Smoking and idiopathic pulmonary fibrosis: A meta-analysis.

INTRODUCTION: In this study, we aimed to systematically explore the relationship between smoking and idiopathic pulmonary fibrosis (IPF). METHODS: The PubMed, Web of Science and Embase databases were searched to systematically identify eligible studies. The Newcastle‒Ottawa Quality Assessment Scale (NOS) was used to evaluate the quality of the selected studies. The pooled odds ratio (OR) and survival hazard ratio (HR) were calculated with a random effects model using Stata 16.0 software. RESULTS: Thirty studies were enrolled. All of the included studies were considered to have intermediate or high quality. Nine studies were suitable for meta-analysis of ORs, and twenty-one studies were suitable for meta-analysis of survival HR. The pooled analysis revealed a significant difference in the risk of IPF between the smoking group and the never smoking group (OR 1.71, 95% CI 1.27-2.30, P < 0.001), indicating that smoking is a risk factor for IPF. When analyzing pooled survival HRs, never smoking was compared to former smoking or current smoking. Former smoking was shown to be a poor prognostic factor for IPF (HR 1.43, 95% CI 1.18-1.74, P < 0.001), but current smoking was not a significant factor. CONCLUSIONS: Our results indicated that smoking is a risk factor for IPF patients. IMPLICATIONS: In this study, we mainly concluded that smoking is a risk factor for IPF and that former smoking is a poor prognostic factor for IPF. To our knowledge, this is the first meta-analysis report focusing on the association between smoking per se and IPF. Through our current study, we hope to further raise awareness of the relationship between smoking and IPF.

Delayed diagnosis for primary tracheobronchial amyloidosis.

OBJECTIVE: To determine clinical features and diagnostic methods for primary tracheobronchial amyloidosis (TBA).
 METHODS: The clinical manifestations and diagnosis of a male patient who had been misdiagnosed for many years were described and analyzed.
 RESULTS: The patient was a 68-year-old male who complained of recurrent cough, expectoration, and progressive dyspnea for more than 30 years. He had been diagnosed with chronic bronchitis, bronchiectasis, and endobronchial tuberculosis in other hospitals and treated with antibiotics frequently and anti-tubercular agents for 3 months. Despite the treatments, the patient's symptoms were progressively worse. Finally, he came to Xiangya Hospital, Central South University, and was clearly diagnosed with primary TBA based on histopathological evidence after bronchoscopy.
 CONCLUSION: TBA, a rare disease resulting from abnormal submucosal amyloid deposition in the trachea and bronchi, may display with many different symptoms. TBA is often misdiagnosed with other pulmonary diseases. The use of bronchoscopic techniques is essential for the diagnosis of TBA. Histopathology remains the gold standard for diagnosis of primary TBA. So, for patients with chronic cough of unknown etiology, bronchoscopy should be performed to obtain biopsy samples for the definitive diagnosis.

[Construction of RBM5 vector, establishment of stably transfected A549 cell line and preliminary research on the function of RBM5 gene].

OBJECTIVE: To establish a stable A549 cell line transfected by RNA binding motif 5 (RBM5) expression vector, and to investigate the effect of RBM5 gene on proliferation of A549 cell line and the expression of DEAH box polypeptide 15 (DHX15). METHODS: The eukaryotic expression vector pcDNA3.1 (+)/RBM5 was constructed by a twostep PCR technique. Then, the recombinant plasmid pcDNA3.1 (+)/RBM5 was verified by DNA sequencing and transfected into the lung adenocarcinoma cell A549. The positive cells with overexpression of RBM5 gene were identified by Western blotting. Flow cytometry was used to analyze the cell cycles of the positive A549 cells [pcDNA3.1 (+)/RBM5-A549] and the negative controls [pcDNA3 .1 (+)- A549]. Finally, RT-PCR was used to detect the expression of DHX15, a splicing-related factor, in the positively transfected A549 cells and the negative controls. RESULTS: A pcDNA3.1 (+)/RBM5 eukaryotic expression vector has been constructed successfully, and the A549 cell line that stably transfected with RBM5 gene has been established. Compared with negative control cells, the percentage of G1 phase cells in the positive cells was increased, while the percentage of S phase was decreased (both P<0.01), and the expression of DHX15 is upregulated (P<0.01). CONCLUSION: RBM5 gene can inhibit the cell cycle and upregulate the expression of DHX15 in A549 cells.

SARS, MERS and COVID-19 among healthcare workers: A narrative review.

In the recent two decades, three global viral infectious diseases, severe acute respiratory syndrome (SARS), middle east respiratory syndrome (MERS), and coronavirus disease (COVID-19), have occurred worldwide. SARS occurred in November 2002, causing 8096 infected cases, as well as 774 deaths. MERS occurred in June, 2012, causing 2519 confirmed cases, along with 866 associated deaths. COVID-19 occurred in December 2019, as of 30 April 2020, a total of 3,024,059 clinical cases have been reported, including 208,112 deaths. Healthcare workers (HCWs) need to be in close contact with these virus-infected patients and their contaminated environments at work, thus leading to be infected in some of them, even a few of them are died in line of duty. In this review, we summarized the infection status of HCWs during the outbreak of SARS, MERS and COVID-19, with in-depth discussion, hoping to provoke sufficient attention to the HCWs infection status by more people.

Impact of Sex and Smoking on the Efficacy of EGFR-TKIs in Terms of Overall Survival in Non-small-Cell Lung Cancer: A Meta-Analysis.

Background: To comprehensively understand the impact of sex and smoking on the efficacy of epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) therapy in terms of overall survival (OS) in non-small-cell lung cancer (NSCLC). Methods: PubMed, Cochrane Library, Embase, and Scopus were searched from inception to March 17, 2019. OS was analyzed based on hazard ratios (HRs) and 95% confidence intervals (CIs) and estimated using the random effects model. Results: Our meta-analysis included 22 studies involving 11,874 patients. In the primary analysis, we found no statistically significant efficacy difference for EGFR-TKI intervention between females and males (pooled HR 0.95, 95% CI 0.87-1.04, P = 0.30) and no obvious efficacy difference between never smokers and ever smokers (pooled HR 0.91, 95% CI 0.76-1.09, P = 0.31). In the subgroup analysis of placebo control treatment, we found that female NSCLC patients who received EGFR-TKI therapy had a longer OS than male patients (pooled HR 0.86, 95% CI 0.75-1.00, P = 0.04), while smoking status showed no significant effect on the efficacy of EGFR-TKI treatment in terms of the OS of NSCLC patients in all subgroup analyses. Conclusion: The efficacy of EGFR-TKI therapy for NSCLC patients is independent of smoking status but dependent on sex, and females have a longer OS than males.

Anti-tumour effects of Keratin 6A in lung adenocarcinoma.

BACKGROUND: To examine the effects of Keratin 6A (KRT6A) protein on the proliferation, migration and invasion abilities of lung adenocarcinoma cells, and to analyse the relationship between the expression level of KRT6A protein and the survival prognosis of lung adenocarcinoma patients. METHODS: Western Blot was used to detect the expression of KRT6A protein in lung adenocarcinoma cell lines. CCK-8 experiment and colony formation assays were performed to detect the proliferation ability. Wound healing assay and transwell migration assay were conducted to detect the migration ability. Transwell invasion assay was conducted to detect the invasion ability. Immunohistochemistry was used to detect the expression of KRT6A protein in lung adenocarcinoma tissues. RESULTS: We first found that the expression of KRT6A protein in lung adenocarcinoma cell lines was low. After overexpressed KRT6A protein in lung adenocarcinoma cells, we then found that KRT6A protein could not only inhibit the proliferation ability of lung adenocarcinoma cells but also inhibit them migration and invasion abilities. In addition, we also found that there had obvious difference in the expression of KRT6A protein in between patients. And through further analysis, we finally discovered that high expression of KRT6A protein was related to favourable prognosis in lung adenocarcinoma patients. CONCLUSIONS: KRT6A protein inhibits the proliferation, migration and invasion abilities of lung adenocarcinoma cells, and high expression of KRT6A protein is a predictor of good prognosis in patients with lung adenocarcinoma.

Progesterone/Org inhibits lung adenocarcinoma cell growth via membrane progesterone receptor alpha.

BACKGROUND: The aim of this study was to determine whether progesterone could inhibit the growth of lung adenocarcinoma cells via membrane progesterone receptor alpha (mPRα) and elucidate its potential mechanism. The relationship between mPRα expression and the survival prognosis of lung adenocarcinoma patients was studied. METHODS: A mPRα knockdown lung adenocarcinoma cell line was constructed and treated with P4 and Org (a derivative of P4 and specific agonist of mPRα). Cell proliferation was assessed using CCK-8 and plate colony formation assays. Protein expression was detected by western blotting. A nude mouse model of lung adenocarcinoma was established to assess the antitumor effect of P4/Org in vivo. RESULTS: We initially determined that mPRα could promote the development of lung adenocarcinoma through the following lines of evidence. High expression of mPRα both at the mRNA and protein level was significantly associated with the poor prognosis of lung adenocarcinoma patients. The downregulation of mPRα inhibited the proliferation of lung adenocarcinoma cells. We further showed that mPRα mediates the ability of P4 to inhibit the growth of lung adenocarcinoma cells through the following lines of evidence: P4/Org inhibited the proliferation of lung adenocarcinoma cells; mPRα mediated the ability of P4/Org to inhibit lung adenocarcinoma cell proliferation; mPRα mediated the ability of P4/Org to inhibit the PKA (cAMP-dependent protein kinase)/CREB (cAMP responsive element binding protein) and PKA/ß-catenin signaling pathways; and P4/Org inhibited the growth of a lung adenocarcinoma tumor model in vivo. CONCLUSIONS: In summary, the results of our study show that progesterone can inhibit lung adenocarcinoma cell growth via mPRα.

Newly emergent acquired EGFR exon 18 G724S mutation after resistance of a T790M specific EGFR inhibitor osimertinib in non-small-cell lung cancer: a case report.

BACKGROUND: T790M mutation is well known as the most common mechanism for resistance to the first- and second-generation tyrosine kinase inhibitors (TKIs) for EGFR mutation in non-small-cell lung cancer. Several third-generation EGFR TKIs, such as osimertinib, have been explored and approved for conquering this resistance; however, acquired resistance to osimertinib is evident and the resistance mechanisms remain complex and incompletely explored. CASE PRESENTATION: A non-smoking 58-year-old female patient was initially diagnosed with lung adenocarcinoma harboring EGFR exon 19 deletion and clinically responded to initial gefitinib treatment. The patient progressed on gefitinib after >1 year and a T790M mutation was detected in tissue biopsy by next-generation sequencing (NGS). Osimertinib treatment was administrated for several months and an acquired rare EGFR G724S mutation was detected via NGS blood sample after osimertinib resistance. CONCLUSION: The specific mechanisms of acquiring drug resistance for EGFR-TKIs have not been fully explored. EGFR G724S mutation might be associated with osimertinib resistance but more studies about the mechanism should be explored.

Correlative analysis of gene mutation and clinical features in patients with non-small cell lung cancer.

BACKGROUND: Lung cancer is the main reason for death associated with cancer all over the world. In most cases of non-small cell lung cancer (NSCLC), patients only express one type of gene mutation, each gene mutation population has different clinicopathological features, and each is expressed differently in different regions of the population. At present, there are few studies on multiple driver genes and clinicopathological features of the population in Hunan, China. METHODS: From February 2016 to December 2017, the Department of Geriatric Respiratory Medicine of Xiangya Hospital of Central South University diagnosed 113 cases of NSCLC. Genetic testing of next-generation sequencing (NGS) was completed, and it conformed to the inclusion criteria. All cases were pathologically confirmed as NSCLC, with the tumor staging being based on the 8th edition of TNM classification. RESULTS: In this study, we included a total of 113 NSCLC cases, including 78 males and 35 females. Histological distributions were mainly adenocarcinoma (ADC, 78.76%) and squamous cell carcinoma (SCC, 21.24%). We found 71 cases had gene-mutations. There was one concurrent mutation of ALK and ROS1, one concurrent mutation of epidermal growth factor receptor (EGFR) and BRAF, one concurrent mutation of EGFR and MET, one concurrent mutation of MET and BRAF, and one concurrent mutation of EGFR and KRAS; there were two cases of concurrent mutation of EGFR and ERBB2. The distribution of each of the mutated genes was as follows: EGFR, 62.82%; ALK, 8.97%; ROS1, 5.13%; MET, 5.13%; ERBB2, 5.13%; RET, 0.00%; BRAF, 2.56%; KRAS, 10.26%. Our study found that in patients with EGFR mutation, the mutation rate of males was 32.05%, and the rate in females was 68.57% (P<0.01); the mutation rate in people aged 60 or above was 40.00% while for those aged lower than 60 it was 46.55% (P>0.05); the mutation rate of ADC was 52.81% and in SCC was 8.33% (P<0.01); the mutation rate in smokers was 32.84% and in non-smokers was 58.70% (P<0.05); the mutation rate in patients of IV stage was 47.37% and the rate in patients of non-IV stage was 22.22% (P>0.05). Our study found that among patients with ALK/ROS1/MET/ERBB2/BRAF/KRAS mutations, the mutation rate in men was 7.69%, 2.60%, 3.85%, 2.56%, 0.00%, and 8.97% respectively, and for females it was 2.86%, 5.71%, 2.86%, 5.71%, 5.71%, and 2.86% respectively; the mutation rate in patients aged 60 and older was 3.64%, 5.45%, 3.64%, 1.82%, 1.82%, and 9.09% respectively; the rate in patients aged lower 60 was 8.62%, 1.72%, 3.45%, 5.17%, 1.72%, and 5.17% respectively; the mutation rate of ADC was 6.74%, 3.37%, 3.37%, 4.49%, 2.25%, and 6.74% respectively, while for SCC, it was 4.17%, 4.17%, 4.17%, 0.00%, 0.00%, and 8.33% respectively; the mutation rate in smokers was 8.96%, 1.49%, 4.48%, 1.49%, 0.00%, and 10.45% respectively, while in non-smokers, it was 2.17%, 6.52%, 2.17%, 6.52%, 4.35%, and 2.17% respectively; the mutation rate in patients of IV stage was 7.37%, 4.21%, 2.11%, 4.21%, 2.11%, and 7.37% respectively, and in patients of non-IV stage, it was 0.00%, 0.00%, 11.11%, 0.00%, 0.00%, and 5.56% respectively. In ALK/ROS1/MET/ERBB2/BRAF/KRAS mutations, there was no statistically significant difference in gender, age, tissue type, smoking history, and stage. Our research shows that the distribution of each mutant type of EGFR mutation was as follows: exon 2, 1/74 (1.35%); exon 4, 1/74 (1.35%); exon 6, 1/74 (1.35%); exon 18, 1/74 (1.35%); exon 19, 25/74 (33.78%); exon 20, 12/74 (16.22%); exon 21, 19/74 (25.68%); exon 22, 1/74 (1.35%); and EGFR amplification, 13/74 (17.57%). CONCLUSIONS: (I) EGFR mutation was more common in non-smoking female patients with ADC and had no significant correlation with age and stage. (II) EGFR mutations were mainly concentrated in exon 19, 20, 21, and EGFR amplification. There was no significant statistical difference between mutations in exons 19, 20, 21, EGFR gene amplification and clinical features. (III) There was no statistically significant difference in the ALK/ROS1/MET/ERBB2/BRAF/KRAS mutations with gender, age, tissue type, smoking history, and tumor stage.

Relationship between resilience, social support as well as anxiety/depression of lung cancer patients: A cross-sectional observation study.

OBJECTIVE: The mood of patients with lung carcinoma would be greatly influenced by the diagnosing and treating processes. This study was aimed to explore the effects of resilience between social assistance and anxiety/depression of patients with lung cancer, which may assist in clinical intervention. DESIGN AND METHODS: A cross-sectional pilot study was conducted on lung cancer patients at Xiangya Hospital of Central South University, China. A total of 289 patients aged 25-81 years were included in this study. RESULTS: Correlational analyses revealed that anxiety/depression was negatively associated with psychological resilience and each dimension of social assistance, including subjective support, objective support along with the supports utilization (P < 0.01). Furthermore, psychological resilience was positively related to subjective support (P < 0.01), support utilization (P < 0.01) along with objective support (P < 0.05). Mediational analyses showed that, on the one hand, resilience could partially mediate the relation between anxiety and subjective support and totally mediate the relationship between support utilization and anxiety. On the other hand, resilience could totally mediate the relation between depression and subjective support and partially mediate the relation between support utilization and depression. However, resilience did not play an intermediary role between anxiety/depression and objective support. CONCLUSION: Lower psychological anxiety and depression would be experienced by lung cancer patients with higher resilience and social support. The level of anxiety and depression would be indirectly affected by social support through the mediation of resilience.

[Effects of matrix metalloproteinase-9 antisense oligonucleotide on the apoptosis and metastasis of the human lung adenocarcinoma cell].

BACKGROUND: Matrix metalloproteinase-9 (MMP-9) is one of significant extracellular matrix catabolic enzymes, which is known to relate to the initiation, progression and growth of the tumor. The aim of this study is to investigate the effects of MMP-9 antisense oligonucleotide (ASODN) on the apoptosis and metastasis of human lung adenocarcinoma A549 cell. METHODS: MTT was used to analyze the effect of MMP-9 ASODN transfection on A549 cell growth. Flow cytometry was used to analyze the cell cycle and apoptosis. MTT chromometry and scratch migration were used to observe the capability of adhesion and immigration of the A549 cell. RESULTS: MMP-9 ASODN inhibited the survival rate of the A549 cell and the action was concentration-and time-dependent. The peak concentration of MMP-9 ASODN was 600 nmol/L at 48 hours after transfection. After transfection of MMP-9 ASODN to A549 cell, the percentage of A549 apoptosis cell was significantly higher than that of control group (P < 0.01), but the adhesion and migration cut down predominantly (P < 0.01). CONCLUSIONS: MMP-9 ASODN can depress the adhesion and migration and inhibit proliferation of adenocarcinoma A549 cell effectively, and can promote apoptosis of the A549 cell.

[Effects and mechanism of decorin on the proliferation of A549 lung adenocarcinoma cells in vitro].

BACKGROUND: Decorin is a member of the small proteglycans in extracellular matrix of tumor microenvironment, which is known to relate to the initiation, progression and growth of the tumor. The aim of this study is to investigate the effects and mechanism of decorin on the proliferation of A549 lung adenocarcinoma cell line in vitro. METHODS: Lung adenocarcinoma cell line A549 was cultured with decorin in a wide range of concentration for different time. Cell activities were studied by MTT. The changes of cell cycle and apoptosis were analyzed by FCM. Decorin mRNA expression was detected by RT-PCR. P21 expression was determined by Western blot. TGF-ß concentration in the culture supernatants was determined by ELISA. RESULTS: The proliferation of A549 cell could be inhibited by decorin in vitro and the inhibition effect was the time- and dose-dependent relationship. Apoptosis of adenocarcinoma cell could be efficiently induced by decorin in a time/dose-dependent manner. Decorin could upregulate the intrinsic decorin mRNA and P21 protein expression, downregulate the TGF-ß, and block cell cycle at G1 phase. CONCLUSIONS: Decorin can inhibit adenocarcinoma cell proliferation and induce apoptosis of adenocarcinoma cells in vitro. The proliferation of A549 cell could be inhibited in vitro by decorin through the mechanism of increasing decorin mRNA, decreasing TGF-ß, increasing P21 protein expression, inhibiting cell cycle and inducing cell apoptosis.

Bronchoscopic Diagnosis and Treatment of Primary Tracheobronchial Amyloidosis: A Retrospective Analysis from China.

Objective. To assess the value of bronchoscopy in the diagnosis and treatment of primary tracheobronchial amyloidosis (TBA), in order to reduce misdiagnosis rates and improve prognosis. Methods. Clinical data of 107 patients with TBA reported from 1981 to 2015 in China were retrospectively analyzed for clinical features, bronchoscopic manifestations, pathologies, treatments, and outcomes. Results. 105 of 107 TBA patients were pathologically confirmed by bronchoscopy. Main bronchoscopic manifestations of TBA were single or multiple nodules and masses within tracheobronchial lumens; local or diffuse luminal stenosis and obstruction; luminal wall thickening and rigidity; rough or uneven inner luminal walls; congestion and edema of mucosa, which was friable and prone to bleeding upon touch; and so forth. 53 patients were treated with bronchoscopic interventions, like Nd-YAG laser, high-frequency electrotome cautery, freezing, resection, clamping, argon plasma coagulation (APC), microwaving, stent implantation, drug spraying, and other treatments. 51 patients improved, 1 patient worsened, and 1 died. Conclusion. Bronchoscopic biopsy is the primary means of diagnosing TBA. A variety of bronchoscopic interventions have good short-term effects on TBA. Bronchoscopy has important value in the diagnosis, severity assessment, treatment, efficacy evaluation, and prognosis of TBA.

Prognostic significance of TCF21 mRNA expression in patients with lung adenocarcinoma.

Several prognostic indicators have shown inconsistencies in patients of different genders with lung adenocarcinoma, indicating that these variations may be due to the different genetic background of males and females with lung adenocarcinoma. In this study, we first used the Gene-Cloud of Biotechnology Information (GCBI) bioinformatics platform to identify differentially expressed genes (DEGs) that eliminated gender differences between lung adenocarcinoma and normal lung tissues. Then, we screened out that transcription factor 21 (TCF21) is a hub gene among these DEGs by creating a gene co-expression network on the GCBI platform. Furthermore, we used the comprehensive survival analysis platforms Kaplan-Meier plotter and PrognoScan to assess the prognostic value of TCF21 expression in lung adenocarcinoma patients. Finally, we concluded that decreased mRNA expression of TCF21 is a predictor for poor prognosis in patients with lung adenocarcinoma.

Benzo(a)pyrene enhances the EMT-associated migration of lung adenocarcinoma A549 cells by upregulating Twist1.

Benzo(a)pyrene (BaP), an important toxic component of cigarette smoke, can cause lung cancer and lead to the progression of lung cancer. In the present study, we investigated the effect of BaP on the migration of lung adenocarcinoma A549 cells. BaP (1 µM) promoted the migration of A549 cells in a time-dependent manner and upregulated the expression of the Twist family BHLH transcription factor 1 (Twist1). BaP also induced upregulation of the mesenchymal markers N-cadherin and vimentin and downregulation of the epithelial marker E-cadherin. When the expression of Twist1 was knocked down in A549 cells that were treated with BaP for 4 weeks (A549BaP-4w), the expression of Twist1 decreased, which inhibited the migration capacity of A549BaP-4w cells, the expression of N-cadherin and vimentin was downregulated and the expression of E-cadherin was upregulated. In addition, morphological observations of A549BaP-4w cells revealed that the epithelial characteristics of A549 cells became mesenchymal characteristics. When the expression of Twist1 was knocked down, the A549BaP-4w cells were transformed back to cells with epithelial characteristics. In conclusion, the results from the present study indicate that BaP enhances the epithelial-mesenchymal transition-associated migration of lung adenocarcinoma A549 cells by upregulating Twist1.

Microarray data re-annotation reveals specific lncRNAs and their potential functions in non-small cell lung cancer subtypes.

Non­small­cell lung cancer (NSCLC) is a leading cause of cancer mortality worldwide. The most common subtypes of NSCLC are adenocarcinoma (AC) and squamous cell carcinoma (SCC). However, the pathophysiological mechanisms contributing to AC and SCC are still largely unknown, especially the roles of long non­coding RNAs (lncRNAs). The present study identified differentially expressed lncRNAs between lung AC and SCC by re­annotation of NSCLC microarray data analysis profiling. The potential functions of lncRNAs were predicted by using coding­non­coding gene co­expressing network. Reverse transcription-quantitative polymerase chain reaction (RT­qPCR) was used to investigate lncRNA expression levels in AC cell lines (A549 and L78), SCC cell lines (H226 and H520) and normal cells (NL­20). Western blotting analysis was used to investigate the protein expression levels in these cell lines. A total of 65 lncRNAs were differentially expressed between AC and SCC including 28 lncRNAs that were downregulated in SCC subtypes compared with those in AC ones, and 37 upregulated lncRNAs in SCC subtypes compared with AC subtypes. Three lncRNAs, sex determining region Y­box 2 overlapping transcript (SOX2­OT), NCBP2 antisense RNA 2 (NCBP2­AS2) and ubiquitin like with PHD and ring finger domains 1 (UHRF1), were predicted to be associated with lung cancer; RT­qPCR confirmed that SOX2­OT and NCBP2­AS2 were associated with lung cancer. Finally, western blot assays demonstrated that there was no difference in ß­catenin and glycogen synthase kinase 3ß (GSK­3ß) expression in cancer cells compared with NL­20, but increased phosphorylated (p­)ß­catenin and p­GSK­3ß was detected in lung cancer cell lines compared with NL­20, particularly in A549 cells. Although these results require further experimental verification, the analysis of lncRNA signatures between AC and SCC has provided insights into the regulatory mechanism of NSCLC development.

Eight potential biomarkers for distinguishing between lung adenocarcinoma and squamous cell carcinoma.

Lung adenocarcinoma (LADC) and squamous cell carcinoma (LSCC) are the most common non-small cell lung cancer histological phenotypes. Accurate diagnosis distinguishing between these two lung cancer types has clinical significance. For this study, we analyzed four Gene Expression Omnibus (GEO) datasets (GSE28571, GSE37745, GSE43580, and GSE50081). We then imported the datasets into the Gene-Cloud of Biotechnology Information online platform to identify genes differentially expressed in LADC and LSCC. We identified DSG3 (desmoglein 3), KRT5 (keratin 5), KRT6A (keratin 6A), KRT6B (keratin 6B), NKX2-1 (NK2 homeobox 1), SFTA2 (surfactant associated 2), SFTA3 (surfactant associated 3), and TMC5 (transmembrane channel-like 5) as potential biomarkers for distinguishing between LADC and LSCC. Receiver operating characteristic curve analysis suggested that KRT5 had the highest diagnostic value for discriminating between these two cancer types. Using the PrognoScan online survival analysis tool and the Kaplan-Meier Plotter, we found that high KRT6A or KRT6B levels, or low NKX2-1, SFTA3, or TMC5 levels correlated with unfavorable prognoses in LADC patients. Further studies will be needed to verify our findings in additional patient samples, and to elucidate the mechanisms of action of these potential biomarkers in non-small cell lung cancer.

Pulmonary histoplasmosis in a immunocompetent patient: A case report and literature review.

In the present study, the case of a 54-year-old male patient diagnosed with pulmonary histoplasmosis is reported, with the aim to increase the understanding of the disease characteristics and thereby facilitate the diagnosis and treatment of pulmonary histoplasmosis. Clinical manifestations, diagnosis, treatment and clinical outcomes of the present case of pulmonary histoplasmosis were described. In addition, 76 histoplasmosis patients with complete clinical data were reviewed by searching the literature for relevant studies published during 1990 and 2015. The disease was mainly manifested as cough in the present case, while imaging examination detected a lump shadow in the right lung, accompanied by exudative lesions. Initially, the patient was suspected to have bacterial pneumonia, but subsequently the diagnosis of pulmonary histoplasmosis was confirmed by lung biopsy. The symptoms were alleviated following itraconazole treatment. The patient was physically stable and had no recurrence during the subsequent follow-up period. In conclusion, pulmonary histoplasmosis is characterized by non-specific clinical and imaging manifestations, and lung tissue biopsy or respiratory pathogen culture are regarded as the diagnostic gold standards. Individualized antifungal medication should be administered based upon the patients' situation in terms of dosage and duration.

Prognostic value of decreased microRNA-133a in solid cancers: a meta-analysis.

OBJECTIVE: Increasing evidence indicates that the decreased expression of microRNA-133a (miR-133a) may be correlated with poor survival for cancer patients. Thus, we performed this meta-analysis to evaluate the prognostic value of decreased miR-133a in solid cancers. METHODS: Eligible studies were gathered by searching on PubMed, Web of Science, and Embase. Using the STATA 12.0 software, the pooled hazard ratios (HRs) and their corresponding 95% confidence intervals (CIs) for total and subgroup analyses were calculated to investigate the possible correlation between decreased miR-133a and overall survival (OS) of patients with cancer. RESULTS: Ten studies were enrolled in this meta-analysis. The pooled result showed that decreased expression of miR-133a predicted poor OS in solid cancer patients (HR =1.62, 95% CI: 1.16-2.24, P=0.004). Compared with the total pooled HR, further analyses indicated that the subgroups of digestive system neoplasms (HR =1.73, 95% CI: 1.20-2.51, P=0.003), frozen tissue preservation (HR =1.89, 95% CI: 1.41-2.53, P<0.001), and multivariate analysis (HR =2.07, 95% CI: 1.42-3.02, P<0.001) exhibited stronger connection between decreased miR-133a expression and OS outcome. CONCLUSION: This meta-analysis suggested that decreased miR-133a was associated with poor OS in patients with solid cancer. Because of the data in our study are limited, additional studies are required to verify the poor prognosis of decreased miR-133a in solid tumors.

PTEN expression is a prognostic marker for patients with non-small cell lung cancer: a systematic review and meta-analysis of the literature.

Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is a known tumor suppressor in non-small cell lung cancer (NSCLC). By performing a systematic review and meta-analysis of the literature, we determined the prognostic value of decreased PTEN expression in patients with NSCLC. We comprehensively and systematically searched through multiple online databases up to May 22, 2016 for NSCLC studies reporting on PTEN expression and patient survival outcome. Several criteria, including the Newcastle-Ottawa Quality Assessment Scale (NOS), were used to discriminate between studies. In total, 23 eligible studies with a total of 2,505 NSCLC patients were included in our meta-analysis. Our results demonstrated that decreased expression of PTEN correlated with poor overall survival in NSCLC patients and was indicative of a poor prognosis for disease-free survival and progression-free survival in patients with NSCLC.