Therapeutic resistance resulting from mutations in @entity8496 / @entity8047 / @entity3963 and XXXX / @entity983 / @entity584 / @entity3470 signaling pathways.

@entity1 @entity8047 @entity5 @entity3963 @entity584 @entity3470 @entity10412 @entity983 @entity8496
Chemotherapy remains a commonly used therapeutic approach for many @entity5 . Indeed chemotherapy is relatively effective for treatment of certain @entity5 and it may be the only therapy (besides radiotherapy) that is appropriate for certain @entity5 . However, a common problem with chemotherapy is the development of drug resistance. Many studies on the mechanisms of drug resistance concentrated on the expression of membrane transporters and how they could be aberrantly regulated in drug resistant cells. Attempts were made to isolate specific inhibitors which could be used to treat drug resistant @entity1 . Unfortunately most of these drug transporter inhibitors have not proven effective for therapy. Recently the possibilities of more specific, targeted therapies have sparked the interest of clinical and basic researchers as approaches to kill @entity5 cells. However, there are also problems associated with these targeted therapies. Two key signaling pathways involved in the regulation of cell growth are the Ras/ @entity8496 / @entity8047 / @entity3963 and @entity10412 / @entity983 / @entity584 / @entity3470 pathways. Dysregulated signaling through these pathways is often the result of genetic alterations in critical components in these pathways as well as mutations in upstream growth factor receptors. Furthermore, these pathways may be activated by chemotherapeutic drugs and ionizing radiation. This review documents how their abnormal expression can contribute to drug resistance as well as resistance to targeted therapy. This review will discuss in detail @entity983 regulation as this is a critical @entity5 suppressor gene frequently dysregulated in @entity1 @entity5 which contributes to therapy resistance. Controlling the expression of these pathways could improve @entity5 therapy and ameliorate @entity1 health.
