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Future development of these technologies, especially siRNA Tze many years for a new class of drugs that may inactivate a specific and helpful HER2 oncogenic function. Resistance downstream HER2 inhibitors quite a few mutational occasions Rts described growth factor receptors in cancer. Ren will activate BRAF mutations in AR, PIK3CA and inactivating mutations or deletions of PTEN. since these genes downstream rts perform rts HER2 and considering that each and every induces these mutations constitutive Signalaktivit t, at least in idea, k downstream can mutations K-dependent rts rtigen tumor development of HER2 HER2 usually means made dependent and-dependent independently decouple the ideal everlasting HER2 inhibitors. In breast cancer and BRAF mutations are rare Ras, but HER2 overexpression happens h PIK3CA mutations typically in h, but only hardly ever.
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