Dr. Cohen Discusses Head and Neck Cancer Pathways

Ezra Cohen, MD
Published: Tuesday, Nov 29, 2011

Ezra Cohen, MD, Associate Professor of Medicine, University of Chicago, discusses the next steps for head and neck cancer signaling pathways, specifically for patients that do not respond to the inhibition of the epidermal growth factor receptor (EGFR).

Cohen explains that every head and neck cancer expresses EGFR to some degree. The amount the tumor depends on the EGFR pathway for its survival varies from a complete reliance to none at all. If inhibiting EGFR is not effective another target may be active parallel or downstream from the pathway.

The mammalian target of rapamycin (mTOR) in the phosphatidylinositol 3-kinase (PI3K)/Akt pathway seems to be a logical choice for inhibition in patients that do not respond to EGFR treatment. If this pathway is active it may be signaling independently from EGFR and would need to be targeted separately.

There are targeted agents that could aid in inhibiting these pathways but it is still unclear exactly which head and neck cancer patients will respond to PI3K/Akt/mTOR inhibitors. The next step is to take a closer look at the patients not responding to EGFR treatment and discover why and if another pathway is active.

Ezra Cohen, MD, Associate Professor of Medicine, University of Chicago, discusses the next steps for head and neck cancer signaling pathways, specifically for patients that do not respond to the inhibition of the epidermal growth factor receptor (EGFR).

Cohen explains that every head and neck cancer expresses EGFR to some degree. The amount the tumor depends on the EGFR pathway for its survival varies from a complete reliance to none at all. If inhibiting EGFR is not effective another target may be active parallel or downstream from the pathway.

The mammalian target of rapamycin (mTOR) in the phosphatidylinositol 3-kinase (PI3K)/Akt pathway seems to be a logical choice for inhibition in patients that do not respond to EGFR treatment. If this pathway is active it may be signaling independently from EGFR and would need to be targeted separately.

There are targeted agents that could aid in inhibiting these pathways but it is still unclear exactly which head and neck cancer patients will respond to PI3K/Akt/mTOR inhibitors. The next step is to take a closer look at the patients not responding to EGFR treatment and discover why and if another pathway is active.


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