This prospective and randomized trial sought to compare large-bore plastic endoprostheses (14 French) and self-expanding metal stents (24 French) in the palliative treatment of obstructive jaundice due to biliary hilar malignancies. Twenty patients with Type II-IV (Bismuth classification) hilar obstruction were randomized to treatment with either plastic or metal stents. Both treatment groups were well matched with regard to all assessed clinical criteria before stenting. Stent placement was uniformly successful in the metal group and in 88.9% of the plastic group. Early stent failure (< 30 days) occurred in two patients of the plastic stent group. Longterm (> 30 days), stent failure was observed in 50% of the plastic group and 18.2% of the metal stent group. All differences were not statistically significant. The number of re-interventions required to manage stent-related problems proved to be significantly higher in the plastic group (2.4 +/- 2.6) compared to the metal group (0.4 +/- 0.5). Hospitalization for treatment of stent complications was also significantly higher in the plastic treatment group. The costs calculated for stents and hospital stay for required re-interventions were therefore higher in the plastic stent group. In conclusion, metal stent insertion for palliation of hilar malignancies does not only offer higher success rates and higher patency rates compared to plastic stent insertion, but is also cost-effective since patients require fewer re-interventions.
The peroxisome proliferator‐activated receptor‐β (PPARβ) has been implicated in tumorigenesis, but its precise role remains unclear. Here, we show that the growth of syngeneic Pparb wild‐type tumors is impaired in Pparb−/− mice, concomitant with a diminished blood flow and an abundance of hyperplastic microvascular structures. Matrigel plugs containing pro‐angiogenic growth factors harbor increased numbers of morphologically immature, proliferating endothelial cells in Pparb−/− mice, and retroviral transduction of Pparb triggers microvessel maturation. We have identified the Cdkn1c gene encoding the cell cycle inhibitor p57Kip2 as a PPARβ target gene and a mediator of the PPARβ‐mediated inhibition of cell proliferation, which provides a possible mechanistic explanation for the observed tumor endothelial hyperplasia and deregulation of tumor angiogenesis in Pparb−/− mice. Our data point to an unexpected essential role for PPARβ in constraining tumor endothelial cell proliferation to allow for the formation of functional tumor microvessels.
The application of iodinated contrast agents during diagnostic x-ray procedures, such as chest CT, leads to a clear increase in the level of radiation-induced DNA damage as assessed with γH2AX foci formation.
These data suggest that the addition of alpha-interferon to octreotide has antiproliferative efficacy in a subgroup of patients with advanced metastatic disease unresponsive to octreotide monotherapy. Prolonged survival was seen in the responder group.
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