Immune Responses Against Autointracellular Pathogenic Genomes or Cancered Cells
Author(s): Feleke Eriso
Cancer, also termed malignancy is a disease characterized by an uncontrolled growth of cells, i.e., an abnormal growth of immortal cells with no apoptosis. More than 100 types of cancer are known, including breast cancer, skin cancer, colon cancer, prostate cancer, and lymphoma. What makes a cell a cancered one is the autointracellular pathogenic genome, or “cancerous genome” located inside that cancered cell. The code of design of constructing or building the body of every species of all living-things is found in its genome; the same is true with the pathogenic genome in building the body of cancered cells (host cells). Three major types of tumor suppressor genes are known to code for proteins that suppress growth of cells: (i) one type tells cells to slow down and stop dividing, (ii) the second type is responsible for fixing changes (repairing) in damaged cells, and (iii) the third type is in charge of apoptosis (the programmed death of cell). If mutations that can inactivate any of these tumor suppressor genes occur, cancer will be onset and allow cancered cells to grow unchecked. The cytotoxic T cells and NK cells are 100% correct in identifying the cancered cell foreign to the body of the patient just as they identify virus-infected cells, because the genome inside the cancered cell is foreign to the body of the patient as it is transformed into a completely different genome from those found in the body of patient. The genome is transformed by a multitude of mutations referred to as driver mutations. The transformed genome is said pathogenic because it causes the dangerous disease called cancer. As the genome is changed or transformed all biological molecules/biomass of its cells produced by the coded information or directives of this changed genome are foreign (nonself) to the body of the patient and that is why the killer immune cells recognize the cancered cell as foreign to the body of the patient and kill it. Unl