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In lung cancer A549 cells, the present study evaluated the associations between p130cas expression and the activation of p38 or Smad2, which are components of two of the main signaling pathways of transforming growth factor-β1 (TGF-β1), i.e., epithelial-mesenchymal transition (EMT) and apoptosis, respectively. TGF-β1-induced EMT was investigated by inspecting cell shape and cell migration, and by testing E-Cadherin, N-Cadherin and Vimentin biomarkers in p130cas-RNA interference (RNAi)-A549 cells. The changes in TGF-β1-induced apoptosis, i.e., cleaved Caspase-3 levels, were additionally analyzed following p130cas-RNAi. p130cas-knockdown decreased the phosphorylated (p)-p38 expression level, and blockaded the TGF-β1-induced activation of p-p38 in the A549 cells. p130cas-knockdown arrested cell migration and impaired TGF-β1-induced EMT in the A549 cells, characterized by changes in cell morphology and biomarker levels. However, p130cas-knockdown had no impact on the activation of Smad2 and the cleavage of Caspase-3. These results indicate that p130cas is a novel molecular ‘rheostat’ that alters the function of the TGF-β1 signaling pathway from tumor suppression to tumor promotion in lung cancer cells. The underlying mechanism warrants further study. [ABSTRACT FROM AUTHOR]

Objective: Our previous study suggested the potential clinical implications of BCAR1 in non-small-cell lung cancer (NSCLC) (Mol Diagn Ther. 2011. 15(1): 31-40). Herein, we aim to evaluate the predictive power of BCAR1 as a marker for poor prognosis in NSCLC cases, verify the carcinogenic roles of BCAR1 in the A549 lung adenocarcinoma cell line, and testify to the BCAR1/phospho-p38 axis. Methods: Between January 2006 and June 2010, there were a total of 182 patients with NSCLC (151 cases with available follow up data, and 31 cases lost to follow-up due to the invalid contact information). We inspected BCAR1, phospho-BCAR1(Tyr410), phospho-p38(Thr180/Tyr182) and p38 expression in NSCLC tissues and matched adjacent normal tissues by immunoblotting and IHC. After BCAR1 -RNA interference in A549 cells, we inspected the protein expression (BCAR1, phospho-BCAR1, phospho-p38 and p38) and performed cell biology experiments (cell growth, migration and cycle). Results: BCAR1 was overexpressed in NSCLC tissues (177/182) and cell lines (A549 and Calu-3). However, it was not detected in the normal adjacent tissue in 161 of the 182 cases. Higher BCAR1 levels were strongly associated with more poorly differentiated NSCLC and predicted poorer prognosis. BCAR1 knockdown caused cell growth arrest, cell migration inhibition and cell cycle arrest of A549 cells. Overexpression of BCAR1 was associated with activation of p38 in NSCLC cases, and BCAR1 knockdown caused reduction of phospho-p38 levels in A549 cells. Conclusion: Overexpression of BCAR1 is a predictor of poor prognosis in NSCLC and plays important carcinogenic roles in carcinogenesis, probably via activation of p38 MAPK. However, further investigations are required immediately. [ABSTRACT FROM AUTHOR]

Objective: This study was designed to evaluate the clinical efficacy of pyloric digital fracture for the prevention of early delayed gastric emptying (DGE) after high-level esophagogastrostomy. Methods: From January 2004 to March 2009, we sequentially enrolled 78 patients after esophagogastrostomy: 48 patients with pyloric digital fracture (DF group) and 30 patients without any drainage procedure (non-DF group). Intraoperative manometric study was performed in 48 patients of the DF group. Postoperative evaluation was performed, including symptomatic questionnaire, radiographic study, and gastric scintigraphy. Results: Intraoperative manometric study revealed that basal pyloric pressure and peak pressure of pylorus in phase III of the migrating motor complex increased significantly after gastric conduit was made and anastomosed, but decreased appreciably following digital fracture. Compared with the peak pressure of IPPW before digital fracture (88.52 ± 19.88 mmHg), it appreciably decreased following digital fracture (40.45 ± 13.52 mmHg). Occurrences of IPPW (in 10 min) and duration time of each occurrence (s) had similar trends for before and after digital fracture (11.5 ± 4.5 vs. 5.0 ± 3.5 and 7.0 ± 2.0 vs. 3.0 ± 1.0, respectively). Postoperative evaluation demonstrated that early DGE occurred in four patients in the non-DF group (13.3%), and there was no DGE patient in the DF group. There was significant difference regarding gastric scores between the DF group and the non-DF group (10.5 ± 3.4 vs. 16.7 ± 3.8, t = 2.8271, P < 0.05). Gastric scintigraphy revealed that either semi-emptying-time or percent of retention at 4 h of the DF group was significantly lower than that of the non-DF group. Conclusion: Pyloric digital fracture can prevent early DGE after high-level esophagogastrostomy efficaciously and conveniently. [ABSTRACT FROM AUTHOR]

Colon redundancy and adhesional obstruction after colonic interposition for corrosive esophageal burns, leading to poor quality of life and malnutrition in young adults, often require surgical revision. Herein, we present our lessons and experiences regarding managements of the late and untoward complications which occurred in the postoperative 15th year following the initial colon interposition. And we review the literatures in the discussion. Prolonged surgical follow-up and appropriate management of coloplasty dysfunction are important for long-term success after coloninterposition for corrosive esophageal burns. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented in response to the article "Establishment of 15 cancer cell lines from patients with lung cancer and the potential tools for immunotherapy" by S. Masakazu, T. Mitsuhiro, and O. Toshihiro in the July 2002 issue.