Cancer: Using the Inflammatory Way to Invade the Host

Inflammation has been implicated in tumor development, invasion and metastasis. Hence, it has been suggested that common cellular and molecular mechanisms are activated in wound repair and in cancer development. In addition, it has been previously proposed that the inflammatory response, which is associated with the wound healing process, could recapitulate ontogeny through the re-expression of the extraembryonic, i.e. amniotic and vitelline, functions in the interstitial space of the injured tissue. If so, the use of inflammation by the cancer-initiating cell can also be supported in the ability to reacquire extraembryonic functional axes for tumor development, invasion and metastasis. Thus, the diverse components of the tumor microenvironment could represent the overlapped re-expression of amniotic and vitelline functions. These functions would favor a gastrulation-like process, that is, the creation of a reactive stroma in which fibrogenesis and angiogenesis appear.

Keywords: Cancer, tumor development, tumor invasion, metastasis, cancerrelated inflammation, angiogenesis, wound healing, myofibroblast, epithelialmesenchymal transition, mesenchymal-epithelial transition lymphangiogenesis, hypoxia, interstitial-lymphatic tumoral axis, Warburg effect, leukocytic cancer cell phenotype, immunotolerance.