Study Explores Which Patients Respond Best to Vectibix

Posted on April 19th, 2010 by

Previous studies have reported that colorectal cancers with mutations in a gene known as KRAS do not respond well to drugs such as Vectibix® (panitumumab). In an effort to expand these findings and further individualize colorectal cancer treatment, researchers evaluated several additional genes. The results were presented at the 101st annual meeting of the American Association for Cancer Research.

Colorectal cancer remains the second leading cause of cancer-related death in the United States. Metastatic colorectal cancer refers to cancer that has spread from the colon to distant sites in the body.

Targeted therapies are anticancer drugs that interfere with specific pathways involved in cancer cell growth or survival. Some targeted therapies block growth signals from reaching cancer cells; others reduce the blood supply to cancer cells; and still others stimulate the immune system to recognize and attack the cancer cell. Depending on the specific “target,” targeted therapies may slow cancer cell growth or increase cancer cell death.

Vectibix inhibits cancer cell growth and survival by targeting a protein known as the epidermal growth factor receptor (EGFR). Vectibix has been approved for the treatment of EGFR-expressing, metastatic colorectal cancer that has progressed on or following fluoropyrimidine-, oxaliplatin-, and irinotecan-containing chemotherapy regimens. 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 explore whether other genes also influence response to Vectibix, researchers evaluated information from a Phase III clinical trial. The study compared Vectibix to best supportive care among patients with metastatic colorectal cancer. Researchers tested samples of tumor tissue for KRAS mutations as well as mutations in NRAS, BRAF, PIK3CA, PTEN, AKT1, EGFR, beta-catenin (CINN1B), and TP53.

  • Vectibix significantly improved progression-free survival among patients without KRAS mutations but did not benefit patients with KRAS mutations.
  • The NRAS gene also influenced response to Vectibix. Patients with NRAS mutations did not appear to benefit from Vectibix.

This study adds to a growing body of knowledge about which patients are most likely to respond to drugs such as Vectibix. The goal of this research is to provide more individualized and more effective cancer therapy.

Reference: Peeters M et al. Use of massively parallel, next-generation sequencing to identify gene mutations beyond KRAS that predict response to panitumumab in a randomized, Phase III, monotherapy study of metastatic colorectal cancer (mCRC). Presented at the 101st annual meeting of the American Association for Cancer Research. Washington, DC, April 17-21, 2010. Abstract LBA 8791.

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