Cancer: Using the Inflammatory Way to Invade the Host
Pp. 214-249 (36)
Jose-Ignacio Arias, Maria-Angeles Aller, Isabel Prieto, Ana Arias, Heping Yang and Jaime Arias
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.
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.
Cátedra de Cirugía, Facultad de Medicina, Universidad Complutense, Pza. de Ramón y Cajal s.n., 28040 MADRID, Spain.