ABSTRACT
Plummer-Vinson syndrome (sideropenic dysphagia) is characterized by dysphagia due to an upper esophageal or a hypopharyngeal web in a patient with chronic iron deficiency anemia. The main cause of dysphagia is the web of the cervical esophagus, and an abnormal motility of the pharynx or the esophagus is found to play a significant role in the above cause. Patients with this syndrome are thought to be precancerous because squamous cell carcinomas of the hypopharynx, oral cavity, or esophagus take place in 10% of those patients. However, for Plummer-Vinson syndrome to be combined with gastric cancer is most unusual. We report the case of a 43-year-old woman who was first found to have stomach cancer under a diagnosis of Plummer-Vinson syndrome and who recovered after surgery.
Subject(s)
Adult , Female , Humans , Anemia, Iron-Deficiency , Carcinoma, Squamous Cell , Deglutition Disorders , Diagnosis , Esophagus , Hypopharynx , Mouth , Pharynx , Plummer-Vinson Syndrome , Stomach NeoplasmsABSTRACT
PURPOSE: This study was undertaken to reveal the molecular mechanism underlying sulindac-induced apoptosis in the human colon cancer cell line HT-29 (mutant p53). METHODS: Apoptosis was determined by using Hoechst 33342 staining, and translocation of proteins was established by using immunofluorescence, immunoelectron microscopy, and Western blotting after ultra- fractionation. RESULTS: This type of apoptosis was associated with decreased mitochondrial membrane potential, a translocation of the apoptosis-inducing factor (AIF) to the nucleus, and morphological evidence of nuclear condensation. However, DNA electrophoresis did not elucidate the ladder pattern of DNA fragments. Instead, a pulse-field gel electrophoresis showed that sulindac led to disintegration of nuclear DNA into-high- molecular-weight DNA fragments of about 100~300 kbp. CONCLUSIONS: Our findings indicate that sulindac induces large-scale DNA fragmentation, suggesting a predominantly AIF-mediated cell-death process, through translocation of the AIF to the nucleus in HT-29 cells.
Subject(s)
Humans , Apoptosis Inducing Factor , Apoptosis , Blotting, Western , Cell Line , Colonic Neoplasms , DNA Fragmentation , DNA , Electrophoresis , Fluorescent Antibody Technique , HT29 Cells , Membrane Potential, Mitochondrial , Microscopy, Immunoelectron , SulindacABSTRACT
PURPOSE: The aim of this study was to determine the feasibility and safety of laparoscopy-assisted gastrectomy (LAG) with lymph node dissection for gastric cancer according to the analysis of postoperative complications. METHODS: The authors attempted LAG with lymph node dissection in 117 consecutive patients with gastric cancer. The clinicopathologic characteristics of the patients, operative outcomes, preoperative comorbidities and postoperative morbidities and mortalities were evaluated using the stomach cancer database of Dong-A university hospital and medical charts. RESULTS: Among the 114 successful patients, 100 had early gastric cancer and 14 had advanced gastric cancer. The mean operation time was 259.2 minutes (range 150~415). The mean number of retrieved lymph nodes was 23.4 (range 6~66). The mean time to the first flatus and postoperative hospital stay were 3.7 and 10.0 days, respectively. The overall operative mortality rate, hospital death rate and the overall rate of postoperative complications were 0, 1.7 and 14.7%, respectively. The major and minor complication rate were 4.3 and 10.4%, respectively. CONCLUSION: LAG with lymph node dissection is technically feasible and receptive as surgical treatment for patients with gastric cancer, although various postoperative complications can arise in LAG as they do in open gastrectomy.