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It has been suggested that patients whose tumors harbor a KRAS Gly13Asp mutation may benefit from anti-EGFR mAb therapy [ 20- 22].
These data again raise the possibility that tumours of this phenotype, expressing elevated PLK1 and harbouring TP53 mutation, may benefit from the use of novel PLK1 inhibitors [ 7].
However, as previously mentioned, evidence is now present that patients harboring the codon 13 c.38 G > A mutation may benefit from anti-EGFR treatment [ 4, 5, 14].
The findings contradict pre-clinical studies that suggest melanomas with BRAF mutation may benefit from inhibition of dual MEK and PI3K pathway inhibition [ 13, 26].
However, evidence is present that patients harboring the codon 13 c.38 G > A mutation may benefit from anti-EGFR treatment [ 4, 5].
In terms of treatment, CMMLs with a RAS pathway mutation may benefit from drugs able to target the RAS/RAF/MAPK pathway [ 33, 34] (e.g. sorafenib), while all CMMLs may benefit from therapy restoring RUNX function.
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Infants with these genetic mutations may benefit from switching to oral sulfonylurea therapy.
Therefore, ovarian cancer patients with KRAS or BRAF mutations may benefit from CI-1040 treatment.
It is possible that cell lines with BRAF and PIK3CA mutations may benefit from the combination.
Notably, several retrospective studies suggested that NSCLC patients with positive HER2 mutations may benefit from HER2-targeted therapy [ 64, 92].
For example, combination therapies to target both oncogenic and TSG mutations may benefit patients within a relevant molecularly defined segment.
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