gms | German Medical Science

130. Kongress der Deutschen Gesellschaft für Chirurgie

Deutsche Gesellschaft für Chirurgie

30.04. - 03.05.2013, München

Increased growth of colorectal liver metastasis following partial hepatectomy

Meeting Abstract

  • Sarah König - Universitätsmedizin Göttingen, Abteilung Allgemein- und Viszeralchirurgie, Göttingen
  • Petra Krause - Universitätsmedizin Göttingen, Abteilung Allgemein- und Viszeralchirurgie, Göttingen
  • Henk Flikweert - Universitätsmedizin Göttingen, Abteilung Allgemein- und Viszeralchirurgie, Göttingen
  • Gabriel Cantanhede - Universitätsmedizin Göttingen, Abteilung Allgemein- und Viszeralchirurgie, Göttingen
  • Ali Seif - Universitätsmedizin Göttingen, Diagnostische Radiologie, Göttingen
  • Gunther Helms - Universitätsmedizin Göttingen, Cognitive Neurology, MR-Research in Neurology and Psychiatry, Göttingen
  • Michael Ghadimi - Universitätsmedizin Göttingen, Abteilung Allgemein- und Viszeralchirurgie, Göttingen

Deutsche Gesellschaft für Chirurgie. 130. Kongress der Deutschen Gesellschaft für Chirurgie. München, 30.04.-03.05.2013. Düsseldorf: German Medical Science GMS Publishing House; 2013. Doc13dgch482

doi: 10.3205/13dgch482, urn:nbn:de:0183-13dgch4827

Veröffentlicht: 26. April 2013

© 2013 König et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Introduction: Nearly 50% of colorectal cancer patients develop metastatic liver tumours. Even after complete resection of the affected liver segments, 5-year survival rates border on only 30%. Dormant tumour cells may rapidly develop into tumour masses. Following partial hepatectomy (PH), regenerative processes lead to both to the restoration of liver parenchyma as well as the undesirable proliferation of tumour cells. This work investigates the influence of PH on the growth and composition of colorectal liver metastasis in a syngeneic rat model.

Material and methods: 1 million CC531 colorectal tumour cells were implanted via the portal vein in WAG/Rij rats followed by a 30% PH a day later. Control groups either received tumour cells followed by a sham surgical procedure or were injected with a buffer solution followed by PH. The animals were examined by magnetic resonance imaging (MRI) under anaesthesia at 2 weeks and euthanized for organ harvesting.

Results: MRI revealed a 2,9-fold increase in relative tumour mass (tumour percentage/liver volume) when compared to the control group (sham-OP). Likewise, mRNA expression of CD44, adopted as a surrogate for tumour mass, was increased 2.3-fold. A series of molecular markers pointing towards metastatic potential and tumour aggressiveness (CD49f, CXCR4, Axin and c-Met) were significantly increased after PH, none of which was specifically associated to the tumour mass alone. Two weeks after PH, liver metastases demonstrated a significantly higher proliferation of Ki67 compared with the sham-OP group. Furthermore, hepatocyte proliferation was enhanced in the surrounding liver tissue and especially in liver parenchyma some distance from the tumour.

Conclusion: The growth of liver metastases was accelerated, owing to the effects of PH. Even after completion of liver regeneration, the growth of tumour cells could still be detected. Tumour composition was not influenced by the conditions associated with liver regeneration. Future investigations should focus on whether the inhibition of cell cycle (i.e. irradiation) may hinder liver regeneration and therefore restrain tumour growth.