Preferential growth of blood-borne cancer cells at sites of trauma--a growth promoting role of macrophages.

Carcinoma and sarcoma after gaining access to the venous circulation are completely trapped in the organs of first encounter, i.e. the lung and vertebrae for cancers draining into the vena cava, or liver for tumours with portal drainage. Systemic dissemination of carcinomas and sarcomas derives from cancer growing in the lung and can be mimicked in experimental rats by injecting cancer cells intra-arterially via the left ventricle. These emboli are arrested in different tissues in proportion to the cardiac output they receive, but the probability of a cancer embolus introduced in this way causing a lesion varies by several orders of magnitude for different tissues. Traumatising tissues by procedures such as surgical incision of the abdomen, gut anastomosis, placing a stitch in the kidney or chemical or surgical partial hepatectomy, greatly enhances the likelihood that a cancer cell trapped in the tissues develops into a metastasis. While several factors contribute to making a wound a more favourable "soil" for metastasis a major mechanism is the release of growth factors from macrophages that have infiltrated the wound.