Perioperative host-tumor inflammatory interactions: a potential trigger for disease recurrence following a curative resection for colorectal cancer

Surg Today. 2008;38(7):579-84. doi: 10.1007/s00595-007-3674-6. Epub 2008 Jul 9.

Abstract

The aim of the present review was to investigate whether host-tumor interactions are causal or consecutive clinical factors associated with surgical stress that influence the long-term survival after a curative resection of colorectal cancer. A Medline/PubMed search was conducted to identify the relevant articles investigating the factors related to surgical stress and their effects on the long-term survival after a curative resection of colorectal cancer. The intraoperative state is defined as a cytokine storm in which ongoing local cytokine production occurs at the site of the tumor, thus further enhancing the autocrine cytokine loop for angiogenic factor production. The postoperative state is defined as tissue regeneration in which surgery-related clinical events enhance the systemic induction of inflammatory cytokines, which in turn synergistically exaggerate the local activation of tumor growth factors. Host-tumor interactions under surgical stress may act synergistically as potent tumor growth factors, and may thus influence long-term survival. Controlling surgical insults and/or regulating perioperative inflammatory responses may therefore lead to new therapeutic approaches for controlling disease recurrence.

Publication types

  • Review

MeSH terms

  • Adenocarcinoma / blood
  • Adenocarcinoma / surgery*
  • Colectomy
  • Colorectal Neoplasms / blood
  • Colorectal Neoplasms / surgery*
  • Cytokines / blood*
  • Hepatocyte Growth Factor / blood
  • Humans
  • Inflammation / blood
  • Inflammation / complications*
  • Interleukin-1 / blood
  • Interleukin-6 / blood
  • Neoplasm Recurrence, Local*
  • Prognosis
  • Stress, Physiological*
  • Vascular Endothelial Growth Factor A / blood
  • Wound Healing

Substances

  • Cytokines
  • Interleukin-1
  • Interleukin-6
  • Vascular Endothelial Growth Factor A
  • Hepatocyte Growth Factor