Neoplastic transformation is accompanied, among others, by the inhibition of apoptosis. Four mechanisms that allow cells to avoid apoptosis are well known: loss of APAF1 (apoptosis-inducing factor 1), up-regulation of caspase inactivating apoptosis inhibitors, expression of FasL (Fas ligands) on the cell surface, and production of caspase 8 inhibiting protein (FLIP FADD like interleukin 1 beta converting proteins). Moreover, the roles of RB1 and TP53 genes in the neoplastic process have been described. Tumor cells can show mutations of genes responsible for the expression of proteins regulating the cell cycle and of proteins controlling apoptosis, e.g. TP53 protein. Neoplastic cells seek to avoid not only apoptosis, but also necrosis, inflammatory cells, and the reaction of the immunological system. The types of neoplastic antigens, i.e. TSA (tumor specific antigens) and TAA (tumor associated antigens), as well as the possibilities of their recognition by the organism burdened with neoplasm, have been described. Furthermore, the mechanisms of weakening the immunological response by neoplastic cells and the role of inflammatory cells and inflammatory response in destroying neoplasms (mainly the cell-based response i.e. cells such as NK, LAK, Tc, Th, and macrophages) have been presented. Macrophages have received special attention because of the role of macrophages associated with tumors (e.g. mammary gland cancer in dogs) in causing an abnormal (non-canonical) course of the Wnt pathway. Paradoxically, the immune response sometimes promotes neoplastic growth by the so-called immune facilitation effect. After the first stage (i.e. the limitation of apoptosis), the necrosis of neoplastic cells and inflammatory infiltration occur, followed by unlimited neoplastic progression due to insufficient immunological anti-neoplastic cell reaction.
