Imaging characteristics of orbital peripheral nerve sheath tumors: Analysis of 34 cases.

BACKGROUND: Peripheral nerve sheath tumors (PNSTs), a rare group of neoplasms in the orbit, comprise only 4% of all orbital tumors. At present, there are very few studies detailing the features of these tumors identified using imaging technology. AIM: To compare the differences in location, morphology, magnetic resonance imaging (MRI) signal intensity/computed tomography (CT) value, and enhancement degree of tumors of different pathological PNSTs types. METHODS: Clinical, pathological, CT, and MRI data were analyzed retrospectively in 34 patients with periorbital sheath tumors diagnosed using histopathology from January 2013 to August 2021. RESULTS: Among 34 cases of orbital peripheral nerve sheath tumors, 21 were schwannomas, 12 were neurofibromas, and 1 was a plexiform neurofibroma. Common clinical symptoms presented by patients with these types of tumors include eyelid swelling, exophthalmos, and limited eye movement. Schwannomas mostly occur in the intramuscular space with small tumor volume and rare bone involvement. Neurofibromas develop in the extrapyramidal space with larger tumor volume and more bone involvement. Radiologically, schwannomas and neurofibromas are characterized by regular morphology and uneven density and signal. One case of plexiform neurofibroma showed tortuous and diffuse growth along the nerve, with a worm-like appearance on imaging. CONCLUSION: Different pathological types of orbital peripheral nerve sheath tumors have unique imaging characteristics. Comprehensive consideration of the patient's clinical and imaging manifestations is of great value in the diagnosis of orbital peripheral nerve sheath tumors.

Bevacizumab-induced esophageal pleural fistula during maintenance therapy without radiation in lung cancer.

BACKGROUND: Esophageal pleural fistula (EPF) is a rare but fatal complication associated with bevacizumab use; however, cases reports of EPF caused by bevacizumab have not been previously published. CASE PRESENTATION: A 66-year-old male patient diagnosed with stage IV lung adenocarcinoma on April 24, 2020 received 6 cycles of platinum-containing dual chemotherapy combined with bevacizumab followed by three cycles of bevacizumab monotherapy. Five days before admission, he experienced chest tightness, dyspnea, and right chest pain. Bed-side X-ray examination revealed a massive right hydrothorax, and food was found in the extracted pleural effusion. EPF was further confirmed by upper gastrointestinal radiography after oral administration of iohexol. The patient underwent jejunostomy as the distal esophagus could not be identified on gastroscopy, and eventually died of septic shock on January 16, 2021. CONCLUSIONS: It is necessary to pay attention to EPF during bevacizumab use in patients with or without risk factors.

S100A2: A potential biomarker to differentiate malignant from tuberculous pleural effusion.

BACKGROUND: S100 calcium binding protein A2 (S100A2)-which has been testified to have an abnormal expression in non-small cell lung cancer (NSCLC)-is considered as an effective biomarker in the diagnosis and prognosis of this malignancy. In this study, we detected the S100A2 levels in pleural effusion, aiming to evaluate its potential value in differentiating malignant pleural effusion (MPE) from tuberculous pleural effusion (TPE). METHODS: We collected pleural effusion from 104 NSCLC patients with MPE and 96 tubercular pleurisy cases. Enzyme-linked immunosorbent assay (ELISA) was performed to measure the levels of S100A2 in these samples. Meanwhile, the serum S100A2 levels were also examined in same subjects. The data concerning the expression of those commonly-used markers, including CEA, CYFRA211 and NSE, were obtained from medical records. RESULTS: Like other classified biomarkers, S100A2 had an over-expression in both pleural effusion and sera of the NSCLC patients compared with controls (P = 0.000), though having a lower P value. Receiver operating characteristic (ROC) analysis showed that the levels of S100A2 in pleural effusion (PE) could distinguish MPE from tuberculous pleurisy (Area Under the Receiver Operating Characteristic Curve (AUC) = 0.887), and its diagnostic value in hydrothorax was obviously higher than in serum (AUC = 0.709). CONCLUSION: Our results indicate that levels of S100A2 are significantly elevated in MPE, and that S100A2 may serve as a diagnostic biomarker for NSCLC patients with MPE. In further studies, we will validate our findings with a larger sample population.

Expression and clinicopathological significance of S100 calcium binding protein A2 in lung cancer patients of Chinese Han ethnicity.

BACKGROUND: S100 family of calcium-binding proteins plays a significant role in the process of many kinds of tumors, including lung cancer. As an important member of this family, S100 calcium binding protein A2 (S100A2) has been confirmed to be associated with many biological processes, and has an abnormal expression in non-small cell lung cancer (NSCLC). However, the S100A2 status in lung cancer is still controversial and undefined. METHODS: We evaluated the pattern and distribution of S100A2 in 109 cases of lung cancer, including five histological types (47 adenocarcinoma, 46 squamous cell carcinoma, 7 small cell carcinoma, 3 large cell carcinoma, and 6 atypical carcinoid), and 30 cases of paired adjacent normal lung tissues by means of immunohistochemistry. RESULTS: Compared with the normal tissues (0/30), S100A2 experienced a dramatically upward trend of positive expression in lung cancer, with a positive rate of 68/109 (P<0.001). Specifically, squamous cell carcinoma, with 34/12, had the highest expression ratio, followed by large cell carcinoma (2/1), adenocarcinoma (31/16), and atypical carcinoid (1/5) respectively, while no S100A2 protein was detected in small cell carcinoma. Meanwhile, we firstly demonstrated that the high expression of S100A2 was significantly associated with the incidence of lymph node metastasis in adenocarcinoma (P=0.013). CONCLUSIONS: The association between high S100A2 expression and NSCLC at the level of tissue, and S100A2 may serve as an effective biomarker for the diagnosis and prognosis of NSCLC in future.

Blockade efficacy of MEK/ERK-dependent autophagy enhances PI3K/Akt inhibitor NVP-BKM120's therapeutic effectiveness in lung cancer cells.

NVP-BKM120 (BKM120) is a new pan-class I phosphatidylinositol-3 kinase (PI3K) inhibitor and has been tested in clinical trials as an anticancer agent. In this study, we determined whether BKM120 induces autophagy and the impact of autophagy induction on BKM120's growth-inhibitory activity. BKM120 potently induced elevation of autophagosome-bound type II LC3 (LC3-II) protein, predominantly in cell lines insensitive to BKM120, thereby inducing autophagy. The presence of lysosomal protease inhibitor chloroquine further enhanced the levels of LC3-II. BKM120 combined with chloroquine, enhanced growth-inhibitory effects including induction of apoptosis, suggesting that autophagy is a protective mechanism counteracting BKM120's growth-inhibitory activity. Interestingly, BKM120 increased p-ERK1/2 levels. When blocking the activation of this signaling with MEK inhibitors or with knockdown of ERK1/2, the ability of BKM120 to increase LC3-II was attenuated and the growth-inhibitory effects including induction of apoptosis were accordingly enhanced, suggesting that the MEK/ERK activation contributes to BKM120-induced authophagy. In mouse xenograft model, we also found that the combination of BKM120 and PD0325901 synergistically suppressed cell growth in human lung cancer cells. Thus, the current study not only reveals mechanisms accounting for BKM120-induced autophagy, but also suggests an alternative method to enhance BKM120's therapeutic efficacy against non-small cell lung cancer(NSCLC) by blocking autophagy with either a lysosomal protease inhibitor or MEK inhibitor.

miRNA-204 suppresses human non-small cell lung cancer by targeting ATF2.

MicroRNAs (miRNAs) play a critical role in cancer development and progression. Deregulated expression of miR-204 has been reported in several cancers, but the mechanism through which miR-204 modulates human non-small cell lung cancer (NSCLC) is largely unknown. In this study, we investigate the expression and functional role of miR-204 in human NSCLC tissues and cell lines. RNA isolation, qRT-PCR, MTT, colony formation assay, cell cycle assay, cell apoptosis assay, cell migration assay, and Western blot were performed. Statistical analysis was performed using SPSS 18.0 software and statistical significance was accepted at p value <0.05. miR-204 level was significantly reduced in NSCLC tissues as compared to that of non-neoplastic tissues. Transient over-expression of miR-204 by transfecting with miR-204 mimics suppressed NSCLC cell proliferation, migration, and induced apoptosis and G1 arrest, whereas inhibition of miR-204 showed the converse effects. Additionally, activating transcription factor 2 (ATF2), an important transcription factor, was demonstrated as a potential target gene of miR-204. Subsequent investigations found a negative correlation between miR-204 level and ATF2 expression in NSCLC tissue samples. Moreover, we observed that miR-204 expression inversely affected endogenous ATF2 expression at both mRNA and protein levels in vitro. Taken together, miR-204 may act as a tumor suppressor by directly targeting ATF2 in NSCLC.

Diagnostic significance of S100A2 and S100A6 levels in sera of patients with non-small cell lung cancer.

Biochemical markers play a significant role in the diagnosis of lung cancer. Recent studies have demonstrated a link involving S100 Calcium Binding Proteins (S100A2, S100A6) and non-small cell lung cancer (NSCLC), but the expediency of their serum levels in NSCLC has not been established. In this study, we evaluate the potential of serum S100A2 and S100A6 levels as diagnostic markers for NSCLC. Enzyme-linked immunosorbent assay (ELISA) was performed to detect the levels of S100A2 and S100A6 in 141 NSCLC patients and 150 healthy subjects. Serum levels of the two proteins in patients with NSCLC were higher compared to healthy controls (P = 0.0002 for S100A2 and P < 0.0001 for S100A6). Moreover, the levels of S100A2 and S100A6 were higher in the sera of stage I/II NSCLC patients compared to healthy controls with P = 0.01 and <0.0001, respectively. Receiver operating characteristic (ROC) analysis showed that S100A2 could distinguish NSCLC patients from healthy controls (AUC = 0.646), and S100A6 could also identify NSCLC (AUC = 0.668). Meanwhile, these two proteins showed notable capabilities for distinguishing stage I/II NSCLC from healthy controls (AUC = 0.708 for S100A2 and AUC = 0.702 for S100A6). Our results indicate that serum levels of S100A2 and S100A6 are significantly elevated in early stage NSCLC and may have the potential for NSCLC biomarker. Further studies with large sample population would help validate our findings.

Expression of the copper transporters hCtr1, ATP7A and ATP7B is associated with the response to chemotherapy and survival time in patients with resected non-small cell lung cancer.

Copper transporter family proteins may regulate the chemoresistance of non-small cell lung cancer (NSCLC) to platinum-based anticancer drugs. The present study aimed to investigate the expression of these proteins in lung cancer tissue specimens for association with clinicopathological data and patient responses to chemotherapy and survival. A total of 54 patients with surgically resected NSCLC that received first-line platinum-based doublet chemotherapy were recruited in the present study, and the paraffin-embedded pre-treatment tumor tissue specimens were subjected to immunohistochemical analysis for the expression of human copper transporter 1 (hCtr1) and copper-transporting p-type adenosine triphosphatase 1 (ATP7A) and 2 (ATP7B). This cohort of patients with NSCLC received platinum-based chemotherapy subsequent to the surgical removal of tumor lesions. ATP7B expression was found to be significantly associated with tumor cell differentiation, while hCtr1 expression was significantly associated with improved chemotherapeutic responses. The median survival time was 20 months in patients possessing tumors with high ATP7A expression, but >66 months in patients possessing tumors with low ATP7A expression at the end of the follow-up (P<0.001). The median survival time at the end of the follow-up was 15 months in patients with low tumor hCtr1 expression, but >66 months in patients with high tumor hCtr1 expression (P<0.001). High hCtr1 and low ATP7A expression were each favorable prognostic factors subsequent to chemotherapy for patients with resected NSCLC. Multivariate analysis revealed that high hCtr1 expression combined with low ATP7A expression, good tumor differentiation and female gender were all favorable independent predictive and prognostic factors for patients with resected NSCLC following chemotherapy. High hCtr1 expression combined with low ATP7A expression was associated with an improved prognosis in patients with resected NSCLC that received platinum-based chemotherapy. Surgery combined with neoadjuvant chemotherapy may improve the survival time of patients with NSCLC.

Expressions of miR-181a and miR-20a in RPMI8226 cell line and their potential as biomarkers for multiple myeloma.

Multiple myeloma (MM) is characterized by clonal proliferation of malignant plasma cells in the bone marrow. The anti-tumor activity of bortezomib (a proteosome inhibitor) in MM is challenged by emergence of drug resistance. MicroRNAs (miR) regulate and orchestrate multiple cellular pathways. We investigate the contribution miR-181a and miR-20a expressions' on cell proliferation and apoptosis in RPMI8226 cell line and their influence on bortezomib treatment. RNA isolation, quantitative real-time PCR (qRT-PCR), cell proliferation assay, cell cycle analysis, and cell apoptosis assay were done. Statistical analysis was performed using SPSS 17.0 software (SPSS, Chicago, IL, USA). P values of less than 0.05 were considered statistically significant. RPMI8226 cells seeded in 96-well plates and treated for 24 h with different concentrations of bortezomib showed dose-dependent growth inhibition; expression of both miR-181a and miR-20a were inhibited by bortezomib. We found decrease of miR-181a (60%) and miR-20a (30%) in cells transfected with 20-nM inhibitor. A relative increase of 14-fold in miR-181a and 11-fold in miR-20a was observed in cells transfected with mimics of the same concentration. Transient low expression of miR-181a/20a inhibited proliferation at day 4, and overexpression of miR-181a promoted proliferation. Cells transfected with miR-181a/20a inhibitor within day 4 showed lower survival rate, and low expression of miR-181a on the fourth day after transfection promoted apoptosis. Our findings suggest that miR-181a/20a has a higher expression in MM. miR-181-a expression is proportional to MM tumor burden and could be a biomaker for monitoring treatment. miR-20a shows the potential of a diagnostic biomarker.

Polymorphisms in C-reactive protein and Glypican-5 are associated with lung cancer risk and Gartrokine-1 influences Cisplatin-based chemotherapy response in a Chinese Han population.

The role of genetics in progression of cancer is an established fact, and susceptibility risk and difference in outcome to chemotherapy may be caused by the variation in low-penetrance alleles of risk genes. We selected seven genes (CRP, GPC5, ACTA2, AGPHD1, SEC14L5, RBMS3, and GKN1) that previously reported link to lung cancer (LC) and genotyped single nucleotide polymorphisms (SNPs) of these genes in a case-control study. A protective allele "C" was found in rs2808630 of the C-reactive protein (CRP). Model association analysis found genotypes "T/C" and "C/C" in the dominant model and genotype "T/C" in the overdominant model of rs2808630 associated with reduced LC risk. Gender-specific analysis in each model showed that genotypes "T/T" and "C/C" in rs2352028 of the Glypican 5 (GPC5) were associated with increased LC risk in males. Logistic regression analysis showed "C/T" genotype carriers of rs4254535 in the Gastrokine 1 (GKN1) had less likelihood to have chemotherapy response. Our results suggest a potential association between CRP and GPC5 variants with LC risk; variation in GKN1 is associated with chemotherapy response in the Chinese Han population.

FOXP4 modulates tumor growth and independently associates with miR-138 in non-small cell lung cancer cells.

Family of forkhead box transcription factors, including forkhead box P4 (FOXP4), plays an important role in oncogenesis. The current study is to evaluate the role of FOXP4 in regulating human non-small cell lung cancer (NSCLC). Quantitative RT-PCR and Western blot were performed to evaluate the gene and protein expressions of FOXP4 in six NSCLC cell lines and 55 NSCLC patients. Lentivirus of small hairpin RNA (FOXP4-shRNA) was used to downregulate FOXP4 in NSCLC cell lines A549 and H1703 cells. Its effect on NSCLC growth, invasion, and cell cycle were evaluated by cell proliferation assay, migration assay, and cell cycle assay, respectively. Dual luciferase assay and Western blot were used to examine whether microRNA-138 (miR-138) was an upstream regulator of FOXP4. The dependence of FOXP4 on miR-138 associated signaling pathway was evaluated by ectopically overexpressing enhancer of zeste homolog 2 (EZH2), a known miR-138 target in NSCLC. FOXP4 was highly expressed in both NSCLC cell lines and NSCLC patients. FOXP4 downregulation by FOXP4-shRNA markedly reduced cancer cell growth and invasion, as well as induced cell cycle arrest in A549 and H1703 cells. MiR-138 was confirmed to be an upstream regulator of FOXP4 and directly regulated FOXP4 expression in A549 and H1703 cells. FOXP4 downregulation-mediated inhibition on cancer cell growth and invasion was independent on overexpressing EZH2, another direct target of miR-138 in NSCLC. Our data demonstrated that FOXP4 was a critical regulator in NSCLC and independently associated with miR-138 regulation.

MicroRNA-15a induces cell apoptosis and inhibits metastasis by targeting BCL2L2 in non-small cell lung cancer.

MicroRNAs (miRNAs) play a critical role in cancer development and progression. Aberrant expression of miR-15a has recently been reported in several cancers, but its role in non-small cell lung cancer (NSCLC) still remains obscure. We investigated the effects of miR-15a on proliferation, apoptosis, and metastasis in A549 cells. Eighteen paired NSCLC and adjacent non-tumor lung tissues were surgically removed and immediately snap frozen until total RNA was extracted and confirmed by two independent pathologists. The targets of miR-15a were predicted by bioinformatics tools. RNA isolation and quantitative real-time PCR (qRT-PCR), Western blot analysis, cell proliferation assay, cell cycle analysis, cell apoptosis assay, and migration and invasion assays were done. The wild type (WT) or mutant type (MT) 3'-untranslated region (UTR) vectors were co-transfected with miR-15a or negative control into A549 cells, and after 24 h of transfection, luciferase activity was measured using the Dual-Glo luciferase assay kit. Statistical analysis was performed using SPSS 13.0 software (SPSS, Chicago, IL, USA). P values of less than 0.05 were considered statistically significant. miR-15a was significantly downregulated in NSCLC than in adjacent non-cancerous tissues. miR-15a overexpression remarkably inhibited cell viability, invasion, and migration and promoted the apoptosis of NSCLC cells. Additionally, inhibition of miR-15a expression had the opposite effects on tumor progression, while cell cycle remained unaltered. Furthermore, we identified that BCL2L2 was a target of miR-15a and negatively regulated by miR-15a at the translational level. miR-15a acts as a tumor suppressor in NSCLC by directly targeting BCL2L2 and may serve as a potential diagnostic biomarker and therapeutic target for NSCLC.

Differentially expressed glycosylated patterns of α-1-antitrypsin as serum biomarkers for the diagnosis of lung cancer.

Lung cancer is the most common malignancy worldwide. Thus, there is a critical need for diagnostic biomarkers with adequate sensitivity and specificity for lung cancer detection. Glycans in glycoproteins are significantly altered in cancer, and may serve as a tool for identifying potential diagnostic biomarkers. Recent studies have reported changes in α-1-antitrypsin (A1AT) glycosylation in lung cancer serum, tissue and cell lines. In this study, a lectin microarray was used to detect glycosylation changes in serum A1AT from patients with lung adenocarcinoma (ADC), squamous cell lung cancer, small-cell lung cancer (SCLC) and benign pulmonary diseases. Differentially expressed glycosylated patterns of A1AT were identified by lectin arrays and were confirmed by lectin-based enzyme-linked immunosorbent assay (ELISA). We found that galactosylated A1AT could distinguish non-small-cell lung cancer (NSCLC) from benign pulmonary diseases (AUC = 0.834); fucosylated A1AT showed exceptional capability in distinguishing ADC from benign diseases (AUC = 0.919) or other lung cancer subtypes (AUC = 0.844), and A1AT containing poly-LacNAc could detect SCLC from benign diseases (AUC = 0.905) or NSCLC (AUC = 0.707). The present study indicates that glycosylated patterns of A1AT may serve as potential biomarkers for detection of lung cancer. Further studies in larger sample sizes are necessary to validate the clinical utility of these markers.

Polymorphisms in the TERT gene are associated with lung cancer risk in the Chinese Han population.

Lung cancer has the highest mortality rate among cancers; however, its nosogenesis is still unclear. Genome-wide association studies have shown that the telomerase reverse transcriptase (TERT) gene, located in the chromosome 5p15.33 region, is one of the genes associated with the risk of lung cancer. In this case-control study, we genotyped 11 tag single-nucleotide polymorphisms of the TERT gene to evaluate their association with lung cancer risk in the Han Chinese population. Two tag single-nucleotide polymorphisms were found to be associated with lung cancer risk on using the χ2-test: rs4246742 [odds ratio (OR)=0.77, 95% confidence interval (CI) 0.60-0.98; P=0.03] and rs2853672 (OR=1.26, 95% CI 1.01-1.57; P=0.045). By using SNPStats software we also found rs2242652 (OR=1.47, 95% CI 1.02-2.13; P=0.04) in the dominant model and rs2736098 (OR=1.38, 95% CI 1.06-1.80; P=0.017), rs2853672 (OR=1.41, 95% CI 1.11-1.80; P=0.0048), and rs4246742 (OR=0.75, 95% CI 0.58-0.97; P=0.029) in the log-additive model. 'T/C-T/T' of rs10069690 conferred an increased risk for male sex in the dominant model (OR=1.80, 95% CI, 1.05-3.08; P=0.03) and 'TC' increased risk for male sex in the overdominant model (OR=1.85, 95% CI, 1.08-3.17; P=0.031). Our findings, combined with previous studies, suggest that polymorphisms in the TERT gene contribute to the risk for lung cancer in the Chinese Han population.

Correlation of CLPTM1L polymorphisms with lung cancer susceptibility and response to cisplatin-based chemotherapy in a Chinese Han population.

The implication of genetic factors in predisposition to cancer is a recognized fact. The Cleft lip and palate transmembrane 1-like (CLPTM1L) gene resides in a locus in the chromosome 5p15.33 region that is associated with lung cancer susceptibility and has a role in carcinogenesis. We conducted a case-control study in a Chinese population of 309 pathologically confirmed lung cancer patients and 310 controls to investigate the effect of variant genotypes within the CLPTM1L locus on susceptibility to lung cancer and sensitivity to cisplatin-based chemotherapy. We genotyped nine single nucleotide polymorphisms (SNPs) within the CLPTM1L locus and examined their correlation with lung cancer risk and treatment response using χ (2) and unconditional logistic regression analysis. We identified rs451360 as a novel SNP associated with lung cancer risk in the Chinese Han population. The "T" allele of rs451360 was associated with decreased risk of lung cancer (p = 0.007, odd ratio (OR) = 0.59, 95 % confidence interval (CI): 0.40-0.87). Significant multiplicative interactions were observed between gender and polymorphisms of rs402710, the "T/T" genotype of which was associated with decreased lung cancer risk in male patients (p = 0.016, OR = 0.35, 95 % CI: 0.17-0.73). CLPTM1L polymorphisms did not affect the tumor sensitivity to cisplatin combination chemotherapy in our study patients. The results of the present study suggest a potential association between CLPTM1L variants and lung cancer risk in the Chinese Han populations.

Atypical presentation of tracheobronchopathia osteochondroplastica: is chronic inflammation a perpetrator?

OBJECTIVE: To report an atypical presentation of tracheobronchopathia osteochondroplastica (TO). CLINICAL PRESENTATION AND INTERVENTION: A 59-year-old man was investigated for productive cough of 1 month. An antimycobacterial combination regime was initiated with a misdiagnosis of endobronchial tuberculosis. At follow-up, the patient reported worsening of his symptoms. CT revealed an increased intensity of the cartilage ring surrounding the trachea, and bronchoscopy showed tracheal stenosis with white, hard nodules on the airway submucosa. Histopathology confirmed the diagnosis of TO. CONCLUSION: This case showed that TO should be considered in patients with cough not explained by noninvasive testing and not responsive to empiric medications.

Combining multiple serum biomarkers in tumor diagnosis: A clinical assessment.

The present study aimed to assess the diagnostic/prognostic value of various clinical tumor markers, including carcinoembryonic antigen (CEA), neuron-specific enolase (NSE), cytokeratin 19 (CYFRA21-1), α-fetoprotein (AFP), carbohydrate antigen-125 (CA-125), carbohydrate antigen-19.9 (CA-19.9) and ferritin, individually or in combination. The electro-chemiluminescence immunization method was performed to detect the levels of seven tumor markers in 560 cancer patients and 103 healthy subjects for comparison. The serum levels of the seven markers measured in cancer patients were higher compared to healthy subjects (P<0.05 for AFP and P<0.001 for the remaining six markers). Different markers had different sensitivity towards different types of tumors. Combining more markers significantly increased the ratios of positive diagnosis in the tumors. The diagnostic sensitivities of combining seven markers were particularly high in digestive, urinary and skeletal tumors (82, 92 and 83%, respectively). Gynecological tumors have exhibited a constant yet relatively low positive diagnosis irrespective of the use of a single marker or combined markers. However, the increase in sensitivity when combining markers was accompanied by a decrease in specificity. Generally, combining more markers increased the tumor detection rates, while a combination of the seven markers provided the highest detection rate. Combined detection showed a particularly high sensitivity in detecting respiratory, digestive and urinary system tumors, with the lowest sensitivity observed in gynecological tumors. As a result, combining tumor markers may play an important role in early tumor detection/diagnosis while the loss of specificity can be tolerated.

Descriptive data on cancerous lung lesions detected by auto-fluorescence bronchoscope: A five-year study.

BACKGROUND: Auto-fluorescence bronchoscopy (AFB) has been used for the identification and localization of intra-epithelial pre-neoplastic and neoplastic lesions within the bronchus. OBJECTIVES: To determine the applicability of AFB for the detection and localization of precancerous and cancerous lesions, in addition to analyzing the morphologic presentation, their association to histological type and the variation between genders. METHODS: A five-year study involving 4983 patients, who underwent routine bronchoscopy [B] examination in a local tertiary teaching hospital, was done. The B examination was performed under intratracheal lidocaine, and samples were obtained using suitable approach. One thousand four hundred and eighty-five pathologically confirmed lung cancer patients were included in the study. The following parameters were studied: Morphological presentation, biopsy sites, histology. Differences between the groups were analyzed using Chi square test. RESULT: One thousand four hundred and eighty-five patients who had hyperplasia or neoplastic lesions were further confirmed as lung cancer pathologically. Lung cancer was more commonly found in the right lung (51.58% vs. 42.82%). The lesion occurred more frequently in the upper lobe than the lower lobe (44.17% vs. 22.42%). Male patients with squamous cell carcinoma showed upper lobe involvement more commonly, while the left main bronchus was more commonly involved in female patients. Adenocarcinoma mostly involved lesion of the upper lobe. Squamous cell carcinoma and small cell carcinoma were the major proliferative types (80.15% and 76.16% respectively). CONCLUSION: AFB is efficient in the detection of pre-invasive and invasive lung lesions. The morphological presentation is associated to the histological type. There is variation in the presentation and histology of cancerous lung lesions between genders.

Pro-apoptotic effects of Paecilomyces hepiali, a Cordyceps sinensis extract on human lung adenocarcinoma A549 cells in vitro.

BACKGROUND: Paecilomyces hepiali (PH) is a derivative of Cordyceps sinensis (CS), a fungus that has been shown to have anti-cancer and pro-apoptotic effects. Here, we aimed to investigate the effect of in vitro PH treatment on cell proliferation, cell cycling, apoptosis, and tumor necrosis factor-alfa (TNF-α) mRNA expression in human lung adenocarcinoma A549 cells (A549). MATERIALS AND METHODS: A549 cells were treated with an aqueous extract of PH at concentrations of 0.25, 0.5, 1, 2, and 4 mg/ml. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was used to evaluate cellular viability and proliferation, while flow cytometry (FCM) was used to examine cell cycling. Apoptosis was assayed using Annexin V Fluorescein Isothiocyanate / Propidium Iodide (V-FITC/PI) and FCM. TNF-α mRNA expression was measured with reverse transcriptase-polymerase chain reaction (RT-PCR). RESULTS: Cell proliferation was significantly suppressed by treatment with 1, 2, and 4 mg/ml of PH extract. Furthermore, the MTT assay showed that cell proliferation was inhibited in a concentration-time-dependent manner. As the concentration of the PH treatment increased, there were fewer cells in the S phase, and more cells in the G0/G1 and G2 phases. After 24 h of treatment, apoptosis was induced by a dose of 2 mg/ml of PH. TNF-α mRNA expression was significantly higher in the intervention groups and was positively associated with treatment concentration. CONCLUSIONS: These results indicate that in vitro treatment with an aqueous extract from PH limits cell proliferation, induces apoptosis, and causes cell cycle arrest of A549 cells; this suggests that it may have potential as a therapy for lung adenocarcinoma.