Reducing Chemotherapy Toxicity for Colon Cancer Patients

Everyone responds differently to medicines. The dose of a drug that cures one person can be ineffective-or even toxic-in someone else. Although many non-genetic factors play a role in how an individual patient responds to a particular drug treatment, many differences in drug response come from genetic variation. Individualizing a drug's dose based on pharmacogenomic information can help a patient get the most benefit from a drug while minimizing side effects.

Take the example of treating colorectal cancer with a chemotherapy regimen that includes Camptosar (irinotecan). A gene, called UGT1A1, produces an enzyme that metabolizes Camptosar. Variations in this gene can influence a patient's ability to break down the drug.

About 10 percent of the North American population has a variation of the UGT1A1 gene that reduces their ability to metabolize Camptosar, leading to high blood levels of the drug and a higher risk of toxic side effects. If these patients are given standard doses of Camptosar, about half will develop severe neutropenia, which can be fatal.
A test, called the Invader UGT1A1 Molecular Assay, can identify whether a patient has the genetic variant affecting the metabolism of Camptosar and thus would be at higher risk for developing severe neutropenia. The drug label says to consider lowering the starting dose of the Camptosar for those patients found to be high risk.

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