Targeting Bacteria to Improve Cancer Therapy

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Science  05 Nov 2010:
Vol. 330, Issue 6005, pp. 766-767
DOI: 10.1126/science.1198310

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The activity of many drugs is constrained by their metabolism. Agents that are administered as precursors (“prodrugs”) require enzymatic conversion to an active form; conversely, drugs given as active small molecules are converted to excretable entities or degraded by metabolic processes. In the clinic, this knowledge of drug metabolism has been exploited to enhance the efficacy of some drugs. On page 831 of this issue, Wallace et al. demonstrate that inhibiting an enzyme (β-glucuronidase) produced by good gut flora can prevent the intestinal metabolism of the anticancer drug irinotecan, thereby diminishing a life-threatening toxicity and conceivably allowing dose escalation that will enhance the drug's efficacy (1).