London: A new strategy involving a three-pronged approach may keep an aggressive form of lung cancer from returning, says a research.

The study done on mice found that the treatment stopped lung cancer cells from developing resistance to chemotherapy.

Cancer often returns after what, at first, seems to be successful treatment.

“This finding ran counter to everything we knew about the way tumours develop resistance,” said Yosef Yarden at Weizmann Institute of Science, Israel.

The team discovered what happens to cancer cells when they are exposed to the receptor-blocking antibody.

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 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 tried to administer another drug, an antibody that is used to treat colon cancer.

This drug also obstructs the passing of the growth signal by stopping EGFR.

The researchers uncovered the chain of protein communication in the new network that ultimately leads to appearance of the sibling growth receptors.

Yarden and his team created new monoclonal antibodies that could target the two main growth receptor siblings, named HER2 (the target of the breast cancer drug Herceptin) and HER3.

The idea was to give all three antibodies together – the two new ones and the original anti-EGFR antibody – to pre-empt resistance to the treatment.

The team tried the three-pronged approach on mouse models of lung cancer that had the secondary, resistance mutation.

In these mice, the tumour growth was almost completely halted.

“Treatment by blocking a single target can cause a feedback loop that ultimately leads to a resurgence of the cancer,” Yarden said.

The study appeared in the journal Science Signalling.