Lyvia Moudombi

Abstract Cellular transformation is initiated by a driver mutation, resulting in the abnormal expression of an oncogene or the loss of a tumor suppressor gene in a normal cell. This event leads to oncogenic stress (OS), describing a disruption of cellular homeostasis which activates stress response pathways and transcriptomic programs that can either promote tumor development or trigger intrinsic safeguards such as senescence or apoptosis.

Ag presenting cells (DCs, macrophages, etc.) can acquire Ags from the extracellular environment via phagocytosis and present them on their MHC-II molecules to trigger CD4 T cells. In addition, all nucleated cells present endogenous Ags via their MHC-I molecules, which is achieved by proteosomal degradation of cytosolic Ags and loading in the ER on MHC-I via transporter associated with antigen processing (TAP). In this way, the immune system can recognize virally infected or malignant cells.