Worldwide, colorectal cancer (CRC) is the 4th and 3rd most common cancer in men and women, respectively. Of all patients, 25% present with liver metastases (LMs) and a further 25-50% will develop LMs during the 2 years following resection of the primary tumour. Remarkably little is known about the biological characteristics that determine the heterogeneity and prognosis of patients with LMs.
We have identified three different histological growth patterns (GPs) of LMs of solid tumours in general and of CRC in particular1 2 . In LMs with a desmoplastic GP the tumour is separated from the liver parenchyma by desmoplastic, inflammatory stroma. In the pushing type, the liver plates are compressed, running parallel to the tumour-liver interface without desmoplastic stroma and with only a mild inflammatory infiltrate. In the replacement GP tumour cells replace the hepatocytes without destruction of the liver architecture. There is no compression, no desmoplastic stroma or inflammatory infiltrate.
We have demonstrated significant biological differences associated with these GPs. Angiogenesis and hypoxia are significantly increased in pushing type LMs1 2 . The GP also differs according to the biological characteristics of the primary tumour, including the histological subtype and the differentiation grade2 . We also demonstrated different expression of the components of the plasminogen system in LMs with different GPs3 . Furthermore, we observed a remarkable tendency toward GP uniformity in multiple LMs arising in the same patient4 . Recently, we have demonstrated that the presence of a pushing component in the GP was an independent predictor for overall survival5 .
Collectively, these data provide compelling evidence that the GPs in LMs of CRC are not a random phenomenon, but the apparent result of different tumour-micro-environment interactions. Current efforts focus on the molecular pathways underlying these GPs and the identification of GP-related biomarkers to guide the treatment of patients with CRC LMs.