Purpose: Epithelial to mesenchymal transitions are vital for tumor growth and metastasis.Several inducers of epithelial to mesenchymal transition are transcription factors that repress E-cadherin expression, such as Snail, Slug, and Twist. In this study, we aimed to examine the expression of these transcription factors in pancreatic cancer. Experimental Design: The expression of Snail, Slug, and Twist was detected by immunohistochemistry in tissue samples from patients with pancreatic ductal adenocarcinoma. Five human pancreatic cancer cell lines (AsPC-1, Capan-1, HPAF-2, MiaPaCa-2, and Panc-1) were analyzed by reverse transcription-PCR, real-time PCR, and Western blotting. An orthotopic nude mouse model of pancreatic cancer was applied for in vivo experiments. Results: Seventy-eight percent of human pancreatic cancer tissues showed an expression of Snail, and 50% of the patients displayed positive expression of Slug. Twist showed no or only weak expression. Snail expression was higher in undifferentiated cancer cell lines (MiaPaCa-2 and Panc-1) than in more differentiated cell lines (Capan-1, HPAF-2, AsPC-1). Expression of Slug was detected in all cell lines with different intensities. Twist was not expressed. After exposure to hypoxia, theTwist gene was activated in all five pancreatic cancer cell lines. Conclusions:The transcription factors Snail and Slug are expressed in pancreatic cancer but not in normal tissue, suggesting a role in the progression of human pancreatic tumors.Twist, activated by hypoxia, may play an important role in the invasive behavior of pancreatic tumors.Pancreatic cancer is the fifth leading cause of cancer-related death in industrial western countries. It is an aggressive disease with <5% survival after 5 years (1, 2). This is largely attributable to late clinical presentation and limitations in diagnostic methods. More than 80% of patients are diagnosed with pancreatic cancer at a locally advanced or metastatic stage, which excludes a curative surgical resection (3). The response to conventional therapies, such as radiotherapy and chemotherapy, is poor and has little effect on the natural progress of this malignancy (4). Understanding the molecular biology of pancreatic cancer and metastasis may provide insight for the development of novel tumor markers or new therapeutic strategies.Epithelial to mesenchymal transition (EMT) is a key step during embryonic morphogenesis and is involved in the progression of primary tumors toward metastasis (5). During EMT, cells undergo a developmental switch from a polarized, epithelial phenotype to a highly motile fibroblastoid or mesenchymal phenotype (6). Tumor cells begin to grow invasive, enter into systemic circulation (''intravasation''), move from the circulatory system into a new host tissue (''extravasation''), and proliferate and grow to a secondary tumor. The cell adhesion molecules E-cadherin and N-cadherin, members of the classic cadherin family, are regarded as inducers of EMT (7,8). E-cadherin is required for the formation o...

Pathogenic events in CD and UC may be associated with different alterations in the mucosal flora of the ileum and colon.

Background-Endoscopic ultrasonography (EUS) and somatostatin receptor scintigraphy (SRS) can detect a high percentage of gastroenteropancreatic neuroendocrine tumours especially in the upper gastrointestinal tract. The ability of these procedures to localise primary tumour lesions and metastases of gastrinomas and insulinomas was evaluated in comparison with transabdominal ultrasonography (US), computed tomography (CT) and magnetic resonance imaging (MRI) . Patients and Methods-In a prospective trial, patients with gastrinomas (n=10) and insulinomas (n=10) diagnosed by clinical signs and laboratory tests were assessed by EUS, SRS, US, CT and MRI. Results-In 10 patients with gastrinoma and 10 patients with insulinoma, a total of 14 separate primary tumour lesions were histologically confirmed for each of the tumour entities. The mean diameter was 2-1 cm for gastrinomas and 1l5 cm for insulinomas. All insulinomas and nine gastrinoma lesions were located in the pancreas. Three gastrinomas were found in the duodenal wall, one in a periduodenal lymph node, and one in the liver. For gastrinomas, sensitivities were 79% with EUS, 86% with SRS and 29% with CT, US, and MRI. For insulinomas, sensitivities were 93% with EUS, 14% with SRS, 21% with CT and 7% with US and

Objective: In children with RET proto-oncogene mutation, curative treatment of medullary thyroid carcinoma (MTC) is possible by prophylactic thyroidectomy. Recommendations on the timing and extent of thyroidectomy are based upon a model that utilises genotype-phenotype correlations to stratify mutations into three risk groups. Design: We evaluated the long-term outcome (mean follow-up 6.4 years, 15 patients more than 10 years, 26 patients more than 5 years) of operated gene carriers stratified into two risk groups (levels 1 and 2) based on the biological aggressiveness of MTC. Results: In 46 RET gene carriers, prophylactic thyroidectomy was carried out between the ages of 4 and 21 years. Level 1 mutations were harboured by 11 patients (codons 790, 791, 804 and 891). Histology was completely normal in two patients; in seven patients C-cell hyperplasia (CCH) and in two patients T1 tumours were diagnosed. All patients with level 1 mutations were cured. Level 2 mutations were harboured by 35 patients (codons 618, 620, 630 and 634). Histology of these patients showed CCH in 11 patients, T1 tumours in 21, T2 tumour in 1, T3 tumour in 1 and Tx in 1 patient. Histology showed no lymph node involvement. Five patients with level 2 mutations failed to be cured; in two patients, persistence of MTC was diagnosed directly after thyroidectomy and in three during follow-up. In two patients carrying a 634 mutation, other endocrinopathies (hyperparathyroidism and bilateral pheochromocytoma) manifested during follow-up. Conclusions: If prophylactic thyroidectomy is done at early ages, cure rate is high. Timing and extent of prophylactic thyroidectomy can be modified by individual RET mutation. 155 229-236 European Journal of Endocrinology

Changes in the specific conductivity during the coagulation and the cooling phase play an important role for the produceable size of a coagulation necrosis and necessitates an adaptation of the therapy parameters during radiofrequency ablation.