Triple treatment keeps cancer from coming back
LUNG cancer is the leading cause of cancer death worldwide, responsible for some 1.59 million deaths a year. That figure is due, in part, to the fact that the cancer often returns after what, at first, seems to be successful treatment. And the recurring cancer is often resistant to the chemotherapy and other drugs that originally drove it into remission.
According to new research by the Weizmann Institute’s Prof. Yosef Yarden, a new strategy involving a three-pronged approach might keep an aggressive form of lung cancer from returning.
The research, says Yarden, arose out of some puzzling results of clinical trials. One class of relatively common lung cancers, which carry a particular mutation in a receptor on the cell membrane, called EGFR, can be treated with a sort of “wonder drug.”
This drug keeps a growth signal from getting into the cell, thus preventing the deadly progression and spread of the cancer. But within a year, those with this mutation invariably experience new cancer growth, usually as a result of a second EGFR mutation.
To prevent this from happening, researchers had tried to administer another drug, an antibody that is today used to treat colorectal cancer. This drug also obstructs the passing of the growth signal by stopping EGFR. Even though the antibody drug should have been able to effectively block the EGFRs – the growth receptors – including those generated by the second mutation, clinical trials of this drug for lung cancer did not produce results.
“This finding ran counter to everything we knew about the way tumors develop resistance,” says Yarden.
How do the cancer cells manage to circumvent the blockade put up by an anti-EGFR antibody?
In the new study, which appeared Thursday in Science Signaling, Yarden and his student Maicol Mancini discovered what happens to cancer cells when they are exposed to the receptor-blocking antibody.
“The blocked receptor has ‘siblings’ – other receptors that can step up to do the job,” says Yarden. Indeed, the team found that when the main receptor (EGFR) continued to be blocked, one of the cell’s communication networks was rerouted, causing the siblings to appear on the cell membrane instead of the original receptor.
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