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Mayo researchers identify dangerous 'two-faced' protein crucial to breast cancer spread and growth
Date:11/17/2008

mor suppressor when it is bound to E-cadherin, and like a tumor promoter when it isn't," Dr. Anastasiadis says.

The researchers believe these findings could help explain why in some solid tumors, such as breast, lung, kidney, and melanoma, loss of E-cadherin is associated with a more aggressive, less treatable prognosis. "We think that when E-cadherin is lost, p120 is now free to turn on growth promotion pathways that can overtake the benefits of targeted chemotherapeutics," he says.

"So in breast cancer that is HER2-positive, anti-HER2 therapies such as Herceptin will not function well if p120 has turned on alternate growth mechanisms," Dr. Anastasiadis says. "A similar effect would also be expected in EGFR-positive lung cancer and anti-EGFR treatment." Both HER2 and EGFR are growth-promotion proteins.

A potential solution would be to design an agent that targets the tumor-promoting function of p120 that is not bound to E-cadherin, he says. "This won't be easy, but based on our current understanding of p120 function we believe it is possible," says Dr. Anastasiadis.


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Contact: Paul Scotti
scotti.paul@mayo.edu
904-953-2299
Mayo Clinic
Source:Eurekalert

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