**1. Introduction**

Cancer arises when a group of cells of a specific tissue type acquires genetic alterations which allow them to grow in an uncontrolled manner eventually invading surrounding tissue and/or traveling to other sites in the body disrupting the normal bodily functions and can result in death. Often the type of acquired genetic alteration in the cancer cell is one which causes the over or under production of a protein important to the regulation of cell growth, or the production of a mutant form of such a protein that is overactive or less active (or not active) or that has a different function than the normal form of the protein. This alteration in expression pattern or altered function contributes to the cancerous state.

The science and art of molecular biology applied to tumor cell lines has provided much information about how mutations contribute to the development of cancers. One group of proteins that are often mutated in cancers are receptor tyrosine kinases. These proteins sit on the cell surface and bind to molecules such as growth factors and result in the growth, maintenance and multiplication of cells. When an activating mutation occurs in a receptor tyrosine kinase the growth factor signal is no longer needed and the cell grows and multiplies uncontrollably, contributing to a cancerous state. While mutations in receptor tyrosine kinases has garnered much attention, and many drugs have been developed targeting them, these kinases are by no means the only relevant kinase family to cancer.

In the past decade there has been rapid growth in the number of FDA approved cancer drugs within the class known as kinase inhibitors. Some kinase inhibitors have become first line targeted therapy for certain tumor types. For example, imatinib (Gleevec) is used effectively to treat Philadelphia chromosome positive (Ph+) chronic myeloid leukemia (CML). The Philadelphia chromosome encodes the mutant BCR-Abl kinase, an oncogenic driver for CML.

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Unfortunately, resistance to kinase inhibitors can develop through up-regulation of the target kinase, or mutation of the target kinase resulting in decreased drug binding.

In the most ideal sense of targeted therapy for cancer, kinase inhibitors have the potential to fulfill the goal of personalized cancer therapy. Studies have shown kinase inhibitors targeting specific kinases that drive a proportion of patients' tumors can provide better outcomes for those patients. Combine this outcome with the possibility of mutant selective kinase inhibitors which may leave tissue that expresses wild-type kinase largely unaffected and provide a potentially better safety profile.
