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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Adenocarcinoma, Antineoplastic Agents, Apoptosis, Benzenesulfonates, Cell Line, Tumor, Cell Proliferation, Cyclin D1, Cyclin E, Esophageal Neoplasms, Extracellular Signal-Regulated MAP Kinases, Humans, Niacinamide, Phenylurea Compounds, Proto-Oncogene Proteins c-akt, Proto-Oncogene Proteins c-bcl-2, Proto-Oncogene Proteins c-myc, Pyridines, STAT3 Transcription Factor, Sorafenib, p38 Mitogen-Activated Protein Kinases.
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Does sorafenib trigger antiproliferative and pro-apoptotic signals in human esophageal adenocarcinoma cells? Context: Current therapies offer scant benefit to patients with advanced esophageal adenocarcinoma. We investigated the effects of Sorafenib, a multifunctional kinase inhibitor, on several growth regulatory pathways that control cell growth and survival in SEG-1 cells derived from Barrett's adenocarcinoma. SEG-1 cells were exposed to acidified medium or taurocholic acid, with and without pre-incubation with Sorafenib. Cyclin D1 and E, c-Myc, and Bcl-2 expression levels as well as STAT3 activations were determined by Western blotting. Cyclin D1 mRNA was measured by real-time PCR. Apoptosis was assessed by TUNEL assay. Sorafenib significantly inhibited SEG-1 cell proliferation stimulated by acid or bile acid treatments and reduced cell survival. This drug significantly reduced the up-regulations of cyclin D1, cyclin E, c-Myc, and Bcl-2 as well as the activation of STAT3 in SEG-1 cells.
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These results support a rational basis for future clinical studies to assess the therapeutic benefit of Sorafenib in esophageal adenocarcinoma. Final Decision: yes