A press release from Amgen has reported that patients with previously treated metastatic colorectal cancer with KRAS wild-type have delayed cancer progression following treatment with Vectibix® (panitumumab) and chemotherapy.
Vectibix is a new targeted therapy that binds to specific targets on cancer cells. Vectibix targets the epidermal growth factor receptor (EGFR), a biologic pathway that is involved in the growth and spread of cancer. Vectibix, which is FDA approved, is often used in combination with chemotherapy for the treatment of colorectal cancer. Vectibix appears to benefit only those patients whose cancers do not contain a mutation in a gene known as KRAS. KRAS mutations occur in an estimated 40-50% of metastatic colorectal cancers and can be identified by testing a sample of tumor tissue.
To evaluate the effectiveness of Vectibix in the second-line treatment of metastatic colorectal cancer, researchers conducted a Phase III clinical trial among 1,186 patients. Study participants were assigned to receive treatment with FOLFIRI chemotherapy alone or FOLFIRI plus Vectibix.
Among patients without KRAS mutations, the addition of Vectibix significantly improved progression-free survival. Among patients with KRAS mutations, the addition of Vectibix did not affect progression-free survival. Vectibix did not significantly affect overall survival in either study group. Side effects of Vectibix included skin rash, low magnesium levels, and diarrhea. Full results from this study are expected to be presented at an upcoming medical meeting.
Comments: These results suggest that the addition of the targeted therapy Vectibix to second-line chemotherapy improves progression-free survival among patients with metastatic colorectal cancers that do not contain KRAS mutations.
Reference: Amgen press release. Vectibix® significantly improved progression-free survival in second-line treatment of KRAS wild-type metastatic colorectal cancer. Available at: http://wwwext.amgen.com/media/media_pr_detail.jsp?releaseID=1321626. Accessed August 24, 2009.
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