Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
9256200 | Pancreatology | 2005 | 7 Pages |
Abstract
Background: There is abundant evidence from in vivo and in vitro studies that Polo-like kinase 1 (PLK1) plays a crucial role in the regulation of proliferative activity of normal and malignant cells. Therefore, PLK1 has been proposed as a new target for antineoplastic treatment strategies. Methods: We conducted an immunohisto-chemical expression study for PLK1 on 86 cases of pancreatic adenocarcinoma as well as on 5 cases of chronic pancreatitis. Additionally, we investigated the correlation of PLK1 expression levels with clinicopathological data and patient survival. Results: PLK1 was found over-expressed in pancreatic neoplasia as early as in pancreatic intraepithelial neoplasia III lesions, whereas benign acinar pancreatic parenchyma and ductal epithelia showed only focal PLK1 positivity. Invasive pancreatic adenocarcinomas were PLK1 positive in 47.7% of cases. No correlation of PLK1 positivity and the extent of tumour spread was evident, nor did PLK1 expression correlate with tumour grade or patient prognosis. Prognostic factors in our study cohort were nodal status and tumour grade. Conclusions: The fact that half of the invasive pancreatic carcinomas strongly overexpressed PLK1 indicates that inhibition of this mitotic key regulator might represent a rewarding approach in the treatment of early and late pancreatic carcinoma.
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Authors
Wilko Weichert, Mathias Schmidt, Juliane Jacob, Volker Gekeler, Jan Langrehr, Peter Neuhaus, Marcus Bahra, Carsten Denkert, Manfred Dietel, Glen Kristiansen,