MIT IDs link between brain tumor proteins

seems that it is not the activation of one receptor that results in cancer. Its the action of multiple receptors that leads to the tumors we see, said Paul Huang, a graduate student in biological engineering and lead author of the paper. A potential way to overcome this is to attack multiple targets instead of just one.

To find out what other proteins are involved in tumor growth, the researchers used a tool known as mass spectrometry to analyze the network of proteins activated by EGFRvIII in GBM tumor cells.

They found that when EGFRvIII is activated, so is another receptor called c-Met. C-Met is normally active during human development, but its turned off in most adult cells.

Until now, there had been no evidence of any cross-talk between c-Met and EGFRvIII in GBM. This discovery could offer an explanation for why GBM tumors are so invasive, because over-activated c-Met has already been implicated in very invasive types of lung and breast cancers.

The researchers dont know yet how EGFRvIII is activating c-Met, and whether other proteins are involved in the activation.

The mechanism underlying this control has yet to be fully characterized, said White. Our data shows that as EGFRvIII is activated, c-Met is activated as well. Whether its direct, or indirect, is something that we are currently deciphering.

The new knowledge of c-Mets involvement could give researchers a potent tool to attack GBM tumors. When the MIT group treated tumor cells with drugs that inhibit EGFRvIII and c-Met, respectively, much lower doses were required to kill the cells than when either drug was given alone.

There are several EGFRvIII inhibitors in clinical trials now, and some have already been approved to treat other cancers. Drug companies are also working on c-Met inhibitors, and Huang estimated that some might be available in five to 10 years.


Contact: Elizabeth Thomson
Massachusetts Institute of Technology

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