A new model, vetted by experiments on lung cancer cells, may help to explain how cancer and other diseases accumulate drug-resistance mutations that can compromise the effectiveness of treatments.
During the past 50 years, researchers have accumulated a massive arsenal in our war on cancer. Well over 500 drugs have been approved to treat tumors, but cancer remains the second leading cause of death in the United States. The problem is partly due to drug resistance—the emergence of treatment-resistant mutants of the original disease. Now a study led by Jeff Maltas of Cleveland Clinic and Case Western Reserve University, both in Ohio, puts forward a model explaining why drug resistance is so common, vetting the model with experiments on lung cancer cells [1]. This model indicates that treatment-resistant mutants can be present in larger-than-expected numbers before treatment begins. The conclusion implies that we cannot understand cancer evolution by looking at individual mutations in isolation; instead, we should consider each tumor as an interacting ecosystem.
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