PubMed · 14146963
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G H JEFFRIES, E WESER, M H SLEISENGER. 1964. MALABSORPTION.. https://pubmed.ncbi.nlm.nih.gov/14146963/
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Protein 4.1 family proteins are thought to interact with membrane proteins and membrane skeletons. Immunohistochemical studies by light and electron microscopy were performed on mouse pancreas with a specific antibody against protein 4.1B. Specific protein 4.1B immunolabeling was observed on endocrine cells in the islets of Langerhans. Protein 4.1B localized along the plasma membranes facing adjacent cells. By immunoelectron microscopy, the immunolabeling of the cells was restricted to the cytoplasmic side just beneath their plasma membrane, including the membranes adjacent to neighboring cells, while the plasma membranes facing endothelial cells were not immunolabeled for protein 4.1B. The immunolocalization of E-cadherin was similar, if not identical, to that of protein 4.1B supporting the idea that protein 4.1B may be functionally interconnected with adhesion molecules. In a transgenic mouse model of pancreatic beta-cell carcinogenesis (Rip1Tag2), the loss of protein 4.1B expression coincided with the phenotypic transition from adenoma to carcinoma. Therefore, we propose a role of protein 4.1B as a connecting and/or signaling molecule between membrane architecture, cell adhesion, and tumor cell invasion in mouse pancreatic endocrine cells.
EAT/mcl-1 (EAT), a bcl-2 related anti-apoptotic gene, is up-regulated at the early stage of differentiation of human embryonal carcinoma cells; cells which serve as a model for early embryogenesis. We generated transgenic mice for the human EAT gene driven by the EF1 alpha promoter in order to elucidate its functional role in vivo. Histologically, these mice exhibited hyperplasia of Langerhans islet cells; pancreatic cell regions composed of both insulin- and glucagon-producing cells. Furthermore, Bax and Bag-1 -- possible heterodimeric partners for EAT in the anti-apoptotic process -- were up-regulated in islets isolated from the EAT transgenic mice. The insulin tolerance test exhibited no significant difference between the EAT transgenic mice and non-transgenic mice, indicating that islet cell hyperplasia was not due to insulin resistance. In conclusion, EAT transgenic mice exhibit hyperplasia of pancreatic beta cells. EAT may inhibit apoptosis of beta cells, allowing these cells to circumvent the process of apoptosis until the adult stage.
OBJECTIVE: To compare the value of the various imaging modalities in the detection of pancreatic islet cell tumors. METHODS: Analysis of the literature to compare the value of ultrasound, CT, MRI, angiography, venous sampling, scintigraphy and PET in the detection of neuroendocrine tumors of the pancreas. RESULTS: For transabdominal ultrasound a sensitivity of 60% has been reported; for endoscopic ultrasound a sensitivity of more than 90%. MRI with a sensitivity of 75-100% is more sensitive compared to CT with a sensitivity of 64-82%. Angiography and venous sampling have a reported sensitivity of 66% and 76%. Somatostatin receptor scintigraphy has a sensitivity of 81-88% with significant differences between the various histological subtypes of the pancreatic islet cell tumors. PET does not play an important role in the detection of neuroendocrine tumors of the pancreas. CONCLUSION: None of the various modalities is superior alone, so that it is often necessary to combine them for diagnostic imaging of pancreatic islet cell tumors.