Escape from HER-family tyrosine kinase inhibitor therapy by the kinase-inactive HER3

Natalia V. Sergina, Megan Rausch, Donghui Wang, Jimmy Blair, Byron Hann, Kevan M. Shokat and Mark M. Moasser ()
Additional contact information
Natalia V. Sergina: University of California
Megan Rausch: University of California
Donghui Wang: University of California
Jimmy Blair: University of California
Byron Hann: University of California
Kevan M. Shokat: University of California
Mark M. Moasser: University of California

Nature, 2007, vol. 445, issue 7126, 437-441

Abstract: Targeted cancer therapies Certain tyrosine kinases are overactive in many cancers, and drugs that inhibit them, such as the leukaemia treatment imatinib, can be successful. But they don't work for all tyrosine kinase-driven cancers, and new work points to a possible reason why. The kinase HER2 is frequently overactive in breast cancers and signals through another family member, HER3. Sergina et al. find that when HER2 is partially blocked by kinase inhibitors, a feedback mechanism causes an increase of active HER3 at the plasma membrane where it continues to signal cancer cell proliferation. So more effective inhibitors that block HER2 completely, and reduce HER3 activity too, may be more effective cancer therapies.

Date: 2007
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DOI: 10.1038/nature05474

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