Using a common antiparasitic medication, scientists found a way to slow the spread of drug-resistant lung cancer. Cancer therapies often face a formidable roadblock when malignant cells acquire resistance to standard targeted treatments like gefitinib. To overcome this hurdle, researchers evaluated a two-pronged therapeutic strategy by pairing gefitinib with mebendazole, an established antiparasitic medication commonly used to treat worm infections. While gefitinib works by shutting down growth signals driven by mutated proteins, mebendazole disrupts the internal structural scaffolding that tumor cells rely on to divide and transport essential materials. By attacking cancer cells simultaneously from two distinct angles, the drug combination imposes severe stress on the tumor's cellular machinery. In preclinical studies, this dual approach significantly slowed tumor progression in models of treatment-resistant non-small cell lung cancer, stretching tumor doubling times compared to single-agent treatments. Laboratory tests revealed that combining low doses of mebendazole with targeted therapy triggered substantial DNA damage and cell death in resistant cancer cells. While clinical trials in humans are still needed before this regimen can enter medical practice, the findings highlight drug repurposing as a promising and cost-effective pathway to overcome treatment resistance in aggressive malignancies. source: El-Tanani, M., Satyam, S. M., Prabhakar, S., et al. (2026). Dual targeting of EGFR signaling and microtubule dynamics enhances replication-associated cellular stress and suppresses tumor growth in gefitinib-resistant non-small cell lung cancer. PLOS ONE.