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Treating based upon EGFR mutations
The table below summarises the different types of EGFR mutations and provides information on whether patients with those mutations are likely to benefit from gefitinib against TKi therapy.
Mok 2009, Kim 2008, Hirsch 2006
Category | EGFR mutation description | % of known activating EGFR mutations | Data supporting sensitivity to gefitinib | |
1 | Exon 19 deletions; L858R | ~90% | Yes | Exon 19 deletions and the L858R mutation constitute ~90% of the EGFR mutations identified to date. In patients with tumours that are positive for these mutations, the current data supports sensitivity to gefitinib. |
2 | T790M/exon 19 deletions; T790M/L858R; G719X; L861Q; S7681 | ~7% | Limited# | NSCLC patients can have tumours that are positive for more than one EGFR mutation type. These are known as double mutations and are predominantly seen with T790M & an exon 19 deletion or T790M & L858R. In patients with tumours with other rare mutations listed here, there is very limited data to support sensitivity or resistance to gefitinib. |
3 | T790M alone; exon 20 insertions; other mutations | ~3% | None# | The exon 20 point mutation T790M (T790M alone), and the exon 20 insertions make up ~3% of the EGFR TK mutations identified to date. In patients with tumours positive for these mutations, there are currently no data to support sensitivity to gefitinib. Some screening methodologies such as sequencing may identify novel EGFR mutations where there will be no clinical or pre-clinical data to guide use of gefitinib. |
#Due to lack of data it is difficult to draw definitive conclusions on the sensitivity or lack of sensitivity to gefitinib in these mutation types, because they only constitute ~10% of all EGFR TK mutations. Few patients in global AstraZeneca studies have been identified with these types of EGFR TK mutations.
A downloadable version of the EGFR mutation report is available from here.