• Toxicological Research
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• v.24 no.2
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• pp.109-112
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• 2008

The G184C and G134A single nucleotide polymorphisms(SNPs) of the CYP1A1 gene result in Ala62Pro and Gly45Asp substitutions, respectively. Here, we tested whether these SNPs are associated with an alteration in lung cancer incidence. We examined 80 Korean subjects with lung cancer and 240 age- and sex-matched controls. For each subject, the CYP1A1 gene was PCR amplified and sequenced. We observed that the odds ratio(OR) for lung cancer was 3.37 higher in subjects with the G184C polymorphism than in controls(95% confidence interval(CI), $0.89{\sim}12.73$, P=0.07). In contrast, the OR for lung cancer was 1.23 in subjects with the G134A polymorphism compared to controls(95% CI, $0.68{\sim}2.20$, P=0.49). The G184C polymorphism exacerbated the effects of smoking on lung cancer development. Gene-smoking interaction analyses revealed that past or present smokers with the G184C polymorphism had a higher incidence of lung cancer(OR, 24.72; 95% CI, $4.48{\sim}136.31$; P<0.01) than control smokers(OR, 6.65; 95% CI, $2.72{\sim}16.28$; P<0.01). However, there was only a slight difference in the ORs for lung cancer between control smokers and smokers with the G134A polymorphism. These findings suggest that the G184C polymorphism, but not the G134A polymorphism, is associated with an increased risk of lung cancer.

• Tuberculosis and Respiratory Diseases
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• v.63 no.5
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• pp.449-453
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• 2007

Totally implanted central venous access devices for chemotherapy (chemoport) are being used increasingly in lung cancer patients. Vascular catheters are associated with various complications including infection, thrombosis as well as spontaneous fractures and embolization of the catheter, which is known as 'pinch-off syndrome'. 'Pinch-off syndrome' refers to the compression of a subclavian central venous catheter between the clavicle and first rib resulting in an intermittent or permanent obstruction, which can lead to tears, transection, or embolization. We report two cases of fractured and embolized implanted subclavian venous catheters in which the fragments were removed percutaneously. A 62-year-old man presented with back pain with a duration of a few weeks. The chest radiograph revealed complete transsection and embolization of the catheter into the right atrium. In addition, a 47-year-old woman with a chemoport had a grade 3 pinch-off sign in a chest radiograph demonstrating complete transsection and embolization of the catheter into the pulmonary artery. Both cases were managed by retrieving the embolized distal fragment percutaneously and removing the proximal section of the catheter.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.2
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• pp.657-662
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• 2014

Background: The epidermal growth factor receptor (EGFR) mutation status of lung cancer is important because it means that EGFR-tyrosine kinase inhibitor treatment is indicated. The purpose of this prospective study is to determine whether EGFR mutation status could be identified with reference to preoperative factors. Materials and Methods: One hundred-forty eight patients with lung cancer (111 adenocarcinomas, 25 squamous cell carcinomas and 12 other cell types) were enrolled in this study. The EGFR mutation status of each lung cancer was analyzed postoperatively. Results: There were 58 patients with mutant EGFR lung cancers (mutant LC) and 90 patients with wild-type EGFR lung cancers (wild-type LC). There were significant differences in gender, smoking status, maximum tumor diameter in chest CT, type of tumor shadow, clinical stage between mutant LC and wild-type LC. EGFR mutations were detected only in adenocarcinomas. Maximum standardized uptake value (SUVmax:$3.66{\pm}4.53$) in positron emission tomography-computed tomography of mutant LC was significantly lower than that ($8.26{\pm}6.11$) of wild-type LC (p<0.0001). Concerning type of tumor shadow, the percentage of mutant LC was 85.7% (6/7) in lung cancers with pure ground glass opacity (GGO), 65.3%(32/49) in lung cancers with mixed GGO and 21.7%(20/92) in lung cancers with solid shadow (p<0.0001). For the results of discriminant analysis, type of tumor shadow (p=0.00036) was most significantly associated with mutant EGFR. Tumor histology (p=0.0028), smoking status (p=0.0051) and maximum diameter of tumor shadow in chest CT (p=0.047) were also significantly associated with mutant EGFR. The accuracy for evaluating EGFR mutation status by discriminant analysis was 77.0% (114/148). Conclusions: Mutant EGFR is significantly associated with lung cancer with pure or mixed GGO, adenocarcinoma, never-smoker, smaller tumor diameter in chest CT. Preoperatively, EGFR mutation status can be identified correctly in about 77 % of lung cancers.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.14
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• pp.5863-5868
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• 2015

Nicotine-derived nitrosamine ketone (NNK) is considered a key tobacco smoke carcinogen inducing lung tumors. Physalis peruviana L (harankash) is considered one plant with marked health benefits. This study aimed to evaluate Physalis peruviana L effect on the toxic effect of NNK induced lung cancer in the rats by using pulmonary histopathological, immunohistochemical and DNA flow cytometric analyses. Sixty adult male rats were divided into four groups, each consisting of fifteen animals. The first group received saline, the second received two successive toxic doses of NNK only while the third received two successive toxic doses of NNK with a single daily dose of Physalis peruviana L. The fourth group received a single daily dose of Physalis peruviana L only. Toxic doses of NNK induced hyperplasia and adenocarcinoma in the lung and positive immunoreactivity for Ki-67 and p53 staining with disturbance of the lung DNA content. Administration of Physalis peruviana L with NNK led to a mild pulmonary hyperplasia and weak expression of Ki-67 and p53 with an improvement in the lung DNA content. Physalis peruviana L may protect against NNK induced lung carcinogenesis due to its antioxidant and anti-proliferative effects.

• Tuberculosis and Respiratory Diseases
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• v.74 no.1
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• pp.32-36
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• 2013

A 43-year-old woman with breast cancer who was on neoadjuvant chemotherapy presented with cough, sputum and mild fever. High-resolution computed tomography showed diffuse ground glass opacities in bilateral lungs and subpleural patchy consolidations. Initially, she was thought to have pneumonia or interstitial lung diseases such as drug-induced pneumonitis and treated with antibiotics and steroids. She subsequently got breast cancer surgery because of disease progression, and concurrent thoracoscopic lung biopsy revealed metastatic carcinoma of the lung from breast cancer. The diagnosis of suspected interstitial lung disease can be made without lung biopsy, but malignancy should always be considered and lung biopsy should be performed in the absence of a definitive clinical diagnosis.

• Journal of Veterinary Clinics
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• v.34 no.1
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• pp.50-53
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• 2017

Two dogs presented to our facility were each diagnosed with a thoracic mass. Radiography and computed tomography revealed isolated primary lung tumors. Partial lung lobectomy was applied in Case 1 and total lung lobectomy in Case 2, using a thoracoabdominal stapler. No complications were observed after surgery in either dog. The outcome of these cases indicates that use of a thoracoabdominal stapler in partial and total lung lobectomy may be recommended for small-breed dogs.

• Tuberculosis and Respiratory Diseases
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• v.56 no.5
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• pp.514-522
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• 2004

Background : Non-steroidal anti-inflammatory drugs (NSAID) are useful in chemoprevention of colorectal cancers. Continuous NSAID administation causes 40% to 50% reduction in relative risk for colorectal cancer. Sulindac possesses an antiproliferative effect and induces apoptosis and tumor regression on colon cancer and other types of cancers. We intended to analyze the effects of sulindac in three non-small cell lung cancer cell lines. Materials and Methods : The human lung cancer cell lines, A549, NCI-H157 and NCI-H460 were used for this study. Viability was tested by MTT assay, and cell death rate was measured by lactate dehydrogenase(LDH) release. Apoptosis was estimated by flow cytometric analysis and nuclear staining. Results: Sulindac was able to decrease the viability of non-small cell lung cancer cells in a dose- and time- dependent manner. In a parallel effect of sulindac on cell death rate, LDH release was increased in sulindac-treated lung cancer cells. Sulindac significantly increased apoptosis characterized by an increase of $sub-G_0/G_1$ fraction and morphological change of nuclei. The rate of apoptotic cells after sulindac treatment in lung cancer cells increased in a time- and dose- dependent manner in flow cytometric analysis. Apoptotic cells were defined as nuclear shrinkage, chromatin condensation and nuclear fragmentation of cells. Conclusion : Sulindac decreases viability and induces the apoptosis of lung cancer cells. Further studies will be needed to elucidate the potential mechanism of sulindac-induced apoptosis in lung cancer cells.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.2
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• pp.647-652
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• 2015

Background: Lung cancer was one of the most common cancers in both men and women all over the world. In this study, we aimed to clarify who could survive after long term chemotherapy in patients with advanced non-small cell lung cancer (NSCLC). Methods: We enrolled 186 patients with stage IV NSCLC after long term chemotherapy from Jun 2006 to Nov 2014 diagnosed in Jiangsu Cancer Hospital. Multiple variables like age, gender, smoking, histology of adenocarcinoma and squamous-cell cancer, number of metastatic sites, metastatic sites (e.g. lung, brain, bone, liver and pleura), hemoglobin, lymphocyte rate (LYR), Change of LYR during multiple therapies, hypertension, diabetes, chronic bronchitis, treatments (e.g.radiotherapy and targeted therapy) were selected. For consideration of factors influencing survival and response for patients with advanced NSCLC, logistic regression analysis and Cox regression analysis were used in an attempt to develop a screening module for patients with elevated survival after long term chemotherapy become possible. Results: Of the total of 186 patients enrolled, 69 survived less than 1 year (short-term group), 45 one to two years, and 72 longer than 3 years (long-term group). For logistic regression analysis, the short-term group was taken as control group and the long-term group as the case group. We found that age, histology of adenocarcinoma, metastatic site (e.g. lung and liver), treatments (e.g. targeted therapy and radiotherapy), LYR, a decreasing tendency of LYR and chronic bronchitis were individually associated with overall survival by Cox regression analysis. A multivariable Cox regression model showed that metastatic site (e.g. lung and liver), histology of adenocarcinoma, treatments (e.g. targeted therapy and radiotherapy) and chronic bronchitis were associated with overall survival. Thus metastatic site (e.g. lung and liver) and chronic bronchitis may be important risk factors for patients with advanced NSCLC. Gender, metastatic site (e.g. lung and liver), LYR and the decreasing tendency of LYR were significantly associated with long-term survival in the individual-variable logistic regression model (P<0.05). On multivariate logistic regression analysis, gender, metastatic site (e.g. lung and liver) and the decreasing tendency of LYR associated with long-term survival. Conclusions: In conclusion, female patients with stage IV adenocarcinoma of NSCLC who had decreasing tendency of LYR during the course therapy and had accepted multiple therapies e.g. more than third-line chemotherapy, radiotherapy and/or targeted therapy might be expected to live longer.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.2
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• pp.495-500
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• 2015

Background: Published studies have reported relationships between X-ray repair cross-complementing group 1 (XRCC1) Arg399Gln polymorphism and lung cancer risk in Chinese population. However, the epidemiological results remained controversial. The objective of this study was to clarify the association of XRCC1 Arg399Gln polymorphism with lung cancer risk in the Chinese population. Materials and Methods: Systematic searches were performed through the database of Medline/Pubmed, Web of Science, Embase, CNKI and WanFang Medical Online. Odds ratios (ORs) with 95% confidence interval (95%CI) were calculated to estimate the strength of the association. Results: Overall, we observed an increased lung cancer risk among subjects carrying XRCC1 codon 399 Gln/Gln genotype (OR=1.36, 95%CI: 1.09-1.71) in the Chinese population on the basis of 19 studies with 5,416 cases and 5,782 controls. We did not observe any association between XRCC1 codon 399 Arg/Gln and Arg/Gln+Gln/Gln polymorphisms and lung cancer risk (OR=1.00, 95%CI: 0.92-1.08 and OR=1.05, 95%CI: 0.97-1.13, respectively). Limiting the analysis to studies with controls in agreement with Hardy-Weinberg equilibrium (HWE), we observed an increased lung cancer risk among subjects carrying XRCC1 codon 399 Gln/Gln genotype (OR=1.18, 95%CI: 1.01-1.38). When stratified by source of control, we observed an increased lung cancer risk among subjects carrying XRCC1 codon 399 Arg/Gln+Gln/Gln genotype on the basis of hospitalized patient-based controls (OR=1.21, 95%CI: 1.04-1.42) and among subjects carrying XRCC1 codon 399 Gln/Gln genotype on the basis of healthy subject-based controls (OR=1.22, 95%CI: 1.04-1.43). Conclusions: Our findings indicated that certain XRCC1 Arg399Gln variants might affect the susceptibility of lung cancer in Chinese population. Larger sample size studies are required to confirm our findings.

• Tuberculosis and Respiratory Diseases
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• v.70 no.3
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• pp.206-217
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• 2011

Background: Transcription factor FOXP3 characterizes the thymically derived regulatory T cells. FOXP3 is expressed by cancer cell itself and FOXP3 expression was induced by TGF-${\beta}$ treatment in pancreatic cancer cell line. However, the expression of FOXP3 expression is not well known in patients with lung cancer. This study was conducted to investigate the expression of FOXP3 in patients with lung cancer and to investigate the regulation of FOXP3 expression by the treatment of TGF-${\beta}$ and DNA methyltransferase inhibitor in lung cancer cell lines. Methods: FOXP3 expression in the tissue of patients with resected non-small cell lung cancer (NSCLC) was evaluated by immunohistochemistry. The regulation of FOXP3 expression was investigated by Western blot and RT-PCR after lung cancer cell lines were stimulated with TGF-${\beta}1$ and TGF-${\beta}2$. The regulation of FOXP3 expression was also investigated by RT-PCR and flow cytometry after lung cancer cell lines were treated with DNA methyltransferase inhibitor (5-AZA-dC). Results: FOXP3 expression was confirmed in 27% of patients with NSCLC. In NCI-H460 cell line, TGF-${\beta}2$ decreased FOXP3 mRNA and protein expressions. In A549 cell line, both TGF-${\beta}1$ and TGF-${\beta}2$ decreased FOXP3 mRNA and protein expressions. 5-AZA-dC increased FOXP3 mRNA expression in NCI-H460 and A549 cell lines. Moreover, 5-AZA-dC increased intracellular FOXP3 protein expression in A549 cell lines. Conclusion: It was shown that FOXP3 is expressed by cancer cell itself in patients with NSCLC. Treatment of TGF-${\beta}2$ and DNA methyltransferase inhibitor seems to be associated with the regulation of FOXP3 expression in lung cancer cell lines.