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Early-phase studies have demonstrated that some neuroblastoma patients with ALK mutations respond to those agents.
It is well recognised that not all KCNJ11 mutations respond to oral sulphonylurea therapy (28).
Furthermore, patients with ABCB4 mutations respond to ursodeoxycholic acid, and hence it is feasible that the SNPs reported in this study will be associated with treatment response.
Most patients with exon 11 mutations respond to treatment with imatinib, while less than half of those with exon 9 mutations respond and are almost twice as likely to recur [ 16- 18].
According to the data for 1170 patients, more than 70% of NSCLCs with EGFR mutations respond to EGFR-TKIs, whereas 10% of tumours without EGFR mutations do so (Table 1).
Previous studies have determined that although cell-based assays overexpressing APP mutations respond to first-generation NSAID GSMs, cell-based assays overexpressing PS1 mutations for the most part do not.
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None of the patients with tumors exhibiting BRAF mutations responded to an EGFR antibody treatment, wheras none of the responders to the treatment had BRAF mutations [ 38].
This suggests that previously reported outliers, i.e., very uncommon cases of mCRC with KRAS mutations responding to therapy [9], [14], [29], [34] may be patients harboring only one of these molecular alterations, thus not concurrently deregulating both MAPK and PI3K pathways.
Four EGFR FISH+ patients with KRAS mutations responded to cetuximab therapy.
None of the nine tumours with KRAS mutations responded to EGFR-TKIs (Pao et al, 2005b).
To begin to address this issue, we examined whether patients with low abundance EGFR sensitizing mutations responded to EGFR TKIs.
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