لخّصلي

Cells usually do not grow on their own, they receive stimulus from the body to start growing according to an event or to continue a regular operation such as growing bones for the youth. Cells may grow on their own, but that is most likely to be the result of a disease such as cancer.
Normal cell signaling starts when the body sends signals with ligands (extracellular material) such as growth factors, inhibitors, or cell adhesion molecules to grow. The receptors on the cell surface receive the signal, and those receptors, in turn, send another signal to the nucleus explains what the body wants the cell to do. In cancer cells, the signaling procedure is the same but uncontrolled, and the signals are not correct. This can happen as a result of many things, such as autocrine stimulation, where the cells create their own growth factors and stimulate their own growth like platelet-derived growth factor (PDGF) which is secreted in the case of glioblastoma.

In addition, the surface receptors on the cell could also cause uncontrolled growth where the production of those receptors is controlled by the protein translation and the gene expression of the cellular strains, but in cancer cells a mutation in those genes could lead to mass production of those proteins which is also called gene implication or to changes in the receptors structure. This production will give the tumor cells a higher opportunity to grow as a result of the overexpressed receptors. This could also lead to independent signaling and activation by ligands that activate the receptors in normal situations. This will also give the tumor cells higher chances of survival because they produce the important factors needed for that. For example: the overexpression of the epidermal growth factor receptor (EGFR) which is founded in the breast and skin and other places in the epithelial tissue and plays a role in cell proliferation, differentiation, and survival, is associated with many tumors such as those in the colon, head, and neck. When the receptor is activated by the ligand, it sends a signal to the nucleus to start proliferating which will end with mitosis and the increase of tumor cells and size.
Recent researchers have discovered many ways to stop this process such as the monoclonal antibody bevacizumab how target the ligands before they bind to their receptor. Or by targeting the receptor itself like cetuximab which is also a monoclonal antibody that binds to the receptor strongly and prevents the other ligands from binding to receptor and stops the growth of the tumor. Or by using small molecule inhibitors which inhibits the receptors function by stopping it from trans ducting the signal to the nucleus such as gefitinib which blocks the tyrosine kinase which an enzyme used for cellular communication and found in some receptors.