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Most patients with an EGFR mutation respond to these drugs; however, a proportion show limited or no tumor response.
In general, about 80% of NSCLCs with EGFR mutation respond to EGFR-TKIs, whereas 10% of tumors without EGFR mutations do so [ 13].
While several patients with KRAS codon 146 mutation respond to anti-EGFR antibody therapy, 7 we assume that further subgroup analyses of RCT may provide information to conclude these issues.
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In the drug's earliest trial, nearly every patient whose tumor cells contained the B-RAF mutation responded to the drug.
The patient harboring this mutation responded to therapy (PR).
The laboratory selection experiment found that L1014F mutation frequency, but not L1014S mutation, responded to deltamethrin selection, suggesting that the L1014F mutation is the key mutation conferring resistance to deltamethrin.
Both patients with a KCNJ11 mutation responded to oral sulphonylurea.
Thus far, few studies have shown EGFR mutation in SQCLC, and patients with activating EGFR mutation responded to TKIs treatment [ 11].
None of the patients bearing BRAF mutation responded to the treatment, in comparison with 24 32%) of 74 patients with BRAF wild-type disease (P=0.016; Table 3C).
In the patient group reported by Heinrich et al (2006b), 37% of the imatinib-resistant GISTs with a primary exon 9 mutation responded to sunitinib, as compared with 5% of cases with a primary exon 11 mutation.
Anecdotal reports of patients with diverse cancers and HER2 amplification or mutation responding to anti-HER2 agents have been published [ 15– 18], implying a potential role for anti-HER2 agents outside of breast and gastric cancer.
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Since I tried Ludwig back in 2017, I have been constantly using it in both editing and translation. Ever since, I suggest it to my translators at ProSciEditing.

Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com