.

					Functional Genome Analysis  (B070) Deutsches Krebsforschungszentrum, Im Neuenheimer Feld 580 D-69120 Heidelberg, Germany.

..
..
  Identification of malignancy factors by analysing cystic tumours of the pancreas
..
..  
In this study, we analysed the transcript profiles of cystic lesions in comparison to normal tissue and the highly malignant and aggressive ductal adenocarcinoma with the objective of identifying factors responsible for malignancy and aggressive growth. Although the cystic forms of pancreatic tumours are only a small portion of the overall number of cases, they represent an appropriate mix of tumour entities for an elucidation of such molecular factors. The transcriptional data presented here permits a highly reproducible differentiation between the various types of cystic tumours and ductal adenocarcinoma. In addition, they could provide a means to understand in detail the molecular elements responsible for the less aggressive nature of the cystic tumours and consequently influence all pancreas carcinomas more effectively.

-  Experimental annotations   -  Array   -  Comprehensive data list

The investigation of the differences in expression profiles between benign, potentially malignant and malignant forms of cystic tumours indicated the involvement of several genes that mostly exhibited an increase in transcript levels with increasing potential for malignancy. In addition, however, there was one striking difference between all potentially malignant and malignant tumour entities on the one hand and the benign SCA lesions as well as normal tissue on the other hand. Only the anti-apoptotic FASTK showed a strong over-expression in all potential malignant tumours, while being at identically low levels in normal pancreas and benign SCA. Down-regulation of the activity of FASTK by siRNA silencing and the effect on various tumour-associated genes support the assumption that FASTK may play an important role in pancreatic cancer with respect to malignancy.

Figure legend: Results of immunohistochemical analyses. Panels A-C show MKP-3 expression in pancreatic tumours. (A) In pancreatic ductal adenocarcinomas, the MKP-3 staining intensity was dependent on the grade of differentiation: on the right a well-differentiated tumour area with moderate expression of MKP-3, on the left a weakly positive, poorly differentiated area. (B) Weak and focal MKP-3 expression was found in the epithelial cell component of MCA. (C) In SCA, no expression of MKP-3 could be detected. Panels D-F: FASTK expression in pancreatic tumours. FASTK was expressed in tumour cells of ductal adenocarcinomas and IPMC (D, E) whereas it was absent in SCA (F).

Bauer et al., 2009, Pancreatology 9, 34-44.

.Overview

.. DKFZ Home Page

Top of page