Objective To investigate the values of combined determination of pleural effusion and serum carcinoembryonic antigen (CEA), cytokeratin 19 fragment (CYFRA21-1), neuron-specific enolase (NSE), and squamous cell carcinoma antigen (SCC-Ag) in diagnosis of lung cancer. Methods 101 patients with pleural effusion were reviewed retrospectively. Expressions of CEA, CYFRA21-1, NSE and SCC-Ag in pleural fluid and serum were detected; the optimum cut-off points resulting from the best sensitivity-specificity balance in the receiver operator characteristic (ROC) curves were constructed. The expressions of the tumor markers were compared among different pathological types of lung cancer. Results The levels of tumor markers in both pleural effusion and serum were significantly higher in patients with lung cancer than the benign group (P < 0.05). The expression levels and positive rate of CEA for lung adenocarcinoma, NSE for small cell lung cancer, and CYFRA21-1and SCC-Ag for pulmonary squamous cell carcinoma were higher than any other single detection (P < 0.05). Combined detection of the tumor markers in pleural fluid and serum improved the detection rate of lung cancer. Conclusions Combined detection of pleural effusion and serum tumor markers has important reference value in the detection of lung cancer and in pathological typing.

Cellular prion protein (PrP(C)) is ubiquitously expressed in the cytomembrane of a considerable number of eukaryotic cells. Although several studies have investigated the functions of PrP(C) in cell proliferation, cell apoptosis, and tumorigenesis of mammals, the correlated functions of chicken PrP(C) (chPrP(C)) remain unknown. In this study, stable chPrP(C)-downregulated Marek's disease (MD) virus-transformed avian T cells (MSB1-SiRNA-3) were established by introducing short interfering RNA (SiRNA) targeting chicken prion protein genes. We found that downregulation of chPrP(C) inhibits proliferation, invasion, and migration, and induces G1 cell cycle phase arrest and apoptosis of MSB1-SiRNA-3 cells compared with Marek's disease virus-transformed avian T cells (MSB1) and negative control cells. To the best of our knowledge, the present study provides the first evidence supporting the positive correlation between the expression level of chPrP(C) and the proliferation, migration, and invasion ability of MSB1 cells, but appears to protect MSB1 cells from apoptosis, which suggests it functions in the formation and development of MD tumors. This evidence may contribute to future research into the specific molecular mechanisms of chPrP(C) in the formation and development of MD tumors.
Animals ; Apoptosis* ; Carcinogenesis ; Cell Cycle ; Cell Proliferation ; Chickens ; Down-Regulation* ; Eukaryotic Cells ; Mammals ; Marek Disease* ; RNA, Small Interfering ; T-Lymphocytes*