Primary fibroblastic osteosarcoma of sternum: A case report.

RATIONALE: Osteosarcoma, a malignant bone tumor, rarely occurs in the sternum, especially the fibroblastic type, and is associated with poor survival. This case report describes a patient with a neoplasm of the sternum who underwent tumor resection 3 times and reconstruction twice because of the high risk of recurrence. PATIENT CONCERNS: A 60-year-old Chinese man presented with a 3-cm palpable bulging mass located in front of his sternum. Chest computed tomography (CT) revealed an anterior chest wall neoplasm with sternal destruction. DIAGNOSIS: Pathological examination revealed that the mass was a low-grade malignant primary fibroblastic osteosarcoma. INTERVENTIONS: Locking plates were used for chest wall reconstruction, demonstrating good structural stability and economic applicability. Regarding the ineffectiveness of current therapies, whole-exome sequencing was conducted, and no targets matched any of the currently available agents. OUTCOMES: No recurrence was found on regular reexamination. LESSONS: Surgery is the first choice of treatment for patients with primary fibroblastic osteosarcoma of the sternum. The reconstruction-locking plate is a good alternative for chest wall reconstruction. Whole-exome sequencing can shed new light on this uncommon disease and help identify novel therapeutic targets.

Protective effect of trichostatin A on CD19+CD5+CD1dhigh regulatory B cells in heart transplantation.

Heart transplantation is widely used for the treatment of several heart diseases. Regulatory B cells (Breg cells) serve a critical role in immune tolerance. However, the role of Breg cells in immune tolerance in the context of allogeneic heart transplantation remains poorly understood. The present study aimed to explore the effect of histone deacetylase (HDAC) inhibitor trichostatin A (TSA)­regulated Breg on the regulation of immune tolerance in heart transplantation. By constructing anallogeneic heart transplantation mouse model, and performing flow cytometry, reverse transcription­quantitative PCR, western blotting and carboxyfluorescein succinimidyl esterstaining assays, TSA­regulated Breg cells and their effects on immune tolerance in heart transplantation were evaluated. The results demonstrated that TSA increased the frequency of CD19+CD5+CD1dhigh Breg cells both in vitro and in vivo. Moreover, TSA treatment increased the frequency of IL­10 and TGF­ß­producing CD19+CD5+CD1dhigh Breg cells, and IL­10 and TGF­ß levels in vitro and in vivo. TSA administration significantly prolonged the survival rate in a heart transplant experiment model. In addition, the IL­10 inhibitor ammonium trichloro(dioxoethylene­o,o')tellurate partially reduced the survival rate and the percentages of CD19+CD5+CD1dhigh Breg cells in mice receiving heart allografts. In contrast, anti­CD20 treatment significantly decreased the survival rate in these mice. Collectively, the present findings suggested that TSA may induce immune tolerance following heart transplantation by regulating CD19+CD5+CD1dhigh Breg cells. These results provide a theoretical basis for the prevention of immunological rejection in cardiac transplantation.

The Crosstalk between lncRNA-SNHG7/miRNA-181/cbx7 Modulates Malignant Character in Lung Adenocarcinoma.

Lung adenocarcinoma (LUAD) is a malignant tumor with poor patient survival and high patient mortality. Long noncoding RNA is profoundly involved in the tumorigenesis of LUAD. The present study explores the effect of small nucleolar RNA host gene 7 (SNHG7) on the progression of LUAD and its underlying mechanisms. SNHG7 was found to be down-regulated in LUAD tissues compared with normal tissues. Altered SNHG7 expression induced changes in cell proliferation and migration both in vitro and in vivo. Mechanistically, it was found that SNHG7 interacted with microRNA mir-181 and sequentially up-regulated cbx7. cbx7, which suppresses the Wnt/ß-catenin pathway in LUAD, was found to be a direct target of mir-181. Taken together, loss of SNHG7 in LUAD up-regulated mir-181 and then down-regulated the tumor suppressor cbx7.

Effect of miR-744 on Ameliorating Heart Allograft Rejection in BALB/c Mice Via Regulation of TNFRSF4 Expression in Regulatory T Cells.

CD134 (TNFRSF4) is a member of the TNFR superfamily, which is specifically expressed on T cells. Previous studies have shown that blocking of CD134L-CD134 interaction reduces the percentage of activated T cells and prevents effector T cell-mediated graft rejection in heart transplantation. However, the role of microRNA-regulated inhibition of the CD134 signal in cardiac transplantation of T-regulatory (Treg) cells is not clear. In this study, we found microRNA 744 (miR-744) agomir administration enhanced the expression levels of miR-744 in CD4+CD25+ Treg cells from heart transplantation mice. Moreover, miR-744 agomir administration significantly enhanced the expression levels of CD62L and Ki67 in CD4+CD25+ Treg cells from heart transplantation mice and further enhanced immunosuppressive function of Treg cells following coculture with CD4+CD25- T cells for different ratios. In addition, miR-744 agomir treatment significantly prolonged survival time and reduced rejection response of heart allografts in vivo, which are involved in downregulation of TNFRSF4 expression. These results provided a novel molecular mechanism of ameliorating heart allograft rejection in Treg cells, which could be used in the treatment of heart allograft rejection clinically.

miR-21 promotes non-small cell lung cancer cells growth by regulating fatty acid metabolism.

BACKGROUND: Lung cancer is one of the most common malignant tumors worldwide. CD36 is a receptor for fatty acids and plays an important role in regulating fatty acid metabolism, which is closely related to tumorigenesis and development. The regulation of miR-21 and its role in tumorigenesis have been extensively studied in recent years. However, the relationship between miR-21 and CD36 regulated fatty acid metabolism in human non-small cell lung cancer remains unknown. METHODS: In this study, lentivirus transfection, qRT-PCR, cell migration, immunofluorescence, and western blot were used to examine the relationship between miR-21 and CD36 regulated fatty acid metabolism and the regulation role of miR-21 in human non-small cell lung cancer. RESULTS: This study demonstrated that up-regulation of miR-21 promoted cell migration and cell growth in human non-small cell lung cancer cells. Moreover, the intracellular contents of lipids including cellular content of phospholipids, neutral lipids content, cellular content of triglycerides were significantly increased following miR-21 mimic treatment compared with control, and the levels of key lipid metabolic enzymes FASN, ACC1 and FABP5 were obviously enhanced in human non-small cell lung cancer cells. Furthermore, down-regulation of CD36 suppressed miR-21 regulated cell growth, migration and intracellular contents of lipids in human non-small cell lung cancer cells, which suggested that miR-21 promoted cell growth and migration of human non-small cell lung cancer cells through CD36 mediated fatty acid metabolism. Inhibition of miR-21 was revealed to inhibit cell growth, migration, intracellular contents of lipids, and CD36 protein expression level in human non-small cell lung cancer cells. In addition, PPARGC1B was a direct target of miR-21, and down-regulation of PPARGC1B reversed the inhibition of CD36 expression induced by miR-21 inhibitor. CONCLUSIONS: These results explored the mechanism of miR-21 promoted non-small cell lung cancer and might provide a novel therapeutic method in treating non-small cell lung cancer in clinic.

Effect of miR-21 on Apoptosis in Lung Cancer Cell Through Inhibiting the PI3K/ Akt/NF-κB Signaling Pathway in Vitro and in Vivo.

BACKGROUND/AIMS: Lung cancer is one of the most common malignancies in the world. Apoptosis-stimulating protein of p53 (ASPP2), a tumorigenesis related protein, plays a critical role in the initiation and development of various types of cancers. However, the effect of ASPP2 on lung cancer remains unknown. The purpose of this study aims to investigate the mechanism of ASPP2 regulated by miR-21 in lung cancer in vitro and in vivo. METHODS: In the study, migration and invasion assays, apoptosis assay, caspase activity assay, TUNEL staining, real time PCR and western blot were used to investigate the mechanism of ASPP2 regulated by miR-21 in lung cancer in vitro and in vivo. RESULTS: We demonstrated that the miR-21 inhibitor induced apoptosis through inhibiting the PI3K/Akt/NF-κB signaling pathway in non-small cell lung carcinoma (NSCLC). Moreover, ASPP2 was directly targeted by miR-21 in NSCLC cells. Down-regulation of miR-21 suppressed cell migration and invasion, as well as the EMT signaling pathway in NSCLC cells. Furthermore, the miR-21 inhibitor induced cell apoptosis via the caspase dependent pathway in NSCLC cells. The miR-21 inhibitor enhanced caspase-3, 8, 9 activity in NSCLC cells. In addition, the caspase inhibitor significantly reduced the apoptosis induced by the miR-21 inhibitor in NSCLC cells. CONCLUSIONS: Our results revealed that the miR-21 inhibitor could induce apoptosis through inhibiting the PI3K/Akt/NF-κB signaling pathway in human NSCLC cells, and might serve as a therapeutic strategy to treat NSCLC.

The effects of low-molecular-weight heparin on lung and pulmonary artery injuries in acute pulmonary embolism rat model via platelet-derived growth factor-ß.

OBJECTIVE: To evaluate the effects of anticoagulant agent (low-molecular-weight heparin, LMWH) on the pulmonary artery intima hyperplasia of rats with acute pulmonary embolism (APE) by assaying platelet-derived growth factor-ß (PDGF-ß). METHODS: A total of 90 Sprague-Dawley rats were randomly assigned into the sham, APE, and LMWH groups with 30 rats in each group. The APE rat models were established by injecting autologous blood clots via external jugular veins. In each group, six mice were sacrificed at the 1st day (D1), 4th day (D4), 7th day (D7), 14th day (D14), and 28th (D28) subsequent to the induction of APE to collect the lungs. Right ventricle pressure (RVP) and mean pulmonary arterial pressure (mPAP) were measured. Western blot and RT-PCR analyses were used to assess PDGF-ß expression at various time points. In addition, changes in lung pathology were evaluated using hematoxylin and eosin (H&E) staining and electron microscope. RESULTS: The overall success rate of establishing APE rat models was 85.7% (60/70). There was no difference in mPAP between the sham group and the APE group at the D1, D4, D7, and D14. However, at the D28, mPAP in the APE group was significantly higher than that in the sham group. There was no difference among the three groups regarding RVP. PDGF-ß expression were decreased in the LMWH group at all time points compared with the sham and APE groups (P < 0.01). Furthermore, pulmonary embolism, alveolar wall necrosis and hemorrhage, and inflammation were significantly attenuated in the LMWH group compared with the sham and APE groups subsequent to the induction of APE. CONCLUSION: LMWH attenuates lung and pulmonary artery injuries and improves prognosis. Decreased PDGF-ß in the lungs may be the important factor in the effects observed.

Expression of Chemokine XCL2 and CX3CL1 in Lung Cancer.

BACKGROUND Chemokines are a family of small proteins secreted by cells with chemotactic activity, and they play important roles in cell adhesion. However, the expression of chemokine XCL2 and CX3CL1 in lung cancers in different pathological stages remains unclear. MATERIAL AND METHODS XCL2 and CX3CL1 expression in lung cancers and adjacent non-cancerous tissues was detected by quantitative PCR and ELISA. The relative expression of both chemokines in lung cancers in different pathological stages was compared by immunohistochemical assay. RESULTS The relative expression level of XCL2 and CX3CL1 in lung cancer was significantly higher compared with adjacent normal tissues (P<0.001). The expression level of both chemokines was significantly increased with higher pathological stages, as indicated by immunohistochemical assay (P<0.05 or P <0.001). Their expression level in cancers with higher numbers of metastatic lymph nodes was also significantly increased compared with cancers with lower numbers of metastatic lymph nodes (P<0.05 or P<0.001). CONCLUSIONS The expression of XCL2 and CX3CL1 increases with increasing degree of malignancy, indicating that both chemokines might be important targets in gene therapy for lung cancer.

Aberrant promoter methylation of cell adhesion-related genes associated with clinicopathologic features in non-small cell lung cancer in China.

PURPOSE: The aim of this study was to investigate the methylation status of three cell adhesion-related genes including CDH1, TSLC1 and TIMP3 in non-small cell lung cancer and explore its association with clinicopathologic features and various environmental risk factors. METHODS: We detected the aberrant methylation presence of these genes by methylation-specific polymerase chain reaction and analyzed the potential correlations with multivariate logistic regression model as well as stepwise logistic regression. RESULTS: For CDH1, promoter methylation was less frequent in adenosquamous carcinomas than adenocarcinomas (OR=0.35, 95%CI=0.13-0.96); pickled food increased the methylation frequency (OR=2.23, 95%CI=1.09-4.54) while light smoking and fruit intake decreased that (OR=0.43, 95%CI=0.19-0.97; OR=0.37, 95%CI=0.15-0.95). For TSLC1, males and toxin exposure increased methylation frequency (OR=6.25, 95%CI=1.05-37.13; OR=2.42, 95%CI=1.01-5.77) while light smoking and radiation exposure decreased that (OR=0.14, 95%CI=0.03-0.60; OR=0.17, 95%CI=0.04-0.87). For TIMP3, males showed lower methylation frequency than females (OR=0.18, 95%CI=0.04-0.88) while central lung cancer, heavy smoking and radiation exposure presented higher aberrant DNA methylation status (OR=2.19, 95%CI=1.07-4.52; OR=6.99, 95%CI=1.32-37.14; OR=2.30, 95%CI=1.04-5.08). CONCLUSIONS: Aberrant promoter methylation of cell adhesion-related tumor suppressor genes in lung cancer displayed varieties of gene-specific correlations with clinicopathologic features and various environmental risk factors.

[Correlation between RARbeta gene promoter methylation and P53 gene mutations in non-small cell lung cancer].

OBJECTIVE: To investigate the correlation between RARbeta gene promoter methylation and P53 gene mutations in non-small cell lung cancer (NSCLC). METHODS: Promoter methylation of RARbeta and P53 mutations of exons 5 through 9 in 198 resected primary NSCLC tissues were determined by methylation-specific PCR and direct sequencing. RESULTS: RARbeta gene promoter methylation and P53 mutation were detected in 58.1% and 36.4% of tumors, respectively. Both were higher in males than in females and in smokers than in nonsmokers. A higher prevalence of RARbeta promoter methylation was found in patients with advanced stage tumors than those with TNM stage I. P53 gene mutations were more frequent in squamous cell carcinoma and adeno-squamous carcinoma than adenocarcinoma. All such differences were statistically significant (P< 0.05). Frequencies of P53 mutations, including G:C>T:A mutations, transversions and missense mutations were significantly higher in tumors with RARbeta methylation than in those without (P< 0.05). A significantly higher prevalence of RARbeta methylation was found in tumors with only G:C>T:A mutation in P53 gene than those without P53 mutations (P< 0.05). This difference (OR=3.737, 95%CI: 1.414-9.873) was still statistically significant (P< 0.05) in smokers (OR=4.020, 95%CI: 1.263-12.800), squamous cell carcinomas (OR=5.480, 95%CI: 1.400-21.446) or patients with advanced tumors (OR=3.446, 95%CI: 1.054-11.267) after adjusting for age and sex. CONCLUSION: RARbeta methylation is associated with G:C>T:A mutations in P53 gene in NSCLC.

[Effects of CYP1A1 and GSTM1 gene polymorphisms and BPDE-DNA adducts on lung cancer].

OBJECTIVE: To investigate the effect of CYP1A1 and GSTM1 genetic polymorphisms and BPDE-DNA adducts on lung tumorigenesis. METHODS: The case control study has included 200 cases of lung cancer and 200 controls. DNA was extracted from blood samples of all subjects. The genotype of both CYP1A1 and GSTM1 were detected with PCR-based restriction fragment length polymorphisms (PCR-RELP). BPDE-DNA adducts were detected with competitive ELISA. RESULTS: CYP1A1 mutant genotype and GSTM1 null genotype with smoke has increased the risk of lung cancer, with OR being 2.406(1.321-4.382), 2.755(1.470-5.163), respectively. The level of BPDE-DNA adducts in patients was greater than control, and the adduct level in ever smokers was higher than never smokers, the difference was statistically significant (P= 0.0252). GSTM1 null genotype individuals with BPDE-DNA level higher than 5 adducts/10(8) nucleotide have increased risk of lung cancer (OR= 1.988, 95%CI: 1.011-3.912). Compared with never smokers with CYP1A1 wild genotype, smokers with CYP1A1 mutation genotype had an increased risk of forming a higher level of DNA adducts (P= 0.0459). Smokers with GSTM1 null genotype formed more DNA adducts compared with never smokers with GSTM1 functional genotype (OR = 2.432, 95% CI: 1.072-4.517). CONCLUSION: GSTM1 null genotype with higher level DNA adducts may increase the risk of lung cancer. DNA adducts form easier in smokers with CYP1A1 mutation genotype and GSTM1 null genotype, which in turn may influence lung tumorigenesis.

Effect of CYP1A1 MSPI polymorphism on the relationship between TP53 mutation and CDKN2A hypermethylation in non-small cell lung cancer.

BACKGROUND AND AIMS: The molecular mechanisms of lung cancer susceptibility have not been fully understood. Although it has been described that germline polymorphisms are associated with either mutation or methylation of genes, the link between gene polymorphisms and gene-gene interactions has not been investigated. Therefore, we conducted this study to determine whether CYP1A1/GSTM1 polymorphisms can affect the relationship between TP53 mutation and CDKN2A hypermethylation in lung cancer. METHODS: This study included 196 primary non-small cell lung cancer (NSCLC) patients. CYP1A1 MSPI and GSTM1 polymorphisms were characterized through PCR-RFLP on DNA isolated from peripheral lymphocytes. TP53 mutations of exons 5 through 9 and CDKN2A promoter hypermethylation in both cancer tissues and corresponding normal tissues were analyzed by direct sequencing and methylation-specific PCR (MSP) respectively. RESULTS: TP53 mutation in the tumor was associated with squamous cell histology and CDKN2A methylation was associated with older age (≥60 years), heavy smoking (>30 pack-years), squamous cell histology and advanced stage (stage II-IV). After adjusting for age, sex, smoking degree, histology type and TNM stage, the correlation between TP53 mutation and CDKN2A methylation was significant in patients with CYP1A1 risk genotype (p = 0.038), but not in those with CYP1A1 homogeneity wild genotype (p = 0.151). CONCLUSIONS: This may suggest that TP53 mutation and CDKN2A methylation specifically interact to promote lung tumorigenesis in subjects with CYP1A1 risk genotype but not in those with CYP1A1 wild-type homozygotes, implying different pathways for the development of lung carcinoma with respect to CYP1A1 polymorphism.

Addition of ulinastatin to preservation solution promotes protection against ischemia-reperfusion injury in rabbit lung.

BACKGROUND: The composition of the lung preservation solution used in lung graft procurement has been considered the key to minimize lung injury during the period of ischemia. Low-potassium dextran glucose (LPDG), an extracellular-type solution, has been adopted by most lung transplantation centers, due to the experimental and clinical evidences that LPDG is superior to intracellular-type solutions. Ulinastatin has been shown to attenuate ischemia-reperfusion (I/R) injury in various organs in animals. We supposed that the addition of ulinastatin to LPDG as a flushing solution, would further ameliorate I/R lung injury than LPDG solution alone. METHODS: Twelve male New Zealand white rabbits were randomly divided into 2 groups. Using an alternative in situ lung I/R model, the left lung in the control group was supplied and preserved with LPDG solution for 120 minutes. In the study group 50,000 U/kg of ulinastatin was added to the LPDG solution for lung preservation. Then re-ventilation and reperfusion of the left lung were performed for 90 minutes. Blood gas analysis (PaO2, PaCO2), mean pulmonary artery pressure (MPAP) and serum TNF-α level were measured intermittently. The pulmonary water index (D/W), tissue myeloperoxidase (MPO) activity, tissue malondialdehyde (MDA) content and morphologic changes were analyzed. RESULTS: The study group showed significantly higher PaO2 and lower MPAP at the end of reperfusion. Serum TNF-α level, left lung tissue MPO and MDA in the study group were significantly lower than those in the control group. D/W and pathologic evaluation were also remarkably different between the two groups. CONCLUSIONS: This study indicated that better lung preservation could be achieved with the use of an ulinastatin modified LPDG solution. Ulinastatin further attenuated lung I/R injury, at least partly by reducing oxidative reactions, inhibiting the release of inflammatory factors and neutrophils immigration.

[Relationship between promoter methylation of p16, DAPK and RAR beta genes and the clinical data of non-small cell lung cancer].

OBJECTIVE: To investigate the effects of promoter methylation of p16, death-associated protein kinase (DAPK) and retinoic acid receptor-beta (RAR beta) genes on clinical data in non-small cell lung cancers, and to study the effect of smoking on the risk of gene methylation. METHODS: The promoter methylation of p16, DAPK and RAR beta genes in 200 primary non-small cell lung cancers and the corresponding nonmalignant lung tissues were determined by methylation-specific PCR. RESULTS: Methylation in the tumor tissues was detected in 51.0% for p16, 60.0% for DAPK, and 58.0% for RAR beta gene, with significant differences (P < 0.05) when compared with those in the corresponding nonmalignant tissues(12.5%, 11.5% and 15.0%) respectively. p16 gene methylation in tumor tissue was associated with age significantly in unconditional logistic regression analysis (P < 0.01) and histologic type (P < 0.05). DAPK gene methylation in tumor tissue was associated significantly with age (P < 0.05), gender (P < 0.05) and clinical type (P < 0.05). RAR beta gene methylation in tumor tissue was associated with clinical type (P < 0.05) and tumor stage (P < 0.05) significantly. The interaction odds ratio (OR) for the gene-gene interaction in tumor tissue between p16 and DAPK was 1.987 (95%CI:1.055-3.743). The results of the gene-smoking analyses revealed that a relationship existed between cigarette smoking and p16 gene methylation (OR = 3.139, 95%CI: 1.046-9.419), the OR for the relationship of DAPK gene methylation and cigarette smoking was 3.585(95%CI: 1.270-10.123) in tumor tissue. The RAR beta gene methylation did not differ based on the smoking status of patients in tumor tissue. CONCLUSION: The p16, DAPK and RAR beta genes methylation are strongly associated with clinical data of non-small cell lung cancer, and methylation of p16 and DAPK genes are associated with tobacco smoking.

Combined effects of serum trace metals and polymorphisms of CYP1A1 or GSTM1 on non-small cell lung cancer: a hospital based case-control study in China.

INTRODUCTION: The limited information for effects of serum trace elements and genetic polymorphisms on lung cancer is available. Based on a hospital based case-control study, the epidemiological questionnaires were completed by face to face interview, and the gene polymorphisms were tested by RFLP-PCR, and serum trace metals were measured by atomic absorption spectrophotometer, and the data was analyzed by the logistic regressive models. RESULTS: The high serum copper level (>1500 ng/ml) or serum copper/zinc ratio (>1) was the risk factors of NSCLC (OR=3.10, 11.03, respectively), but the ORs of the higher serum Zn (>1200 ng/ml), Se (>50 ng/ml) or Cr(3+) (>600 ng/ml) for NSCLC were all significantly less than 0.20 (all p<0.01) indicating strong protection against NSCLC. While the OR of CYP 1A1 variants carriers with a higher serum Cu or Cu/Zn ratio level was around 3.38 and 12.59, respectively, the risk of CYP1A1 variants carriers with a higher serum Zn is 0.18, Se 0.04 or Cr(3+) 0.28. Similarly, compared with the carriers of GSTM1 power with a lower serum Zn, Se or Cr(3+), the OR of the carriers of GSTM1 null with a higher serum Zn, Se and Cr(3+) was separately 0.16, 0.07 and 0.26, highlighting the protection against NSCLC. CONCLUSIONS: Our findings suggested that CYP1A1 or GSTM1 variants may significantly modify the associations between level of serum trace metals (Cu, Zn, Se or Cr) and NSCLC, indicating the intriguing pathogenesis of lung cancer.

[Some research development on non-small cell lung cancer genetics and genetic expression].

Non-small cell lung cancer is the major cancer causing death among the malignant tumors. Early detection non-small cell lung cancer can detect the patients in time and get the treatment in time, to obtain the relative good therapy results. So, it is necessary to develop a method being able to accurately determine the non-small cell lung cancer at the early stage. Currently, the lung cancer marker detection is of certain importance in the non-small cell lung cancer diagnosis. Large volume of molecular biology research demonstrate that gene polymorphism is the important factor of the lung cancer occurrence. Furthermore, the importance of genetic expression changes that occur during lung cancer development has been realized gradually. In the future non-small lung cancer research, a comprehensive method combing epidemiological, genetic and genetic expression research seems very important.

Combined effects of cigarette smoking, gene polymorphisms and methylations of tumor suppressor genes on non small cell lung cancer: a hospital-based case-control study in China.

BACKGROUND: Cigarette smoking is the most established risk factor, and genetic variants and/or gene promoter methylations are also considered to play an essential role in development of lung cancer, but the pathogenesis of lung cancer is still unclear. METHODS: We collected the data of 150 cases and 150 age-matched and sex-matched controls on a Hospital-Based Case-Control Study in China. Face to face interviews were conducted using a standardized questionnaire. Gene polymorphism and methylation status were measured by RFLP-PCR and MSP, respectively. Logistic regressive model was used to estimate the odds ratios (OR) for different levels of exposure. RESULTS: After adjusted age and other potential confounding factors, smoking was still main risk factor and significantly increased 3.70-fold greater risk of NSCLC as compared with nonsmokers, and the ORs across increasing levels of pack years were 1, 3.54, 3.65 and 7.76, which the general dose-response trend was confirmed. Our striking findings were that the risk increased 5.16, 8.28 and 4.10-fold, respectively, for NSCLC with promoter hypermethylation of the p16, DAPK or RAR beta gene in smokers with CYP1A1 variants, and the higher risk significantly increased in smokers with null GSTM1 and the OR was 17.84 for NSCLC with p16 promoter hypermethylation, 17.41 for DAPK, and 8.18 for RAR beta in smokers with null GSTM1 compared with controls (all p < 0.01). CONCLUSION: Our study suggests the strong combined effects of cigarette smoke, CYP1A1 and GSTM1 Polymorphisms, hypermethylations of p16, DAPK and RAR beta promoters in NSCLC, implying complex pathogenesis of NSCLC should be given top priority in future research.

Diagnosis and treatment of pulmonary mucosa-associated lymphoid tissue lymphoma.

BACKGROUND: Primary non-Hodgkin's lymphoma in lung is very rare, and the most common among them is mucosa-associated lymphoid tissue lymphoma (MALToma), whose clinical features and laboratory characteristics are poorly defined, making diagnosis difficult. The purpose of this study was to study the diagnosis and treatment of pulmonary MALToma. METHODS: The clinical data of 12 patients treated for MALToma between August 1992 and December 2005 were analyzed. RESULTS: No specific symptoms or signs, or results of bronchoscopy, ultrasonagraphy or bone marrow examination could be found in the 12 patients. Only radiography was useful in diagnosis, though the final diagnosis of all the patients was based on histology and immunohistochemistry. Two patients also had gastric MALToma. Operations were performed on 6 patients, including 5 radical operations and 1 partial resection: 4 patients also received adjuvant chemotherapy. One patient experienced recurrence 152 months after the operation, while the other 5 patients have survived disease-free. Four patients were treated with chemotherapy alone, two of whom experienced complete remission and the others partial remission. The final 2 patients received no treatment and had survived for 7 and 27 months respectively. All the patients were still alive at the most recent follow-up, 7 to 160 months (mean 71.3 months). CONCLUSIONS: Except radiography, no specific clinical manifestations could be identified for pulmonary MALToma. The final diagnosis should be based on histology and immunohistochemistry. Several treatment methods can be used to achieve good outcomes.

[Selective determination of dopamine in the presence of high concentration of ascorbic acid with L-cysteine modified glassy carbon electrodes].

OBJECTIVE: To establish an assay system for determination of dopamine (DA) in the presence of ascorbic acid (AA) with L-cysteine modified glassy carbon electrode. METHODS: L-cysteine was modified onto glassy carbon electrode electrochemically, and with this modified electrode, dopamine was determined by linear sweep stripping voltammetry. RESULTS: L-cysteine polymer-modified electrode had strong catalytic effect towards the electrochemical oxidation of DA. The modified electrode showed good properties in determination of DA with coexisting AA. Under selected conditions, the linearity of DA was in the range of 2.0 x 10(-7) - 1.0 x 10(-4) mol/L with the detection limit of 2.0 x 10(-8) mol/L. The stability, reliability and recovery of this L-cysteine-modified electrode based on electrochemical method were also satisfactory. CONCLUSION: L-cysteine-modified electrode can avoid the interference by AA for determination of DA.