Inflammation is considered to regulate tumor progression, invasion, migration and metastasis. The interstitial inflamed microenvironment in which the cancer cell develops is considered in this review as a space surrounded by a heterogeneous endothelium, made up of tumor neoendothelium, postcapillary venule endothelium, lymphatic endothelium and high endothelial venule endothelium. Through this barrier, the endothelium would exchange substrates and inflammatory mediators with the host organism. At the same time, the systemic inflammatory response associated with tumor development could be considered as an upregulation of extraembryonic functions, as those that are developed by the coelomic-amniotic and trophoblastic-yolk sac or vitelline structures. The coupling of these extraembryonic functions in the interstitial tumor space would induce a process of epithelial-mesenchymal transition leading to cancer cell proliferation, migration and metastasis. Likewise, the fundamental alterations of the systemic inflammatory response could represent a phylogenetic recapitulation of ancestral survival mechanisms, which would also explain the resistance of the cancer cell and its strong ability to survive, even in very adverse environmental situations.