Abstract

A mutated K-RAS gene is the originator of several characters of colorectal cancer among them tumor initiation, growth, survival, metastasis formation and even immune response. Thus; the aim of our experiments is to establish if the tumor samples express the K-RAS mutation before starting the monoclonal antibody-based therapy. Otherwise it makes no sense to block the receptor binding site if the signaling cascade is independent of the binding of the ligand to the receptor. Colorectal cancer, a cancer resulting from uncontrolled cell growth in the colon or rectum is the fourth most common cause of cancer death. The stage of its development affects the method of treatment of this disease. A prominent method to treat this type of cancer is the blockage of the EGFR by monoclonal antibodies. This kind of approach however seems only to be efficient as long as there is no mutation of K-Ras, a GTPase thought to play an important role at an early stage of the development of colorectal cancer. In case of a mutation in the RAS protein, the Ras GTPase is activated to such an extent that the subsequent over activation of downstream signaling pathways leads to tumor genesis.