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Cancer

Polytherapy for lung cancer

Nature Reviews Drug Discovery volume 14, page 680 (2015)Cite this article

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Drug resistance in most oncogene-driven cancers is typically addressed after it has emerged. Here, Hrustanovic et al. investigate the potential of using an upfront polytherapy that targets both the primary oncoprotein and a critical effector of the oncoprotein. First, they identified that EML4–ALK-driven lung adenocarcinoma cells are dependent on RAS–MAPK signalling. In vitro and in individuals with EML4–ALK-positive lung adenocarcinoma, MAPK pathway reactivation was associated with resistance to ALK inhibitors. In preclinical models of EML4–ALK lung adenocarcinoma, co-inhibition of ALK and MEK1/2 increased the magnitude and duration of the initial clinical response.

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References

  1. Hrustanovic, G. et al. RAS–MAPK dependence underlies a rational polytherapy strategy in EML4–ALK-positive lung cancer. Nat. Med. 21, 1038–1047 (2015)

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  1. Sarah Crunkhorn
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Crunkhorn, S. Polytherapy for lung cancer. Nat Rev Drug Discov 14, 680 (2015). https://doi.org/10.1038/nrd4753

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