Background: Photodynamic therapy is a viable option for lung cancer treatment, and many studies have shown that it is capable of inducing cell death in lung cancer cells. However, the precise mechanism of this cell death has not been fully elucidated. To investigate the early changes in cancer cell transcription, we treated A549 cells with the photosensitizer DH-I-180-3 and then we illuminated the cells. Methods: We investigated the gene expression profiles of the the A549 lung cancer cell line, using a DEG kit, following photodynamic therapy and we evaluated the cell viability by performing flow cytometry. We identified the genes that were significantly changed following photodynamic therapy by performing DNA sequencing. Results: The FACS data showed that the cell death of the lung cancer cells was mainly caused by necrosis. We found nine genes that were significantly changed and we identified eight of these genes. We evaluated the expression of two genes, 3-phosphoglycerate dehydrogenase and ribosomal protein S29. The expressed level of carbonic anhydrase XII, clusterin, MRP3s1 protein, complement 3, membrane cofactor protein and integrin beta 1 were decreased. Conclusion: Many of the gene products are membrane-associated proteins. The main mechanism of photodynamic therapy with using the photosensitizing agent DH-I-180-3 appears to be necrosis and this may be associated with the altered production of membrane proteins. (Tuberc Respir Dis 2007; 63: 52-58)
Background: Pleural effusion develops in approximately 40% of pneumonia patients. In 5-10% of these cases, it progresses to complicated parapneumonic effusion (CPPE) or empyema that requires drainage. The prognostic factors of CPPE and empyema remain to be clarified. We examined the treatment outcomes of CPPE and empyema and elucidating their prognostic factors. Methods: One hundred and fifteen patients with CPPE or empyema, who were diagnosed and treated in Kyungpook National University Hospital (Daegu, Korea) between September 2001 and December 2005, were retrospectively analyzed. All the data was acquired from their chart review, and regarding treatment results, the time to defervescence and the length of hospital stay were analyzed. Results: The treatment was successful in 101 patients with a success rate of 87.8%. Multivariate analysis showed the level of pleural fluid lactate dehydrogenase (LDH) to be a significant prognostic factor (odds ratio [OR] 7.37; 95% confidence interval [CI], 1.63 to 33.37; p=0.009). Pussy pleural fluid (r=0.236; p=0.01) and the frequency of urokinase use (r=0.257; p=0.01) correlated with the time to defervescence. However, there was no clinical factor that correlated with the length of hospital stay. Conclusion: The pleural fluid LDH level is a useful prognostic factor for monitoring treatment results of CPPE and empyema. (Tuberc Respir Dis 2007; 63: 24-30)
Background: In pathogenesis and prognosis of lung cancer, significance of enormous types of genetic expression were very compounding and undetermined. We performed this study to search association between clinical characteristics and expression of COX-2, MMP-9 and p53 in non-small cell lung cancer. Methods: Ninety-one patients with adenocarcinoma or squamous cell carcinoma were enrolled. We had searched clinical data retrospectively and performed immunohistochemical staining for COX-2, MMP-9 and p53. We had analyzed significance of these three genes in clinical features and prognosis for survival. Results: 1) In squamous cell carcinoma, male was predominant and was significantly correlated with smoking. 2) Major prognostic determinants for overall survival were curative resection. 3) Expression of COX-2 was more frequent in adenocarcinoma than in squamous cell carcinoma. 4) Negative staining of COX-2, MMP-9 and p53 was more frequent in squamous cell carcinoma than adenocarcinoma. 5) Survival duration was longer in the group with positive expression of p53 and negative for COX-2 and MMP-9 (median duration of survival = 165.6 weeks) than groups with the other expressional patterns. 6) Significant correlation was found between expression of MMP-9 and COX-2. In squamous cell carcinoma, expression of MMP-9, COX-2 and mutant p53 were mutually correlated. 7) COX-2 expression was significant prognostic factor for survival in resected cancer group. In unresected inoperable non-small cell lung cancer group, MMP-9 was statistically significant prognostic factor for overall survival. Conclusion: COX-2 and MMP-9 might have some roles for progression or prognosis in some selected patients with non-small cell lung cancer. COX-2 and MMP-9 may have some roles for disease progression or prognosis in selected patients with NSCLC. (Tuberc Respir Dis 2007; 63: 31-41)
Background: TRAIL is a cytokine that selectively induces apoptosis in various cancer cell lines. Gefitinib is new targeted drug applied in lung cancer that selectively inhibits EGFR tyrosine kinase. However, lung cancers have shown an initial or acquired resistance to these drugs. This study examined the effect of IGF-1R and its blockade on enhancing the sensitivity of lung cancer cell lines to TRAIL and gefitinib. Methods: Two lung cancer cell lines were used in this study. NCI H460 is very sensitive to TRAIL and gefitinib. On the other hand, A549 shows moderate resistance to TRAIL and gefitinib. The IGF-1R blockade was performed using adenoviruses expressing the dominant negative IGF-1R and shRNA to IGF-1R and AG1024 (IGF-1R tyrosine kinase inhibitor). Results: The adenovirus expressing dominant negative IGF-1R(950st) induced the increased expression of defective IGF-1R on the lung cancer cell surface, and the adenovirus-shIGF-1R effectively decreased the level of IGF-1R expression on cell surface. The genetic blockade of IGF-1R by the adenovirus-dnIGF-1R and AG1024 increased the sensitivity of A549 cells to TRAIL. The reduction of IGF-1R by transduction with ad-shIGF-1R also increased the sensitivity of the A549 cells to gefitinib. Conclusion: The blockade of IGF-1R through various mechanisms increased the sensitivity of the lung cancer cell line that was resistant to TRAIL and gefitinib. However, further studies using other cell lines showing acquired resistance as well as in vivo animal experiments will be needed. (Tuberc Respir Dis 2007; 63: 42-51)
Background: Surgical lung biopsy is required to establish the etiology and stage of interstitial lung disease(ILD). and this procedure can be safe and meaningful for making clinical decisions. We wanted to determine the safety of surgical lung biopsy(SLB) in patients with interstitial lung disease(ILD). Methods: We conducted a retrospective review of 40 patients with suspected ILD and they underwent surgical lung biopsy from January 2001 to June 2006 at Chungnam University Hospital. We analyzed retrospectively according to their age, gender, pulmonary function, chest tube duration, the arterial blood gases, the procedural technique, and the requirement for supplemental oxygen and mechanical ventilation(MV) at the time of SLB. Results: The mean age of the patients was 56.4±16.13 years(range: 21 to 77 years). Overall, the 30-day and 90-day mortality rates were 15% and 20%, respectively. The predictors of perioperative mortality were either the need for mechanical ventilation(MV) at the time of SLB or the need for supplemental oxygen prior to undergoing SLB. Among the 32 patients who were 90-day survivors, the proportion of those patients using the oxygen supplement was 28.1% (n=9). All 8 patients who were 90-day non-survivors used oxygen supplement (p=0.000). The use of the MV was 12.5% (n=4) in the 90-day survivors (n=32) and 62.5% (n=5) in the 90-day non-survivors (n=8); there was a significant difference between the 90-day survivors and non-survivors (p=0.000). Conclusion: Patients who require MV and supplemental oxygen are associated with an increased risk for death following SLB. (Tuberc Respir Dis 2007; 63: 59-66)
Antiphospholipid syndrome (APS) causes recurrent thromboses and morbidity during pregnancy, including fetal loss. This malady is associated with the persistent presence of anticardiolipin antibody or lupus anticoagulant. The pulmonary manifestations of antiphospholipid syndrome include pulmonary thromboembolism, pulmonary hypertension, acute respiratory distress syndrome, etc. Pulmonary thromboembolism is often the initial manifestation of antiphospholipid syndrome and a timely diagnosis is critical due to the high mortality rate. We herein report on a 19-year-old man with pulmonary thromboembolism that was caused by primary antiphospholipid syndrome. He presented with blood-tinged sputum, fever and epigastric pain, and his chest computerized tomography showed pulmonary thromboembolism. The other possible causes of pulmonary thromboembolism were excluded and the diagnosis of primary antiphospholipid syndrome was confirmed by the lupus anticoagulant that was present on two occasions six weeks apart. We also discuss the nature and management of antiphospholipid syndrome, along with a brief review of the relevant literatures. (Tuberc Respir Dis 2007; 63: 72-77)
Schwannoma represents approximately 40% of neurogenic tumors arising in the mediastinum, and develops along the sympathetic or parasympathetic chain, intercostals nerve, and spinal ganglia. It is usually asymptomatic, and is confronted accidentally but can produce chest pain, cough and dyspnea. However, dyspnea with pleural effusion is rare in patients with benign schwannoma. We encountered two cases of benign schwannoma with pleural effusion. Both cases had similar initial symptoms and the characteristics of a mass but the characteristics of pleural effusion analysis were different. The benign schwannoma was confirmed in two cases using VATS (video-assisted tharawswpic surgery). (Tuberc Respir Dis 2007; 63: 78-82)
Idiopathic pulmonary fibrosis (IPF) is strongly associated with lung cancer compared with the general population. However, other types of idiopathic interstitial pneumonia (IIP) are rarely associated with lung cancer. We describe a case of a primary lung cancer associated with IIP other than IPF, which was considered to be nonspecific interstitial pneumonia (NSIP), and NSIP disappeared spontaneously after treating the primary lung cancer. (Tuberc Respir Dis 2007; 63: 83-87)
Wegener’s granulomatosis is a disease with an unknown etiology that is characterized by necrotizing granulomatous vasculitis involving the upper and lower respiratory tract and the kidneys. The typical pulmonary findings are bilaterally involved multiple variable sized nodules. We report a case of Wegener’s granulomatosis that presented as a single lung mass. A male patient presented with a nasal obstruction, arthralgia, cough, and intermittent dyspnea. The chest radiograph showed a mass, approximately 4.5 cm in diameter, in the right lower lobe. Lung cancer or tuberculosis was initially considered. However, the clinical, laboratory and pathological findings of the mass indicated Wegener’s granulomatosis. The patient was administered prednisolone and cyclophosphamide, and improved temporarily. Unfortunately, the immunocompromised patient expired as a result of respiratory failure with pneumonia. (Tuberc Respir Dis 2007; 63: 88-93)
The spontaneous regression (SR) of cancer is defined as the complete disappearance of a malignant disease without adequate treatment. SR is a very rare biological event, particularly in a pulmonary sarcoma. We report the first documented case of an endobronchial sarcoma that regressed spontaneously in Korea. We encountered a rare case of a 72-year-old woman with an undiagnosed intrapelvic cystic mass, who presented with a smooth surfaced endobronchial tumor obstructing the orifice of the right lower lobe bronchus on a bronchoscopic examination. She had a prior history cervical cancer and adenocarcinoma in the right middle lobe lateral segment of her lung for which she had undergone radiation therapy. The tumor was diagnosed as an endobronchial sarcoma by the histopathology findings and immunohistochemistry. It was unclear if the tumor was a primary sarcoma of the lung or a metastatic lesion of an intrapelvic cystic mass because she refused a diagnostic exploratory laparotomy. Two months later, obstructive pneumonia of the right lower lobe with parapneumonic effusion developed with fever above 38.5℃ for 10 days. After recovering from pneumonia, she was followed up regularly in the outpatient clinic without any specific treatment. One year later after treating the obstructive pneumonia, the follow-up bronchoscopy revealed complete SR of endobronchial sarcoma. It is believed that the obstructive pneumonia accompanied by fever above 38.5℃ for 10 days might have played a role in this SR. (Tuberc Respir Dis 2007; 63: 94-99)