• Asian Pacific Journal of Cancer Prevention
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• 제13권8호
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• pp.3627-3630
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• 2012

The epithelial cell adhesion molecule (EpCAM) is a pan-epithelial differentiation antigen that is expressed on almost all carcinomas. However, a role in rat liver carcinogenesis has never been reported previously. Thus, its expression was investigated herein in rat liver tumors induced by diethylnitrosamine (DEN). Twenty male 5-week-old F344 rats were used in this experiment. Mini-osmotic pumps containing doses of 47.5 mg of DEN were inserted into the abdominal cavity of each animal to initiate liver carcinogenesis. All animals were sacrificed at 26 weeks after DEN treatment. At necropsy, hepatic masses were processed for histopathological examination, which revealed forty-four hepatocellular adenomas (HCAs) and twenty hepatocellular carcinomas (HCC). Tumors were immunohistochemically analyzed for EpCAM, proliferating cell nuclear antigen (PCNA) and co-localization of the two. EpCAM expression was mainly detected in hepatic tumor cells, showing a cytoplasmic staining pattern. However, expression was also slightly observed in normally-appearing surrounding hepatic cells. PCNA expression was highly detected in tumor cells, showing nuclear staining. Double staining of EpCAM and PCNA in tumors showed many cells with co-localization. Taken together, EpCAM and PCNA expression were increased in DEN-induced tumors and many tumor cells showed co-expression. It is suggested that EpCAM may increase during DEN-induced tumors, possibly associated with cell proliferation.

• Asian Pacific Journal of Cancer Prevention
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• 제14권2호
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• pp.695-700
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• 2013

Background: Mutations affecting the epidermal growth factor receptor (EGFR) are good predictors of clinical efficacy of EGFR tyrosine kinase inhibitors (TKI) in patients with non-small cell lung cancer. Serum carcinoembryonic antigen (CEA) levels are also regarded as predictive for the efficacy of EGFR-TKI and EGFR gene mutations. This study analyzed the association between EGFR gene mutations and clinical features, including serum tumor marker levels in lung adenocarcinomas patients. Patients and Methods: A total of 70 lung adenocarcinoma patients with complete clinical data and pathological specimens were investigated. EGFR gene mutations at exons 19 and 21 were assessed. Serum tumor markers were detected by protein chip-chemiluminescence at the corresponding time, and correlations were analyzed. Results: Mutations of the EGFR gene were detected in 27 of the 70 patients and the serum CEA and CA242 concentrations were found to be significantly associated with the incidence of EGFR gene mutations (P<0.05). The AUCs for CEA and CA242 were 0.724 (95% CI: 0.598~0.850, P<0.05) and 0.769 (95% CI: 0.523~0.800, P<0.05) respectively. Conclusions: Serum CEA and CA242 levels are associated with mutations of the EGFR gene in patients with lung adenocarcinomas.

• IMMUNE NETWORK
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• 제3권2호
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• pp.118-125
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• 2003

Background: Disialoganglioside GD2 is a tumor-associated antigen that is overexpressed on tumor cells of neuroectodermal origin, such as melanoma and neuroblastoma. Anti-idiotypic antibodies that mimic GD2 may induce more effective immune responses than GD2 antigen itself, because they are protein antigens and are known to be able to break immune tolerance. In this study, to explore the potential of anti-idiotypic antibodies as tumor vaccines, the ability of anti-idiotypic antibodies (Ab2) to induce anti-anti-idiotypic antibodies (Ab3) that bind to the original antigen GD2 was investigated. Methods: Six monoclonal anti-idiotypic antibodies (1A8, 1G5, 2B6, 3A4, 3D6, 3H9) to monoclonal antibody M2058, which is a monoclonal antibody to GD2, were produced in mice. Three (1A8, 3A4, 3H9) of them were selected based on their ability to inhibit the binding of Ab1 to D142.34 (murine melanoma cell expressing GD2). These 3 different Ab2 were injected into rabbits, and rabbit Ab3 induced by each of them were characterized. Results: Ab3-containing sera from two rabbits immunized with 1A8, 3A4, or 3H9 bound significantly (P<0.05) to D142.34 but not to B78.96 (GD2-negative cell), and bound significantly (P<0.05) to isolated GD2 but not to GD1a. Ab3-containing sera from two rabbits immunized with 3A4 or 3H9 inhibited significantly (P<0.05) the binding of Ab1 M2058 to D142.34, and inhibited significantly (P<0.05) the binding of Ab1 M2058 to the Ab2. Conclusion: These results suggest that anti-idiotypic antibodies 3A4 and 3H9 have a potential to be used as vaccines against tumors expressing GD2 by inducing GD2-specific antibodies (Ab3).

• Journal of Korean Neurosurgical Society
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• 제38권5호
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• pp.390-392
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• 2005

A case of chordoid meningioma occurring in a 61-year-old woman who did not have a Castleman's disease is presented. The patient had suffered from headache and motor dysphasia. Laboratory findings are normal. The tumor, located in the left frontal region and associated with peritumoral edema, was totally resected. Surgical specimen revealed a solid mass with irregular surface that measured $3.5{\times}4.5{\times}4cm$. Immunohistochemical staining revealed that the tumor cells expressed epithelial membrane antigen[EMA] focally, but not S-100 protein and glial fibrillary acid protein [GFAP], and the Ki-67 proliferative index of the tumor was 9%. The neoplasm was diagnosed chordoid meningioma of the World Health Organization[WHO] grade II. After total resection, her preoperative headache and dysphasia were disappeared.

• Radiation Oncology Journal
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• 제17권1호
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• pp.30-35
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• 1999

목적 : 자궁경부암의 치료후의 재발이나 병소의 지속을 발견하기 위한 종양표지자로서의 squamous cell carcinoma antigen(SCC) 와 carcinoembryonic antigen(CEA) 의 의의를 확인하고 향후의 치료시에 참고하고자 한다. 대상 및 방법 : 1995년 10월부터 1998년 8월까지 단국대학병원 치료방사선과에서 원발성 자궁경부암으로 근치적 방사선치료를 시행 받은 환자 중 22례를 대상으로 하였고 방사선치료전에 MRI 나 초음파를 시행하여 종양의 체적을 구하였으며 방사선치료 전에 SCC 와 CEA를 측정하였고 치료 후에도 주기적으로 SCC 와 CEA를 측정 하여 분석 하였다 결과 : 방사선 치료전에 측정한 SCC 치는 전체 22례 중 68.2$\%$ 에서 상승되어 있었으며, CEA 치는 측정이 이루어진 21례 중 19.0$\%$에서 상승되어 있었다. 종괴의 부피와 치료전의 SCC 치의 관련성은 극단적으로 벗어난 1례를 제외하면 상관계수가 0.59382 로 상당히 컸다. 종괴의 부피증가에 따른 CEA 치의 증가경향은 없었다. 치료후의 SCC 치는 9.1$\%$ 에서 CEA 치는 측정이 이루어진 21례 중 4.8$\%$ 에서 상승되어 있었다. 방사선치료 전에SCC 치가 상승되어 있었던 15례 중 14례에서 완전관해의 소견을 보였으며 그 14례 중 SCC 치가 정상 범위로 낮아진 경우가 13례(92.9$\%$) 였다. SCC 치가 치료 전에 상승되어 있다가 치료 후에 정상화 된 13례 중 5례에서 SCC 치의 정상 범위 이상의 재상승이 나타났는데 그 중 4례는 국소실패(3례) 혹은 국소 및 주변 림프절 실패(1례) 였고 나머지 1례는 임상적으로 무병상태(NED) 이다. 따라서 재발과 관련된 SCC 치 상승의 민감도는 100$\%$, 특이도는 93.8$\%$, 양성예측도는 85.7$\%$ 였다. SCC 의 재상승이 있은 후 임상적 재발을 발견할 때까지의 시간차이(lead time) 는 평균 1.2개월이었다. CEA 는 치료전 높았던 4례 모두에서 치료 후 완전 관해시에 정상화 되었고 이들 중 재발한 경우는 없었다. 결론 : 본 연구에서 SCC 와 CEA 는 치료전의 값이 상승되어 있었던 경우는 치료에 대한 반응과 재발을monitor 하는데 좋은 종양표지자로 나타났다. 그러나 치료전 SCC 치가 민감도가 높은데 비해 CEA 치는 민감도가 낮으며 CEA 와 SCC 를 모두 측정한 경우가 SCC 만 측정한 경우에 비해 예후의 관찰에 유리한 점이 없었다.

• Journal of Microbiology and Biotechnology
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• 제9권3호
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• pp.346-351
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• 1999

Tumor cells may alter the expression of proteins involved in antigen processing and presentation, allowing them to avoid recognition and elimination by cytotoxic T cells. In order to investigate whether the major histocompatibility complex (MHC) class I-mediated antigen processing machinery is preserved in human lung cancer cell lines, we examined the expression of multiple components of the MHC class I antigen processing pathway, including transporter associated with antigen processing (TAP), $\beta_2$-microglobulin, MHC class I molecules, and chaperones which have not been previously examined in this context. Row cytometry analysis showed that the cell surface expression of MHC class I molecules was downregulated in all of the cell lines. While some cell lines showed no detectable expression of MHC class I molecules, pulse-chase experiments showed that MHC class I molecules were synthesized in the other cell lines but not transported from the endoplasmic reticulum to the cell surface. Low or nondetectable levels of TAP1 and/or TAP2 expression were demonstrated by Western blot analysis in all of the cell lines, representing a variety of lung tissue types. In some cases, this was accompanied by loss of tapasin expression. Our findings suggest that downregulation of antigen processing may be one of the strategies used by tumors to escape immune surveillance. This study provides further information for designing the potential therapeutic applications such as immunotherapy and gene therapy against cancers.

• 한국생물공학회:학술대회논문집
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• 한국생물공학회 2005년도 생물공학의 동향(XVII)
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• pp.186-186
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• 2005

• Asian Pacific Journal of Cancer Prevention
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• 제13권7호
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• pp.3265-3270
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• 2012

Clinically, elevated cancer antigen 125 (CA-125) in blood predicts tumor burden in a woman's body, especially in the ovary, but cannot differentiate between malignant or benign. We here used intensive modern proteomic approaches to identify predictive proteins in the serum of women with elevated CA-125 to differentiate malignant from benign ovarian tumors. We identified differentially expressed proteins in serum samples of ovarian cancer (OC) patients, benign ovarian tumor (BT) patients, and healthy control women using mass spectrometry-based quantitative proteomics. Both the OC and BT patients had elevated CA-125. Quantitation was achieved using isobaric tags for relative and absolute quantitation. We obtained 124 quantified differential serum proteins in OC compared with BT. Two proteins, apolipoprotein A-4 (APOA4) and natural resistance-associated macrophage 1, were verified using Western blotting. Proteome profiling applied to OC cases identified several differential serum proteins in the serum of women with elevated CA-125. A novel protein, APOA4, has the potential to be a marker for malignant tumor differentiation in the serum of women with elevated CA-125.

• IMMUNE NETWORK
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• 제5권3호
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• pp.157-162
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• 2005

Background: 1-8D gene is a member of human 1-8 interferon inducible gene family and was shown to be overexpressed in fresh colon cancer tissues. Three peptides 1-6, 3-5 and 3-7 derived from human 1-8D gene were shown to have immunogenicity against colon cancer. Methods: To study tumor immunotherapy, of three peptides we established an active immunization model using HHD mice. $D^{b-/-}{\times}{\beta}2$ microglobulin $({\beta}2m)$ null mice transgenic for a chimeric HLA-$A2.1/D^{b-}\;{\beta}2m$ single chain (HHD mice) were challenged with B16/HHD/1-8D tumor cells and were immunized with irradiated peptide-loaded RMA- S/HHD/B7.1 transfectants. In therapy model tumor growth was retarded in HHD mice that were injected with 3-5 peptide-loaded RMA-S/HHD/B7.1. In survival test vaccination with 1-8D-derived peptide protects HHD mice from tumor progression after tumor challenge. Results: These studies show that peptide 3-5 derived from 1-8D gene can be the most effective candidate for the vaccine of immunotherapy against colon cancer and highlight 1-8D gene as putative colon carcinoma associated antigens. Conclusion: We demonstrated that RMA-S/HHD/ B7.1 loaded with 1-8D peptides, especially 3-5, immunization generates potent antitumor immunity against tumor cells in HHD mice and designed active immunization as proper immunotherapeutic protocols.

• Tuberculosis and Respiratory Diseases
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• 제72권6호
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• pp.507-510
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• 2012

Carbohydrate antigen 19-9 (CA19-9) is a specific tumor marker of the biliary, pancreatic and gastrointestinal tracts. CA19-9 is occasionally elevated in serum in patiens with benign pulmonary diseases such as bronchiectasis, idiopathic interstitial pneumonia or collagen disease-associated pulmonary fibrosis. Intralobar pulmonary sequestration is an uncommon congenital lung anomaly. It is dissociated from the normal tracheobronchial tree and is supplied by an anomalous systemic artery. There have been some reports of elevation of CA19-9 in this lesion. We report a case of intralobar pulmonary sequestration with elevated serum CA19-9 in a 29-year-old man who was diagnosed with bronchiectasia of left lower lung field on general check up. He had no evidence of any malignant disease in pancreatobiliary or gastrointestinal tracts. Elevated serum CA19-9 level might be encountered with benign pulmonary disease such as pulmonary sequestration.