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W Although these promising therapeutic years tze a consequence of the HER2 oncogene hypothesis is E schr Ge nonspecific mechanisms of its usefulness to validate the hypothesis and are described here. Readers are completely several excellent reviews on this Ndigen NPI-2358 tze cover this year targeting HER2. Many immunological methods have continued to ensure that the defense mechanisms of the h Yourself to target cancer cells overexpressing HER2, and they are. Beyond the scope of audit Moreover tze many years specifically to suppress the expression of HER2 over the years progressed and developed. Z w choose As antisense, ribozymes and siRNAs years tze to inhibit the expression of the HER2 protein. These terms are not yet k clinically effective products that the validity of the hypothesis in patients with HER2 test can cause oncogene.
Future development of these technologies, particularly siRNA Tze years for a new class of drugs that can inactivate a specific and effective HER2 oncogenic function. Resistance downstream HER2 inhibitors many mutational events 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 work rts HER2 and since each induces these mutations constitutive Signalaktivit t, at least in theory, k downstream can mutations K-dependent rts rtigen tumor growth of HER2 HER2 means made dependent and-dependent independently decouple the best permanent HER2 inhibitors. In breast cancer and BRAF mutations are rare Ras, but HER2 overexpression occurs h PIK3CA mutations frequently in h, but only rarely.
With a PTEN mutation There are no data that overexpress HER2 coexistence mutation to determine resistance to TKI PIK3CA in breast cancer. Interestingly, the cell line used h H Frequently BT474 Moasser Page 11 Oncogene. Author manuscript 6th, April 2011 PMC. commonly referred to as a model of HER2 verst RKT with trastuzumab sensitive and ITC hosts a mutation in exon I of the database unweighted hnlichen cosmic and PIK3CA. PTEN mutations are rare in breast cancer, but reduced PTEN may have a biological significance and is h Frequently visited h in breast cancer. Loss of PTEN in EGFR TKI resistance shown in versts RKT induce breast cancer cell line, but anything similar effect was demonstrated in a HER2