• Tuberculosis and Respiratory Diseases
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• v.67 no.2
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• pp.145-147
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• 2009

Etoposide is a semi-synthetic derivative of podophyllotoxin that is effective against many cancers including small cell lung cancer. We report a case of etoposide-induced anaphylaxis in a 51-year-old woman who tolerated etoposide during her first cycle chemotherapy regimen. During the second cycle, she complained of generalized urticaria and dyspnea 5 minutes after being infused with etoposide. She recovered completely with antihistamine, corticosteroid and fluid replacement. The intradermal skin test with etoposide showed a clear positive immediate reaction. This case suggests that etoposide can induce IgE-mediated anaphylaxis.

• Tuberculosis and Respiratory Diseases
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• v.68 no.4
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• pp.226-230
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• 2010

Androgen deprivation therapy, which is the standard treatment for metastatic prostate cancer, includes nonsteroidal antiandrogenic drugs, such as flutamide, nilutamide and bicalutamide. Of them, bicalutamide rarely induces interstitial pneumonia. We report a case of bicalutamide-induced interstitial pneumonia. A 68-year old male diagnosed with prostate cancer and multiple bone metastases presented with dry cough and low grade fever for 3 days. He had taken bicalutamide (50 mg/day) for 13 months. High resolution computed tomography revealed ground glass opacity in his right upper lung. The laboratory studies showed no eosinophilia in the serum and bronchoalveolar lavage fluid. Despite the use of antimicrobial agents for 2 weeks, the extent of the lung lesions increased to the left upper and right lower lung. He had no environmental exposure, collagen vascular disease and microbiological causes. Under the suspicion of bicalutamide-induced interstitial pneumonia, bicalutamide was stopped and prednisolone (1 mg/kg/ day) was initiated. The symptoms and radiologic abnormalities were resolved with residual minimal fibrosis.

• Tuberculosis and Respiratory Diseases
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• v.44 no.3
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• pp.661-668
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• 1997

The majority of lung cancers associated with hyperamylasemia are adenocarcinomas. Here we report an unusual case of a 54-year-old male patient who complained of dyspnea, anterior chest wall discomfort and facial edema for one month, presenting with a huge mediastinal mass and hyperamylasemia complicated by pericardial effusion. Histological evaluation of mediastinal mass revealed small cell carcinoma and pericardium showed nonspecific inflammation with fibrosis. The serum amylase had an electrophoretic mobility similar to that of salivary gland enzyme. There were no evidence of a salivary or pancreatic causes of hyperamylasemia. After chemotherapy, parenchymal lung lesions improved and hyperamylasemia disappeared. For the management of pericardial effusion, a pericardial window was formed. We concluded that the striking increase in serum amylase was due to the ectopic production of this enzyme by the tumor.

• Molecules and Cells
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• v.27 no.5
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• pp.503-513
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• 2009

Proteoglycans located in basement membranes, the nanostructures underling epithelial and endothelial layers, are unique in several respects. They are usually large, elongated molecules with a collage of domains that share structural and functional homology with numerous extracellular matrix proteins, growth factors and surface receptors. They mainly carry heparan sulfate side chains and these contribute not only to storing and preserving the biological activity of various heparan sulfate-binding cytokines and growth factors, but also in presenting them in a more "active configuration" to their cognate receptors. Abnormal expression or deregulated function of these proteoglycans affect cancer and angiogenesis, and are critical for the evolution of the tumor microenvironment. This review will focus on the functional roles of the major heparan sulfate proteoglycans from basement membrane zones: perlecan, agrin and collagen XVIII, and on their roles in modulating cancer growth and angiogenesis.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.12
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• pp.4745-4751
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• 2014

Oxidative stress is caused by an imbalance in the redox status of the body. In such a state, increase of free radicals in the body can lead to tissue damage. One of the most important species of free radicals is reactive oxygen species (ROS) produced by various metabolic pathways, including aerobic metabolism in the mitochondrial respiratory chain. It plays a critical role in the initiation and progression of various types of cancers. ROS affects different signaling pathways, including growth factors and mitogenic pathways, and controls many cellular processes, including cell proliferation, and thus stimulates the uncontrolled growth of cells which encourages the development of tumors and begins the process of carcinogenesis. Increased oxidative stress caused by reactive species can reduce the body's antioxidant defense against angiogenesis and metastasis in cancer cells. These processes are main factors in the development of cancer. Bimolecular reactions cause free radicals in which create such compounds as malondialdehyde (MDA) and hydroxyguanosine. These substances can be used as indicators of cancer. In this review, free radicals as oxidizing agents, antioxidants as the immune system, and the role of oxidative stress in cancer, particularly breast cancer, have been investigated in the hope that better identification of the factors involved in the occurrence and spread of cancer will improve the identification of treatment goals.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.12
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• pp.7271-7275
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• 2013

Objective: To investigate the association between the gene polymorphisms of angiotensin-converting enzyme (ACE) and digestive system cancer risk. Method: A search was performed in Pubmed, Medline, ISI Web of Science and Chinese Biomedical (CBM) databases, covering all studies until Sep 1st, 2013. Statistical analysis was performed by using Revman5.2 and STATA 12.0. Results: A total of 15 case-control studies comprising 2,390 digestive system cancer patients and 9,706 controls were identified. No significant association was found between the I/D polymorphism and digestive cancer risk (OR=0.93, 95%CI = (0.75, 1.16), P=0.53 for DD+DI vs. II). In the subgroup analysis by ethnicity and cancer type, no significant associations were found for the comparison of DD+DI vs. II. Results from other comparative genetic models also indicated a lack of associations between this polymorphism and digestive system cancer risks. Conclusions: This meta-analysis suggested that the ACE D/I polymorphism might not contribute to the risk of digestive system cancer.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.10
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• pp.4147-4156
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• 2015

Lung cancer is a serious health problem and leading cause of death worldwide due to its high incidence and mortality. More than 80% of lung cancers feature a non-small cell histology. Over few decades, systemic chemotherapy and surgery are the only treatment options in this type of tumor but due to their limited efficacy and overall poor survival of patients, there is an urge to develop newer therapeutic strategies which circumvent the problems. Enhanced knowledge of translational science and molecular biology have revealed that lung tumors carry diverse driver gene mutations and adopt different intracellular pathways leading to carcinogenesis. Hence, the development of targeted agents against molecular subgroups harboring critical mutations is an attractive approach for therapeutic treatment. Targeted therapies are clearly more preferred nowadays over systemic therapies because they target tumor specific molecules resulting with enhanced activity and reduced toxicity to normal tissues. Thus, this review encompasses comprehensive updates on targeted therapies for the driver mutations in non-small cell lung cancer (NSCLC) and the potential challenges of acquired drug resistance faced i n the field of targeted therapy along with the imminent newer treatment modalities against lung cancer.

• Tuberculosis and Respiratory Diseases
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• v.71 no.6
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• pp.417-424
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• 2011

Background: Recent evidences have revealed metabolic functions of p53 in cancer cells; adaptation or survival to metabolic stress and metabolic shift toward oxidative phosphorylation. However, further studies in clinical setting are needed. We investigated whether p53 protein expression, as a surrogate marker for loss of p53 function, is associated with metabolic features of stage I non-small cell lung cancer (NSCLC), focusing on tumor necrosis and maximal standardized uptake value (SUVmax) on $^{18}F$-fluorodeoxyglucose positron emission tomography. Methods: Clinical information was obtained from retrospective review of medical records. p53 expression was assessed by immunohistochemical staining. Results: p53 protein expression was detected in 112 (46%) of 241 NSCLC cases included in this study. p53 expression was independently associated with the presence of necrosis (odds ratio [OR], 2.316; 95% confidence interval [CI], 1.215~4.416; p=0.011). Non-adenocarcinoma histology (OR, 8.049; 95% CI, 4.072~15.911; p<0.001) and poorly differentiation (OR, 6.474; 95% CI, 2.998~13.979; p<0.001) were also independently associated with the presence of necrosis. However, p53 expression was not a significant factor for SUVmax. Conclusion: p53 protein expression is independently associated with the presence of necrosis, but not SUVmax.

• Tuberculosis and Respiratory Diseases
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• v.65 no.1
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• pp.52-56
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• 2008

Sarcoidosis is a systemic granulomatous disease that primarily affects the lung and lymphatic system of the body. Since Brincker first noted a statistically significant increase of malignant tumors among sarcoidosis patients, there have been several reports on simultaneously developed sarcoidosis and malignancy. A 30-year-old man was admitted to our hospital because of multiple enlarged mediastinal lymph nodes. The patient had been well until approximately 10 days before admission, when he developed a cough. Chest X-ray and computed tomography (CT) of the chest that were performed at the outpatient department revealed multiple enlarged mediastinal lymph nodes. Cervical lymph node biopsy revealed both non-caseating granuloma and metastatic papillary carcinoma, whereas the mediastinal lymph node showed only non-caseating granuloma. The thyroid gland surgical specimen showed papillary carcinoma. We report here on a case of a 30-year-old man who had sarcoidosis and thyroid cancer, and we include a review of the literature.

• Tuberculosis and Respiratory Diseases
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• v.76 no.1
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• pp.15-22
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• 2014

Background: Apoptosis plays a role in the development of pleural effusion. Caspase-cleaved cytokeratin 18, a marker for epithelial cell apoptosis, was evaluated in pleural effusion. Methods: A total of 79 patients with pleural effusion were enrolled. The underlying causes were lung cancer (n=24), parapneumonic effusion (n=15), tuberculous effusion (n=28), and transudates (n=12). The levels of M30, an epitope of caspase-cleaved cytokeratin 18, were measured in blood and pleural fluids using enzyme-linked immunosorbent assay along with routine cellular and biochemical parameters. The expression of M30 was evaluated in the pleural tissues using immunohistochemistry for M30. Results: The M30 levels in pleural fluid were significantly higher in patients with tuberculosis ($2,632.1{\pm}1,467.3U/mL$) than in patients with lung cancer ($956.5{\pm}618.5U/mL$), parapneumonic effusion ($689.9{\pm}413.6U/mL$), and transudates ($273.6{\pm}144.5U/mL$; all p<0.01). The serum levels were not significantly different among the disease groups. Based on receiver operating characteristics analysis, the area under the curve of M30 for differentiating tuberculous pleural effusion from all other effusions was 0.93. In the immunohistochemical analysis of M30, all pathologic types of cancer cells showed moderate to high expression, and the epithelioid cells in granulomas showed high expression in tuberculous pleural tissues. Conclusion: Caspase-cleaved cytokeratin 18 was most prominently observed in tuberculous pleural effusion and showed utility as a clinical marker. The main source of M30 was found to be the epithelioid cells of granulomas in tuberculous pleural tissues.