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Patients who have colorectal cancer with
RAS
mutations in exon 2 are unlikely to respond to EGFR blockers. A retrospective analysis of tumors containing other, less common
RAS
mutations confirms that any
RAS
mutation is associated with EGFR resistance.
KRAS
mutation is an established predictive biomarker of resistance to anti–epidermal growth factor receptor (EGFR) therapy in patients with metastatic colorectal cancer.
1
–
4
Specifically, patients with
KRAS
mutations in exon 2 do not have a response to anti-EGFR therapy and may have inferior outcomes if this therapy is combined with an oxaliplatin-containing chemotherapy regimen.
2
,
5
More accurate selection of patients according to the genetic status of the tumor may improve the benefit–risk profile of anti-EGFR therapy.
Activating mutations in
RAS
(
KRAS
or
NRAS
) in addition to
KRAS
mutations in exon 2 have been suggested as negative predictive biomarkers . . .