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ABSTRACT: Sensitive detection of black powder (BP) by stand-alone ion mobility spectrometry (IMS) is full of challenges. In conventional air-based IMS, overlap between reactant ion O2-(H2O)n peak and sulfur ion peak occurs severely; and common doping methods, providing alternative reactant ion Cl-(H2O)n, would hinder the formation of ionic sulfur allotropes. In this work, an ion mobility spectrometer embedded a titration region (TR-IMS) downstream from ionization region was developed for selective and sensitive detection of sulfur in BP with CH2Cl2 as titration reagent. Sulfur ions were produced via reactions between sulfur molecules and O2-(H2O)n ions in the ionization region and the remaining O2-(H2O)n ions that entered the titration region were converted to Cl-(H2O)n ions, which avoided the peak overlap as well as the negative effect of CH2Cl2 on sulfur ions. The limit of detection for sulfur was measured to be 5 pg. Furthermore, it was demonstrated that this TR-IMS was qualified for detecting less than 5 ng BP and other nitro-organic explosives.
Analytical Chemistry 04/2013; · 5.86 Impact Factor
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Xiaomei Liu,
Yaguang Fan,
Yong Jiang,
Jian Xiang,
Jixian Wang,
Zhijuan Sun,
Guanhua Ren,
Shuxiang Yao,
Runsheng Chang,
Yongcheng Zhao,
Youlin Qiao, Qinghua Zhou
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ABSTRACT: Smoking is a major cause of lung cancer. Studies of lung cancer among miners have shown that occupational exposure also played an important role. The aim of this study is to investigate radon, cigarette use and other risk factors of lung cancer in Yunnan tin miners and to provide a scientific basis for the prevention and control of occupational lung cancer.
A prospective cohort study was conducted among Yunnan tin miners, the associations between potential risk factors for lung cancer were analyzed by multivariate Cox regression model. Effects of age at first radon exposure and radon exposure rate on lung cancer risk were analyzed. The relationship between cumulative working level month and lung cancer was analyzed according to smoking status. The joint effect of tobacco use and cumulative radon exposure was analyzed based on additive and multiplicative models.
Increased risk of lung cancer was associated with age at enrollment, tobacco use, prior bronchitis, and cumulative arsenic and radon exposure, while higher education level was associated with decreased lung cancer risk. An inverse effect of radon exposure rate was observed. There was no significant association between lung cancer risk and first radon exposure age. There was a significant additive interaction between tobacco use and radon exposure on lung cancer risk.
Several risk factors may contribute to the high incidence of lung cancer in Yunnan tin miners. Further studies are warranted to evaluate joint effect of different risk factors.
Zhongguo fei ai za zhi = Chinese journal of lung cancer 04/2013; 16(4):184-90.
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ABSTRACT: Lung cancer is one of the malignant tumors with fastest growing rates in incidence and mortality in our country, also with largest threat to human health and life. However, the exact mechanisms underlying lung cancer development remain unclear. The microenvironment of tumor hypoxia was discovered in 1955, but hypoxia in lung cancer tissues had not been successfully detected till 2006. Further studies show that hypoxia not only functions through the resistance to radiotherapy, but also regulates lung cancer development, invasion, metastasis, chemotherapy resistance and prognosis through an important oncogene HIF (hypoxia inducible factor), with its regulators PHD (prolyl hydroxylase domain) and pVHL (product of von Hippel-Lindau gene). Therefore, hypoxia, HIF, PHD and pVHL should be considered as potential therapeutic targets for lung cancer pathogenesis and progression.
Zhongguo fei ai za zhi = Chinese journal of lung cancer 04/2013; 16(4):216-20.
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ABSTRACT: Lung cancer is one of the most common diseases that endanger health and life of people domestically. A number of recurrence and death of lung cancer originated from metastasis. As a key step in metastasis of lung cancer, epithelial to mesenchymal transition involved down-regulation of E-cadherin, as well as regulated by EMT transcription factors. HATs and HDACs is a protein family that catalyzes acetylation and deacetylation of histones. Not only they have vital functions in tumor pathogenesis, but also participate in the EMT of lung cancer. HATs and HDACs interact with certain EMT transcription factors. Moreover, the function of these EMT transcription factors may be regulated by acetylation, which has influence on EMT program in lung cancer. Therefore, this review introduces the event of HATs and HDACs function in EMT of lung cancer, and investigate the molecular mechanism of their interaction. Then, the potential of HDAC inhibitor utilization in the inhibition of EMT and lung cancer therapy were discussed, as to pave the way for the related basic research and clinical practice.
Zhongguo fei ai za zhi = Chinese journal of lung cancer 04/2013; 16(4):211-5.
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ABSTRACT: Persistent STAT3 activation is a critical event in tumorigenesis and metastatic progression. Recent studies have found higher levels of STAT3 in metastatic tissues than in primary tumor tissues. We speculated that such increased STAT3 activity might be attributed to a loss of function or reduction in expression of metastasis inhibitory protein during cancer progression, and we therefore examined the role of tumor metastasis-suppressor nm23-H1 in the activation of STAT3 in the A549 lung cancer cell line. We found that IL-6-dependent induction of tyrosine phosphorylation and activation of STAT3 were influenced by nm23-H1 inhibition. IL-6-induced STAT3(Tyr705) phosphorylation was significantly enhanced in A549 cells transfected with siRNA specific for nm23-H1, and the effect of nm23-H1 depletion on IL-6-induced STAT3(Tyr705) phosphorylation was reversed by ectopic expression of shRNA-resistant nm23-H1 protein. Moreover, STAT3 directly bound to the STAT3 binding site on the nm23-H1 promoter and activated its expression. Thus, we have identified a new feedback mechanism that might provide insight into an in-built metastasis-suppression function in tumor cells and which could be a logical new target for treatment of early metastatic disease.
Biochemical and Biophysical Research Communications 04/2013; · 2.48 Impact Factor
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ABSTRACT: Methylseleninic acid (MSA) is an artificially developed selenium compound. It has been proven that MSA could inhibit growth and metastasis on many tumor cells. This study investigated whether MSA has an impact on the growth and metastasis of L9981-Luc lung cancer transplanted model in nude mice or not.
A transplantated tumor model was established in nude mice. Fifteen nude mice were randomly divided into three groups: the control group treated with normal saline (0.2 mL/d), the MSA group treated with MSA solution (0.2 mL), and the cisplatin (DDP) group injected intraperitoneally with DDP (4 mg/kg/w). Inhibition of MSA on tumor growth and tumor metastasis was observed using the IVIS Imaging System 200 Series.
A significant difference was obserced in the primary tumor bioluminescence among the three groups (P=0.002) on 21 days post-inoculation. Primary tumor bioluminescence in the DDP group (P=0.001) and in the MSA group (P=0.031) was significantly lower than that in the control group (P=0.001). No significant difference in the metastasis bioluminescence of the thoracic area was indicated among the three groups (P>0.05).
MSA can inhibit the growth of planted tumor of transgenic lung cancer cell lines L9981-Luc in nude mice. MSA may also suppress the distant metastasis of the transplanted tumor of transgenic lung cancer cell lines L9981-Luc in nude mice.
Zhongguo fei ai za zhi = Chinese journal of lung cancer 02/2013; 16(2):67-72.
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ABSTRACT: Resistance to antineoplastic drugs is a common problem in cancer treatments. Epithelial-mesenchymal transition (EMT), which plays an important role in the process of drug resistance, may provide opportunity to solve this problem. This article reviews the characteristics of EMT, relationship between EMT and drug resistance, mechanism of EMT in tumor drug resistance in details.
Zhongguo fei ai za zhi = Chinese journal of lung cancer 01/2013; 16(1):54-57.
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ABSTRACT: BACKGROUND: Up to know, no any study on using human bone marrow mesenchymal stem cells (hBMSCs) as cells carrier of tumor suppressor gene (IL-24) was reported. The aim of this study is to study the efficiency of transduction of hBMSCs by constructing the lentiviral vector in co-expressing enhanced green fluorescent protein (EGFP) gene and human IL-24 gene, and to lay a foundation for gene therapy of tumor in the future. METHODS: The lentivector which contain IL-24 and EGFP constructed by recombinant DNA technology were co-transfected to 293FT cells with ViraPowerTM Lentiviral Packaging Mix. The recombinant lentivirus infected with hBMSCs were selected and purified by puromycin. Expression of IL-24 mRNA and IL-24 protein levels were detected by real-time quantitative PCR (qPCR) and ELISA. RESULTS: The recombinant lentiviral vector of co-expressing IL-24 gene and EGFP gene were successfully constructed by multisite Gateway technology, virus can be packaged, purified and concentrated successfully, and the virus titer was 7.25×10⁷ PFU/mL. The efficiency of recombinant lentivirus to transduce hBMSCs can reach 100% after selection. The result of qPCR showed that the level of IL-24 mRNA expression in transduced group was significantly higher than that in non-transduced group (P<0.05); ELISA detection confirmed that IL-24 protein expression of transduced group was positive in supernatant and the concentration of IL-24 protein is 40 μg/L, while the non-transduced group was negative. CONCLUSIONS: Lentiviral vector carrying recombinant IL-24 gene can effectively transduce hBMSCs and express IL-24 protein.
Zhongguo fei ai za zhi = Chinese journal of lung cancer 01/2013; 16(1):7-11.
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ABSTRACT: The EML4-ALK fusion gene has been recently identified in a small subset of non-small cell lung cancer (NSCLC) patients who respond positively to ALK inhibitors. The characteristics of the EML4-ALK fusion gene in Chinese patients with NSCLC are poorly understood. Here, we report on the prevalence of EML4-ALK, EGFR status and KRAS mutations in 208 Chinese patients with NSCLC. EGFR mutations were found in 24.5% (51/208) of patients. In concordance with previous reports, these mutations were identified at high frequencies in females (47.5% vs 15.0% in males; P<0.05); never-smokers (42.3% vs 13.9% in smokers; P<0.05), and adenocarcinoma patients (44.2% vs 8.0% in non-adenocarcinoma patients; P<0.05). There were only 2.88% (6/208) patients with KRAS mutations in our study group. We identified 7 patients who harbored the EML4-ALK fusion gene (3.37%, 7/208), including 4 cases with variant 3 (57.1%), 2 with variant 1, and 1 with variant 2. All positive cases corresponded to female patients (11.5%, 7/61). Six of the positive cases were non-smokers (7.69%, 6/78). The incidence of EML4-ALK translocation in female, non-smoking adenocarcinoma patients was as high as 15.2% (5/33). No EGFR/KRAS mutations were detected among the EML4-ALK positive patients. Pathological analysis showed no difference between solid signet-ring cell pattern (4/7) and mucinous cribriform pattern (3/7) in ALK-positive patients. Immunostaining showed intratumor heterogeneity of ALK rearrangement in primary carcinomas and 50% (3/6) of metastatic tumors with ALK-negative staining. Meta-analysis demonstrated that EML4-ALK translocation occurred in 4.84% (125/2580) of unselected patients with NSCLC, and was also predominant in non-smoking patients with adenocarcinoma. Taken together, EML4-ALK translocations were infrequent in the entire NSCLC patient population, but were frequent in the NSCLC subgroup of female, non-smoker, adenocarcinoma patients. There was intratumor heterogeneity of ALK rearrangement in primary carcinomas and at metastatic sites.
PLoS ONE 01/2013; 8(1):e52093. · 4.09 Impact Factor
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Jundong Gu,
Yanjun Wen,
Siwei Zhu,
Feng Hua,
Hui Zhao,
Hongrui Xu,
Jiacong You,
Linlin Sun,
Weiqiang Wang,
Jun Chen, Qinghua Zhou
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ABSTRACT: Aberrant methylation of CpG islands acquired in tumor cells in promoter regions plays an important role in carcinogenesis. Accumulated evidence demonstrates P(16INK4a) gene promoter hypermethylation is involved in non-small cell lung carcinoma (NSCLC), indicating it may be a potential biomarker for this disease. The aim of this study is to evaluate the frequency of P(16INK4a) gene promoter methylation between cancer tissue and autologous controls by summarizing published studies.
By searching Medline, EMBSE and CNKI databases, the open published studies about P(16INK4a) gene promoter methylation and NSCLC were identified using a systematic search strategy. The pooled odds of P(16INK4A) promoter methylation in lung cancer tissue versus autologous controls were calculated by meta-analysis method.
Thirty-four studies, including 2 652 NSCLC patients with 5 175 samples were included in this meta-analysis. Generally, the frequency of P(16INK4A) promoter methylation ranged from 17% to 80% (median 44%) in the lung cancer tissue and 0 to 80% (median 15%) in the autologous controls, which indicated the methylation frequency in cancer tissue was much higher than that in autologous samples. We also find a strong and significant correlation between tumor tissue and autologous controls of P(16INK4A) promoter methylation frequency across studies (Correlation coefficient 0.71, 95% CI:0.51-0.83, P<0.0001). And the pooled odds ratio of P(16INK4A) promoter methylation in cancer tissue was 3.45 (95% CI: 2.63-4.54) compared to controls under random-effect model.
Frequency of P(16INK4a) promoter methylation in cancer tissue was much higher than that in autologous controls, indicating promoter methylation plays an important role in carcinogenesis of the NSCLC. Strong and significant correlation between tumor tissue and autologous samples of P(16INK4A) promoter methylation demonstrated a promising biomarker for NSCLC.
PLoS ONE 01/2013; 8(4):e60107. · 4.09 Impact Factor
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ABSTRACT: Ion mobility spectrometry (IMS) is a key trace detection technique for explosives and the development of simple, stable and efficient nonradioactive ionization source is highly demanded. A dopant-assisted negative photoionization (DANP) source has been developed for IMS, which uses a commercial VUV krypton lamp to ionize acetone as the source of electrons to produce negative reactant ions in air. With 20 ppm of acetone as the dopant, a stable current of reactant ions of 1.35 nA was achieved. The reactant ions were identified to be CO3-(H2O)n (K0 = 2.44 cm2 V-1 s-1) by atmospheric pressure time of flight mass spectrometry, while the reactant ions in 63Ni source were O2-(H2O)n (K0 = 2.30 cm2 V-1 s-1). Finally, its capabilities for detection of common explosives including ammonium nitrate fuel oil (ANFO), 2,4,6-trinitrotoluene (TNT), N-nitrobis(2-hydroxyethyl)-amine dinitrate (DINA) and pentaerythritol tetranitrate (PETN) were evaluated, the limits of detection of 10 pg (ANFO), 80 pg (TNT), and 100 pg (DINA) with a linear range of two orders of magnitude were achieved. The time of flight mass spectra obtained using DANP source clearly indicated that PETN and DINA can be directly ionized by the ion-association reaction of CO3- to form PETN•CO3- and DINA•CO3- adduct ions, which result in good sensitivity for the DANP source. The excellent stability, good sensitivity, especially the better separation between the reactant and product ion peaks make the DANP be a potential nonradioactive ionization source for IMS.
Analytical Chemistry 12/2012; · 5.86 Impact Factor
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ABSTRACT: Members of transforming growth factor -β(TGF-β) family are the main inducers of epithelial-mesenchymal transition (EMT) during embryogenesis and cancer pathogenesis. However, a significant crosstalk between TGF-β and other signals occurs during the induction of EMT. nm23-H1 was first metastasis suppressor gene to be identified on the basis of an inverse relationship between nm23-H1 expression and metastasis stage. Despite extensive studies, the mechanism underlying its ability to suppress metastasis is far from elucidated. We demonstrated here that the nm23-H1 negatively regulated TGF-β1-dependent induction of EMT in non-aggressive lung cancer cell line. nm23-H1 knockdown significantly enhanced TGF-β1-induced suppression of epithelial marker E-cadherin and upregulation of mesenchymal markers β-catenin and fibronectin. The invasive and migratory potential of lung cancer cells upon TGF-β1 treatment was also markedly enhanced by nm23-H1 knockdown. On the other hand, the effect of nm23-H1 depletion on TGF-β1-induced EMT was reversed by ectopic re-expression of shRNA-resistant nm23-H1 protein. Furthermore, TGF-β1-induced EMT potentiated by nm23-H1 depletion was partially dependent on transcriptional factor Snail expression. Finally, we found Src kinase is involved in regulation of TGF-β1-induced EMT by nm23-H1. Our results suggest a means of restoring nm23-H1 to suppress TGF-β1-induced EMT that may exploited therapeutically for the management of metastasis diseases.
Experimental Cell Research 11/2012; · 3.58 Impact Factor
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ABSTRACT: BACKGROUND: Docetaxel is the first line treatment for castration resistant prostate cancer (CRPC). However, docetaxel resistance rapidly develops. Identifying the critical mechanisms giving rise to docetaxel resistance is the major challenge in advanced prostate cancer. METHODS: The effects of docetaxel on human DU145, PC3, LNCaP, and C4-2 prostate cancer cells were examined in cell culture, and p53 expression were analyzed by Western blot analysis. The potential role of p53 in docetaxel sensitivity in prostate cancer cells was tested by either p53 silencing using shRNA or p53 overexpression by introducing wild-type p53. RESULTS: We found that DU145 (mutant p53) and PC3 (p53 null) cells were less sensitive than LNCaP and C4-2 cells expressing functional p53 in response to docetaxel. Docetaxel treatment induces considerably higher apoptosis in LNCaP and C4-2 cells than in DU145 and PC3 cells in a dose dependent manner. Docetaxel increases the levels of ser15 phosphorylation of p53 in a dose dependent manner in both LNCaP and C4-2 cells, while has no effect on the levels of ser15 phosphorylation of p53 in DU145 cells. These results suggest that p53 phosphorylation is associated with docetaxel sensitivity in prostate cancer cells. To further confirm whether p53 activation can induce cell sensitivity to docetaxel treatment, we used p53 shRNA to knock down p53 expression in C4-2 cells and determined the cells response to docetaxel treatment. Knockdown of p53 significantly down regulated p53 phosphorylation and blocked docetaxel induced apoptotic cell death compared to the vector control. To further confirm this observation, we established a stable knock out p53 in C4-2 cells. Down regulation of p53 in the stable p53 knock out C4-2 cells significantly inhibited docetaxel induced apoptotic cell death. We also used wild-type (WT) p53 to over express p53 in DU145 cells, and found that expression of WT-p53 in DU145 cells increased their sensitivity to docetaxel. CONCLUSIONS: These results demonstrate that docetaxel induces p53 phosphorylation and that p53 status is a crucial determinant of docetaxel sensitivity in prostate cancer cells. Prostate © 2012 Wiley Periodicals, Inc.
The Prostate 09/2012; · 3.48 Impact Factor
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ABSTRACT: The concentration of propofol in patient's exhaled air is an indicator of the anesthetic depth. In the present study, a membrane inlet ion mobility spectrometer (MI-IMS) was built for the on-line measurement of propofol. Compared with the direct sample introduction, the membrane inlet could eliminate the interference of moisture and improve the selectivity of propofol. Effects of membrane temperature and carrier gas flow rate on the sensitivity and response time have been investigated experimentally and theoretically. Under the optimized experimental conditions of membrane temperature 100 °C and carrier gas flow rate 200 mL min(-1), the calculated limit of detection (LOD) for propofol was 1 ppbv, and the calibration curve was linear in the range of 10-83 ppbv with a correlation coefficient (R(2)) of 0.993. Finally, the propofol concentration in an anaesthetized mouse exhaled air was monitored continuously to demonstrate the capability of MI-IMS in the on-line measurement of propofol in real samples.
Talanta 08/2012; 98:241-6. · 3.79 Impact Factor
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ABSTRACT: Lung cancer is the leading cause of cancer related death, 90% of lung cancer patients die of metastasis. Many microRNAs (miRNAs) are deregulated in cancer. They are involved in tumorigenesis and function as oncogenes or tumor suppressor genes. Recent studies show that miRNAs may be responsible for tumor metastasis. Several functional studies show that miR-26a plays an important role in carcinogenesis; however, none of these studies is related to tumor metastasis. In the present study, we investigated the effect of miR-26a on metastasis potential of lung cancer cells. Our data showed that miR-26a expression level was higher in lymph node metastasis tumor tissues than in primary tumor tissues. Ectopic expression of miR-26a dramatically enhanced lung cancer cell migration and invasion abilities. Metastasis-related genes matrix metallopeptidase 2 (MMP-2), vascular endothelial growth factor (VEGF), Twist and β-catenin were upregulated. Phosphatase and tensin homolog (PTEN) was a direct target of miR-26a. Further mechanistic study revealed that miR-26a increased AKT phosphorylation and nuclear factor kappa B (NFκB) transcriptional activation. Our study demonstrated that miR-26a enhanced lung cancer cell metastasis potential via modulation of metastasis-related gene expression, and activation of AKT pathway by PTEN suppression, suggesting that miR-26a might be a potential therapeutic candidate in patients with metastatic lung cancer.
Biochimica et Biophysica Acta 08/2012; 1822(11):1692-704. · 4.66 Impact Factor
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ABSTRACT: Primary lung lymphoma (PLL) presenting as a primary pulmonary lesion is rare and usually affects elderly people. Here we describe a 25-year-old Chinese man diagnosed with primary lung lymphoma, which presented as a huge lung tumor mimicking a primary lung cancer and involving the superior vena cava. He underwent double-sleeve reconstructions of bronchus and pulmonary arteries with right upper- and middle-lobe lobectomy along with replacement of the superior vena cava with a graft, and was then given standard chemotherapy of CHOP plus Rituximab. The patient has been well, showing no local recurrence or distal metastasis during a 27-month follow-up.
World Journal of Surgical Oncology 06/2012; 10:131. · 1.12 Impact Factor
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Yibing Yao,
Yu Fan,
Jun Wu,
Haisu Wan,
Jing Wang,
Stephen Lam,
Wan L Lam,
Luc Girard,
Adi F Gazdar,
Zhihao Wu, Qinghua Zhou
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ABSTRACT: To identify a panel of tumor associated autoantibodies which can potentially be used as biomarkers for the early diagnosis of non-small cell lung cancer (NSCLC). Thirty-five unique and in-frame expressed phage proteins were isolated. Based on the gene expression profiling, four proteins were selected for further study. Both receiver operating characteristic curve analysis and leave-one-out method revealed that combined measurements of four antibodies produced have better predictive accuracies than any single marker alone. Leave-one-out validation also showed significant relevance with all stages of NSCLC patients. The panel of autoantibodies has a high potential for detecting early stage NSCLC.
Biochemical and Biophysical Research Communications 06/2012; 423(3):613-9. · 2.48 Impact Factor
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ABSTRACT: Extramedullary plasmacytoma occurring as a primary pulmonary lesion is rare. The present report describes a 42-year-old Chinese man diagnosed with primary pulmonary plasmacytoma following left lower lobectomy. Of note, an extremely rare immunoglobulin G lambda paraprotein was documented in the patient's serum by immunofixation electrophoresis. The patient has been well, showing no local recurrence or multifocal disease during a 15-month follow-up.
Canadian respiratory journal: journal of the Canadian Thoracic Society 05/2012; 19(3):e28-30. · 1.56 Impact Factor
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ABSTRACT: Inflammatory pseudotumor was a kind of rare benign tumor of the lung, whose incidence was only about 0.7% in all kinds of tumors of the lung. Multiple inflammatory pseudotumor in both lungs were rare, which were often misdiagnosed to metastatic tumor or disseminated pulmonary tuberculosis. The literature reports were scarce too. This report introduces one case of multiple inflammatory pseudotumor in both lungs that we met in clinical works, and discusses the diagnosis and treatment of it.
Zhongguo fei ai za zhi = Chinese journal of lung cancer 04/2012; 15(4):246-8.
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ABSTRACT: Lung cancer is the leading cause of cancer-related death and thus a major health problem nowadays. No early diagnostic method is ideal up to now. Changes in DNA methylation occur on early stage of lung cancer. Detection of DNA methylation is expected to be an important method in early diagosis of lung cancer.
Zhongguo fei ai za zhi = Chinese journal of lung cancer 04/2012; 15(4):234-41.
