 상변화를 이용한 축열재로서 심물질인 1-도데카놀을 멜라민수지로 계면중합법에 의하여 마이크로 캡슐화 하는데 있어서 계면활성제인 SSMA(sulfonated styrene-maleic anhydride)의 화학적 특성에 따른 마이크로 캡슐의 성능과 이에 따른 축열 성능을 비교하였다.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• 제27권5호
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• pp.373-384
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• 2001

Cellular proliferation is an intricately regulated process mediated by the coordinated interactions of critical growth control genes. Two of these factors in mammalian cells are the p53 and mdm-2 genes. A protein product of the mem-2 oncogene has been recently shown to associate with the protein encoded by the tumor suppressor gene p53. The p53 tumor suppressor protein is stabilized in response to DNA damage and other stress signals and causes the cell to undergo growth arrest or apoptosis, thus preventing the establishment of mutations in future cellular generations. Mutation or loss of p53 is a very common event in tumor progression. It occurs in about 50% of all tumors analysed including of colon, lung, breast and liver. The cellular mdm-2 gene, which has potential transforming activity that can be activated by overexpression, is amplified in a significant percentage of human sarcoma and in other mammalian tumors. Proteins encoded by the mdm-2 gene are able to bind to the p53 protein and, when overexpressed, can inhibit p53's transcriptional activation function, thus mdm-2 can act as a negative regulator of p53 function. Experimental study was performed to observe the relationship between p53 gene mutation and mdm-2 protein expression and apply the results to the clinical activity. 36 golden syrian hamster each weighing $60{\sim}80g$ were used and painted with 0.5% DMBA by 3 times weekly on the right buccal cheek(experimental side) for 6, 8, 10, 12, 14 and 16 weeks. Left buccal cheek(control side) was treated with mineral oil as the same manner to the right side. The hamsters were sacrificed on the 6, 8, 10, 12, 14 & 16 weeks. Normal and tumor tissues from paraffin block were examined for histology and immunohistochemistry observation, and were completely dissected by microdissection and DNA from both tissue were isolated by proteins K/phenol/chloroform extraction. Segments of the hamster p53 exons 5, 6, 7 and 8 were amplified by PCR using the oligonucleotide primers, and then confirmational change was observed by SSCP respectively. The results were as follows : 1. Dysplasia at 6 weeks, carcinoma in situ at 8 weeks and invasive carcinoma from 10 weeks could be observed in experimental groups. 2. p53 mutations were detected in 10 of the 36(28%) and the exons 6(6 of the 10 : 60%) was the most hot spot area among the highy conserved region(exons 5, 6, 7 & 8). 3. Immunohistochemical study confirmed 22 of the 36(61%) of p53 expression involving 10 of p53 mutations. 4. mdm-2 expression of was showed in 3 of the 36(8%) involving 1 of the 22 of p53 expression and 2 of the 14 of p53 non-expression. From the above results, mutation of p53 gene or expression of p53 protein may have the influence of the DMBA induced carcinoma of hamster buccal pouch but the expression of mdm-2 protein may not have relationship with tumorigenesis.

• Journal of Gastric Cancer
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• 제5권3호
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• pp.200-205
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• 2005

목적: Zinc finger를 가진 KLF4는 위장관 상피세포의 항상성 유지에 중요한 역할을 하는 종양억제유전자이다. 연구자들은 KLF4 단백의 발현 변화가 위암의 발생에 관여하는지를 파악하고 위암의 병리 지표들과 연관성이 있는지를 알아보고자 하였다. 대상 및 방법: 84예의 파라핀 포매된 위암조직에서 암세포들을 각각 3군데에서 펀치하여 새로운 파라핀 블록으로 옮겨 위암의 tissue microarray를 제작하였다. Tissue microarray 절편에서 KLF4 단백에 대한 항체로 면역화학염색을 실시한 후 발현 양상을 병리 지표들인 조직학적 소견, 침습 정도, 림프절 전이 및 복막파종 등과의 연관성을 조사하였다. 결과: KLF4 단백은 위점막의 표면과 소와 상피세포의 세포질과 핵에서 주로 발현되고 있었고 조사된 위암 84예 중 43예(51.2%)에서 발현이 현저히 저하되어 있거나 소실되어 있었다. 이러한 KLF4 단백의 발현 소실은 조직학적 소견, 침습 정도, 림프절 전이 및 복막파종과는 통계적으로 연관성이 없었다. 결론: 이러한 연구 결과는 KLF4 단백의 발현 소실이 위장관 상피세포의 비정상적인 성장과 분화를 유도하고 위암의 발생 초기에 관여한다는 것을 의미한다.