The role of the host–tumor interface and cell hybridization in invasive cancer

Abstract

Available data indicate that growth of invasive tumors is enhanced by homeostatic mechanisms of the host involved in normal tissue regeneration and repair. To achieve this, malignant cells may (i) induce degeneration of normal cells at the host–tumor interface, (ii) hybridize in situ with activated host stem cells, required for replacement of lost mature tissue cells, (iii) the resulting malignant/normal cell hybrids may exhibit an antigenic similarity to normal cells, (iv) thereby preventing recognition by the immune system, (v) and exploiting normal mechanisms of tissue regeneration by the host. In addition, primary cancers with allotypic determinants may utilize other homeostatic mechanisms evolved in mammals to promote fetal allograft survival. They may have a potential to grow in another (secondary) host. Novel approaches to cancer prevention and control may depend on a better understanding of the mechanisms by which normal cellular growth are controlled, and hybridization prevented.