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126. Kongress der Deutschen Gesellschaft für Chirurgie

Deutsche Gesellschaft für Chirurgie

28.04. - 01.05.2009, München

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Aberrant Expression of Checkpoint-Kinases in pancreatic carcinomas

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  • F. Traub - Department of General and Transplant Surgery, Comprehensive Cancer Center, Erberhard Karls University Tuebingen, Germany
  • J. Gaedcke - Department of General Surgery, Georg-August-University Goettingen, Germany
  • D. Zieker - Department of General and Transplant Surgery, Comprehensive Cancer Center, Erberhard Karls University Tuebingen, Germany
  • S. Kupka - Department of General and Transplant Surgery, Comprehensive Cancer Center, Erberhard Karls University Tuebingen, Germany
  • C. Zug - Department of General and Transplant Surgery, Comprehensive Cancer Center, Erberhard Karls University Tuebingen, Germany
  • M. Ghadimi - Department of General Surgery, Georg-August-University Goettingen, Germany
  • corresponding author B.L.D.M. Brücher - Department of General and Transplant Surgery, Comprehensive Cancer Center, Erberhard Karls University Tuebingen, Germany
  • A. Königsrainer - Department of General and Transplant Surgery, Comprehensive Cancer Center, Erberhard Karls University Tuebingen, Germany

Deutsche Gesellschaft für Chirurgie. 126. Kongress der Deutschen Gesellschaft für Chirurgie. München, 28.04.-01.05.2009. Düsseldorf: German Medical Science GMS Publishing House; 2009. Doc09dgch11663

doi: 10.3205/09dgch637, urn:nbn:de:0183-09dgch6373

Published: April 23, 2009

© 2009 Traub et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.en). You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.

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Introduction: Over the past two decades, research aimed at understanding and fighting the complex mechanisms of cellular transformation which lead to tumor development and helped to improve the detection and treatment of many cancers. However, some tumors have not benefited from these advances. Among them, tumors from the pancreas, which are rapidly invasive, metastatic, and resistant to standard therapies.

Material and methods: Ttissue from 42 patients with pancreatic cancer and from 12 patients with pancreas adenoma or server pancreatitis was analysed for the expression of CHK1, ATM and ATR (mRNA) and compared with histological normal tissue. The gene promoter methylation status was examined, to exclude an epigenetic phenomenon.

Results: In 63% of pancreas cancers a suppression of CHK1 was detected. Compared to histological normal tissue no hypermethylation could be detected. For ATM and ATR a non-uniformly expression pattern was observed. ATR was significant overexpressed in about ~66% of carcinoma tissue. 9 patients had a significant suppression of ATR expression. An overexpression of ATR was detected in two-thirds of the adenoma / pancreatitis tissues. Regarding ATM again a mixed expression was found. A signifikant overexpression or suppression could not be detected.

Conclusion: The expression of the tumor suppressor gene CHK1 was significantly reduced in carcinoma tissue of the pancreas, while the regulating gene ATR showed a significant overexpression. An epigenetic cause for this result could be excluded via methylenation assay. In further investigations the function of ATM and ATR as well as for CHK1 will be analysed using SNP screening.