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Overcoming Drug Resistance In Cancer

Overactive epidermal growth factor receptor () signaling has been linked to the development of .

Several have been developed to treat these EGFR-associated cancers; however, many patients have developed resistance to these drugs and are therefore no longer responsive to .

In a recent research article published in the Journal of Clinical Investigation, Goutham Narla and colleagues at Case Western Reserve University sought to better understand the molecular players in the EGFR signaling pathway in hopes of finding new drug targets for EGFR-associated cancers.

Using cancerous human lung tissue and a mouse model of EGFR-associated , The Narla team discovered that two tumor suppressor genes, KLF6 and FOXO1, function to disrupt overactive EGFR signaling.

After treating the cancerous lung tissue and cancer-prone mice with an FDA-approved drug called trifluoperazine hydrochloride (TFP), which increases the activity of FOXO1, they restored the effectiveness of the anti-EGFR drug erlotinib and reduced tumor growth.

Their work identified new drug targets for EGFR-associated cancers and suggests that combinatorial regimens may improve treatment outcome.

TITLE: Targeting the FOXO1/KLF6 axis regulates EGFR signaling and treatment response

http://www.jci.org/articles/view/62058?key=9eb9f31baf7df0c3365e

Source

Journal of Clinical Investigation