Overexpression of Polo-Like Kinase 1 Is a Common and Early Event in Pancreatic Cancer

Vol. 5, No. 2-3, 2005

Free Abstract Article (References) Article (PDF 356 KB)

Original Paper

Overexpression of Polo-Like Kinase 1 Is a Common and Early Event in Pancreatic Cancer
Wilko Weichert^a, Mathias Schmidt^c, Juliane Jacob^a, Volker Gekeler^c, Jan Langrehr^b, Peter Neuhaus^b, Marcus Bahra^b, Carsten Denkert^a, Manfred Dietel^a, Glen Kristiansen^a

^aInstitute of Pathology and
^bDepartment of General, Visceral and Transplantation Surgery, Charité University Hospital, Berlin, and
^cAltana Pharma AG, Konstanz, Germany

Address of Corresponding Author

Pancreatology 2005;5:259-265 (DOI: 10.1159/000085280)

Key Words

Polo-like kinase
Pancreatic carcinoma
Immunohistochemistry
Pancreatic intraepithelial neoplasia
Prognosis

Abstract

Background: There is abundant evidence from in vivo and in vitro studies thatPolo-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 immunohistochemical 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 overexpressed 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.

Author Contacts

Dr. Wilko Weichert
Institute of Pathology, Charité University Hospital
Schumannstrasse 20/21
DE-10117 Berlin (Germany)
Tel. +49 30450536006, Fax +49 30450536922, E-Mail wilko.weichert@charite.de

Article Information

Received: August 10, 2004
Accepted after revision: September 28, 2004
Published online: April 22, 2005
Number of Print Pages : 7
Number of Figures : 2, Number of Tables : 2, Number of References : 26

Medline Abstract (ID 15855824)

Download Citation

Cited In

For non-native English speakers and international authors who would like assistance with their writing before submission, we suggest American Journal Experts for their scientific editing service.