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  • 1
    ISSN: 1433-0385
    Keywords: Key words: Pancreatic cancer ; CA 19 ; 9.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung. Bei 96 Patienten (duktales Pankreascarcinom, n = 34; periampulläres Carcinom, n = 43; chronische Pankreatitis, n = 19) wurde der Stellenwert des Tumormarkers CA 19–9 in der Differentialdiagnose bei Raumforderungen im Pankreaskopf retrospektiv überprüft. Die Sensitivität betrug für das duktale Carcinom 73,5 % und für den periampullären Tumor 48,8 % bei einer Spezifität von 63,2 %. Das carcinoembryonale Antigen war nur bei jedem 5. Patienten erhöht. Durch Kombination beider Tumormarker ließ sich die Sensitivität serologischer Tests nicht steigern. Die schlechte Spezifität von 63 %, die beim Vorliegen eines Verschlußikterus bis auf 33 % sinkt, erlaubt keine zuverlässige präoperative Differenzierung zwischen einem Carcinom und einer chronischen Pankreatitis. Ein postoperativ erhöhter CA-19–9-Serumspiegel weist auf persistierendes Tumorgewebe hin und ist mit einer statistisch signifikant schlechteren Prognose als bei normalen Marker verbunden.
    Abstract: Schlüsselwörter: Pankreascarcinom – CA 19–9.
    Notes: Summary. In 96 patients (ductal pancreatic carcinoma, n = 34; periampullary carcinoma, n = 43; chronic pancreatitis, n = 19) the role of CA 19–9 in the diagnosis of lesions of the head of the pancreas were evaluated. The sensitivity for ductal pancreatic carcinoma was 73.3 %, for periampullary carcinoma 48.8 %, and specificity was 63.2 %. Carcinoembryonic antigen was elevated only in every fifth patient. Even when combining the two tumor markers no increase in sensitivity could be observed. The low specificity of 63 %, which decreased to 33 % in the case of obstructive jaundice, does not allow adequate preoperative differentiation between cancer patients and those with chronic pancreatitis. In cases of postoperatively elevated CA 19–9 level the prognosis is worse than in patients with normal tumor markers.
    Type of Medium: Electronic Resource
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  • 2
    Publication Date: 2013-04-13
    Description: Rationale: High–angiotensin-converting enzyme (ACE)-levels are associated with cardiovascular disease, but little is known about the regulation of its expression. Objective: To assess the molecular mechanisms regulating endothelial ACE expression focusing on the role of the AMP-activated protein kinase (AMPK) and miR-143/145. Methods and Results: Shear stress decreased ACE expression in cultured endothelial cells, an effect prevented by downregulating AMPKα2 but not AMPKα1. AMPKα2 –/– mice expressed higher ACE levels than wild-type littermates resulting in impaired hindlimb vasodilatation to the ACE substrate, bradykinin. The latter response was also evident in animals lacking the AMPKα2 subunit only in endothelial cells. In cultured endothelial cells, miR-143/145 levels were increased by shear stress in an AMPKα2-dependent manner, and miR-143/145 overexpression decreased ACE expression. The effect of shear stress was unrelated to an increase in miR-143/145 promoter activity and transcription but could be attributed to post-transcriptional regulation of precursor–miR-143/145 by AMPKα2. The AMPK substrate, p53, can enhance the post-transcriptional processing of several microRNAs, including miR-143/145. We found that shear stress elicited the AMPKα2-dependent phosphorylation of p53 (on Ser15), and that p53 downregulation prevented the shear stress–induced decrease in ACE expression. Streptozotocin–induced diabetes mellitus in mice was studied as a pathophysiological model of altered AMPK activity. Diabetes mellitus increased tissue phosphorylation of the AMPK substrates, p53 and acetyl-coenzyme A carboxylase, changes that correlated with increased miR-143/145 levels and decreased ACE expression. Conclusions: AMPKα2 suppresses endothelial ACE expression via the phosphorylation of p53 and upregulation of miR-143/145. Post-transcriptional regulation of miR-143/145 may contribute to the vascular complications associated with diabetes mellitus.
    Keywords: ACE/Angiotension receptors, Cell signalling/signal transduction, Endothelium/vascular type/nitric oxide
    Print ISSN: 0009-7330
    Electronic ISSN: 1524-4571
    Topics: Medicine
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