esults defend the potential importance of DNA-PK-EGFR interaction in the regulation of radiosensitivity of tumor cells. Can stimulate the overexpression of EGFR different intracellular Re signaling pathways that confinement for activating a series of transcription factors NF kB, LiCH 3 and STAT, which are connected exactly for resistance to cancer therapy and result in a poor prognosis. The EGFR signaling pathway is activated by its phosphorylation on tyrosine residues, thus preventing the phosphorylation event k Nnte lead to sensitization of cells to IR. It was reported that the inhibition of EGFR tyrosine kinase radiosensitize and apoptosis in malignant glioma and childhood ependymoma. Another recent study examined the F Ability of a specific inhibitor of EGFR, cetuximab, the radiation resistance Esophagus carcinoma cell line of human radiationresistant KYSE 150R Feedb To make ngig, and showed that could cetuximab effectively reduce the resistance of radiation in these cells. cross-talk between signal mediator protein in RTK, the Ras, mitogen activated protein kinase Raf, phospholipase Cg, and contain protein kinase C are also important in cell proliferation and growth. These molecules are known to be clearer or constitutively active in cancer cell growth and maintain the property to give resistance to apoptosis. Ras gene is known to play an r The center in more than 30% of all cancers. Overexpression of Ras is proposed that a major cause for radioresistance. Ras-induced radioresistance caused by constitutive levels Nilotinib AMN-107 of activated ERK1 / 2 or other downstream mediators. Cengel et al. have shown that genetic inactivation of K ras or N rows in the c lon human tumor cells obtained ht leads radiosensitivity.
Culling strategies with Ras have also been shown radiosensitize head and neck cancer cell lines. The r In another pathway phosphatidylinositol 3-kinase AKT was involved in the development of radioresistance. PI3K AKT f Promotes the proliferation of cancer cells, survive and inhibits apoptosis. IR is known that the activation of Akt, which is an essential mediator of the way and he, therefore, the per signaling he survive Opened to induce a contribution to radioresistance. AKT, a serine / threonine kinase, was also studied as a major player in the development of radioresistance in human cancers. For more insights into his r Followed by the studies that have shown when their effects act arrange by phosphorylation of proteins as prosurvival Bad signaling and apoptosis regulating kinase 1, cell cycle progression by phosphorylation inhibitors cyclin-dependent Ngigen kinases such as p21 and p27, the cellular metabolism through the phosphorylation of glycogen synthase kinase-3 gene transcription by phosphorylation of transcription factors such as family members FKHR and protein synthesis and translation by phosphorylation of proteins such as mTOR. In fact, IkBa kinase in NF-kB activation involved also known that a substrate of AKT and activation of AKT can therefore stimulate NF be kB activity t. The activation of PI3K has been shown that the activity of t of DNA polymerase beta, one of the repair enzymes, which supplies preconcentrated, purified, a survival rate signal in Freund Erythroleuk When the IR to improve suspended.