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Common deworming drug helps restore lung cancer's sensitivity to targeted therapy in mice

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Common deworming drug helps restore lung cancer's sensitivity to targeted therapy in mice

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A form of lung cancer, which is found in about 10%–15% of Western patients and 40%–50% of Asian patients, is driven by a mutation in the epidermal growth factor receptor (EGFR) gene. Gefitinib is a go-to drug that shuts down this protein's signals. However, over time, cancer cells develop resistance to the drug and keep dividing even while treatment is underway, rendering gefitinib powerless. A recent study published in PLOS One has found a way out of this resistance trap.

Rather than developing an entirely new drug to resensitize drug-resistant lung cancer cells and significantly slow tumor growth, researchers turned to an existing deworming drug, mebendazole (MBZ), pairing it with gefitinib. The two drugs attacked cancer in different ways. Gefitinib targeted the tumor's growth signaling pathway, while mebendazole disrupted microtubules, the internal cellular scaffolding cancer cells rely on to divide and transport proteins.

With gefitinib alone, the survival rate of resistant lung cancer cells was 92.7%, and with MBZ alone, it was 80%. However, combining a low dose of MBZ with gefitinib dropped cell survival to 37.7%.

Lung cancer is a growing public health crisis, with the numbers of people who get it and die from it continuing to rise each year. It is the second most common cancer and the main cause of cancer deaths worldwide. 8 million deaths, making up 15% of all new cancer cases and a quarter of all cancer-related deaths.


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