Don't let it to air: A cautionary tale of the potential consequences of surgery of residual cancer

In this issue of the BBI, Haldar et al. demonstrate that major surgical stress from laparotomy caused a significant increase in post-operative metastatic burden in a mouse model of cancer. They identified this metastatic outbreak was driven by a novel mechanism of direct, surgery-induced activation of the primary tumour which, if left in situ, released pro-metastatic factors (IL-6, IL-8, and VEGF). Surgical stress induced significant changes in the transcriptional programming of the primary tumor, with marked activation of NF-cB and down-regulation of IRF-1. Pharmaceutical blockade of post-operative 8-adrenergic and prostanoid signalling, by administration of pro-pranolol and etodolac, prevented post-operative activation of the primary tumour and metastatic disease.

Automated summary

In this study, Haldar et al. demonstrated that laparotomy-induced surgical stress significantly increased post-operative metastatic burden in a mouse model of cancer. They found that this metastatic outbreak was driven by a novel mechanism of direct surgery-induced activation of the primary tumor, leading to the release of pro-metastatic factors (IL-6, IL-8, and VEGF). The study also revealed significant changes in the transcriptional programming of the primary tumor due to surgical stress, with activation of NF-cB and down-regulation of IRF-1. Pharmacological blockade of post-operative adrenergic and prostanoid signaling prevented the activation of the primary tumor and metastatic disease.