53 research outputs found
CLINICAL IMPLICATION OF NEUROENDOCRINE DIFFERENTIATION IN PROSTATIC ADENOCARCINOMAS
Specimens from 75 cases of prostatic adenocarcinoma of different M.D.
Anderson degrees of malignancy were stained immunohistochemically for
neuron-specific enolase (NSE), prostatic specific antigen (PSA) and
prostatic acid phosphatase (PAP). None of these tumors presented on
hematoxylin-eosin sections any features suggesting neuroendocrine
differentiation; nevertheless, 18.7% of the tumors were at least
focally NSE positive, Because of the synchronous antigenic expression of
the NSE-positive cells to PSA and PAP, the authors suggest that
prostatic exocrine and neuroendocrine cells derive from a common
precursor stem cell. The possibility of a more aggressive biological
behavior of these tumors in comparison to the conventional carcinomas is
discussed. The probable clinical necessity for a combined therapeutic
approach is also investigated
Modulation of vascular endothelium by imatinib: A study on the EA.hy 926 endothelial cell line
In this study the EA.hy 926 endothelial cell line-simulating endothelial cells-was treated with imatinib in order to define a possible anti-angiogenic role for imatinib. Dose and time response experiments were performed. Cell morphology was studied, while migration efficiency, intercellular permeability and VE-cadherin expression were assayed, both in the presence and in the absence of imatinib. Imatinib-induced EA.hy 926 cell apoptosis was also examined. Results showed that imatinib reduced the endothelial cell population, changed cell monolayer morphology and reduced cell-to-cell cohesiveness. Migration efficiency was significantly decreased while intercellular permeability was 2.76-fold increased in the presence of imatinib. Indirect immunofluorescence microscopy showed nearly complete down-regulation of VE cadherin in imatinib-treated cells. Furthermore, apoptotic activity was detected in imatinib-treated cells. Altogether our results support an antiangiogenic profile for imatinib that possibly contributes to its therapeutic potential. © E.S.I.F.T. srl
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