The right combination: Overcoming drug resistance in cancer

Public release date: 1-Jun-2012
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Contact: Sarah Jackson
press_releases@the-jci.org
Journal of Clinical Investigation

Overactive epidermal growth factor receptor (EGFR) signaling has been linked to the development of cancer. Several drug therapies 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 drug treatment. 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 lung cancer, 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 drug therapy regimens may improve treatment outcome.

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TITLE:

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

AUTHOR CONTACT:

Goutham Narla

Case Western Reserve University and University Hospitals, Cleveland, OH, USA

Phone: 347-255-0885; E-mail: Goutham.Narla@mssm.edu

View this article at: http://www.jci.org/articles/view/62058?key=9eb9f31baf7df0c3365e

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AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.

Public release date: 1-Jun-2012
[ | E-mail | Share ]

Contact: Sarah Jackson
press_releases@the-jci.org
Journal of Clinical Investigation

Overactive epidermal growth factor receptor (EGFR) signaling has been linked to the development of cancer. Several drug therapies 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 drug treatment. 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 lung cancer, 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 drug therapy regimens may improve treatment outcome.

###

TITLE:

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

AUTHOR CONTACT:

Goutham Narla

Case Western Reserve University and University Hospitals, Cleveland, OH, USA

Phone: 347-255-0885; E-mail: Goutham.Narla@mssm.edu

View this article at: http://www.jci.org/articles/view/62058?key=9eb9f31baf7df0c3365e

---

[ | E-mail | Share ]

?

AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.

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