A 14-year-old, spayed female, poodle was presented with dysuria and hematuria. A mass that appeared hypoechoic on ultrasound and hypoattenuating on computed tomography (CT) extended from the bladder neck to the urethra. Magnetic resonance imaging (MRI) showed the mass invading the muscular layer of the bladder, urethra, and prostate with distinct margins. Transitional cell carcinoma (TCC) was confirmed with the CADET-BRAF test. This study describes the CT and MRI features of suspected TCC lesions involving the bladder, prostate, and urethra. MRI showed superior soft tissue contrast resolution, enabling evaluation of invasion of the muscular layer of the bladder and urethra.

Endoscopic treatment of chronic pancreatitis by stent insertion is an accepted procedure, but various complications can be induced, including proximal migration of the stent. Many techniques are used to retrieve proximally migrated, pancreatic stents. We here report a case of a proximally migrated stent into the dorsal duct of a pancreas divisum, which was retrieved endoscopically by using a mini-snare. A 39-year-old female patient had chronic pancreatitis with divisum. A stent was inserted into the dorsal duct to relieve the chronic pain. After two months, sudden epigastric pain developed due to proximal migration of the stent. The pancreatic stent was retrieved successfully with one endoscopic attempt using a mini-snare. The epigastric pain resolved after retrieval of the stent. Our observation is that pancreatic stent migration may cause severe abdominal pain and that endoscopic retrieval is possible.
Abdominal Pain ; Adult ; Chronic Pain ; Female ; Humans ; Pancreas* ; Pancreatitis, Chronic ; Stents*

BACKGROUND: Endoscopic mucosal resection (EMR) is now widely accepted as a useful treatment method for gastric adenoma and early gastric cancer (EGC) because of its minimal invasiveness and satisfactory post-procedure results. The purpose of this study is to define the follow-up results and usefulness of EMR. METHODS: We analyzed 54 cases from June 2000 through September 2004. Endoscopy with histological examination was carried out every 3 months for 1 year after EMR. RESULTS: The patients consisted of 42 men and 12 women, and the mean age was 60 years old. The histological results were 42 gastric adenoma and 12 EGC cases. There were 9 cases that had the histological diagnosis changes after EMR. Complete resections was performed for 48 cases and the en block resections were 33 of 34 cases (97%) and piecemeal resections were done in 15 of 20 cases (75%). Recurrence was seen in 4 cases (7.1%), and the mean recurrence period was 7 months. There were 3 gastric adenomas of 42 cases (7.1%), one case of EGC of 12 cases (8.3%), one en block resection of 34 cases (2.9%) and three piecemeal resections of 20 cases (15%). CONCLUSIONS: EMR is a safe and useful treatment method for gastric adenoma and EGC. However, EMR has some limitations that EGC may have lymph node metastases or multiple tumors. So, periodic follow-up is very important. As we acquire more clinical experience, EMR may be accepted as the standard treatment method for gastric adenoma and EGC.
Adenoma* ; Diagnosis ; Endoscopy ; Female ; Follow-Up Studies* ; Humans ; Lymph Nodes ; Male ; Middle Aged ; Neoplasm Metastasis ; Recurrence ; Stomach Neoplasms*

Redox adaptation is an important concept that explains the mechanisms by which cancer cells survive under persistent endogenous oxidative stress and become resistant to certain anticancer agents. To investigate this concept, we determined the expression levels of peroxiredoxins (Prxs), antioxidant enzymes in drug-resistant non-small cell lung carcinoma cells. Prx II was remarkably increased only in A549/GR (gefitinib-resistant) cells compared with A549 cells, consistent with methylation/demethylation. Prx II was highly methylated in the A549 cells but was demethylated in the A549/GR cells. The elevated expression of Prx II resulted in the downregulation of reactive oxygen species (ROS) and cell death and upregulation of cell cycle progression in the A549/GR cells. When Prx II mRNA in the A549/GR cells was knocked down, the levels of ROS and apoptosis were significantly recovered to the levels of the controls. In addition, signaling molecules involved in apoptosis were increased in the A549/GR-shPrx II cells. There was no difference in the expression of MAPK/ERK between the A549/GR cells and A549/GR-shPrx II cells, but the phosphorylation of JNK was increased in the A549/GR cells and was markedly decreased in the A549/GR-shPrx II cells. Colony number and tumor growth were significantly decreased in the A549/GR-shPrx II cells compared with the A549/GR cells. Our findings suggest that Prx II has an important role in cancer cell survival via the modulation of signaling molecules involved in apoptosis and the phosphorylation of JNK by the downregulation of ROS levels in A549/GR cells.
Animals ; Antineoplastic Agents/*therapeutic use ; Apoptosis/drug effects ; Carcinoma, Non-Small-Cell Lung/*drug therapy/genetics/metabolism/pathology ; Cell Line, Tumor ; Drug Resistance, Neoplasm ; Female ; Humans ; Lung/drug effects/metabolism/pathology ; Lung Neoplasms/*drug therapy/genetics/metabolism/pathology ; Mice, Inbred BALB C ; Mice, Nude ; Oxidative Stress/drug effects ; Peroxiredoxins/*genetics/metabolism ; Quinazolines/*therapeutic use ; Reactive Oxygen Species/metabolism

Redox adaptation is an important concept that explains the mechanisms by which cancer cells survive under persistent endogenous oxidative stress and become resistant to certain anticancer agents. To investigate this concept, we determined the expression levels of peroxiredoxins (Prxs), antioxidant enzymes in drug-resistant non-small cell lung carcinoma cells. Prx II was remarkably increased only in A549/GR (gefitinib-resistant) cells compared with A549 cells, consistent with methylation/demethylation. Prx II was highly methylated in the A549 cells but was demethylated in the A549/GR cells. The elevated expression of Prx II resulted in the downregulation of reactive oxygen species (ROS) and cell death and upregulation of cell cycle progression in the A549/GR cells. When Prx II mRNA in the A549/GR cells was knocked down, the levels of ROS and apoptosis were significantly recovered to the levels of the controls. In addition, signaling molecules involved in apoptosis were increased in the A549/GR-shPrx II cells. There was no difference in the expression of MAPK/ERK between the A549/GR cells and A549/GR-shPrx II cells, but the phosphorylation of JNK was increased in the A549/GR cells and was markedly decreased in the A549/GR-shPrx II cells. Colony number and tumor growth were significantly decreased in the A549/GR-shPrx II cells compared with the A549/GR cells. Our findings suggest that Prx II has an important role in cancer cell survival via the modulation of signaling molecules involved in apoptosis and the phosphorylation of JNK by the downregulation of ROS levels in A549/GR cells.
Animals ; Antineoplastic Agents/*therapeutic use ; Apoptosis/drug effects ; Carcinoma, Non-Small-Cell Lung/*drug therapy/genetics/metabolism/pathology ; Cell Line, Tumor ; Drug Resistance, Neoplasm ; Female ; Humans ; Lung/drug effects/metabolism/pathology ; Lung Neoplasms/*drug therapy/genetics/metabolism/pathology ; Mice, Inbred BALB C ; Mice, Nude ; Oxidative Stress/drug effects ; Peroxiredoxins/*genetics/metabolism ; Quinazolines/*therapeutic use ; Reactive Oxygen Species/metabolism