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New hope for ways to overcome drug resistance in lung cancer

Published on July 13, 2006 at 4:10 AM · No Comments

Scientists have suggested it may be possible to reverse drug resistance in lung cancer patients, thereby improving the effectiveness of chemotherapy, according to research published in the EMBO Journal.

Most lung cancer deaths are the result of tumours becoming drug resistant, which blocks the cancer-killing effects of chemotherapy. Now Cancer Research UK scientists have discovered the molecular basis of how a type of cancer called small cell lung cancer becomes resistant to treatment. They have identified a number of key proteins in the process that might also promote drug resistance in other forms of cancer.

The research raises the prospect of developing drugs to counteract this type of drug resistance and enable existing chemotherapy to successfully treat more lung cancer patients.

Lung cancer is the most common cancer in the world today and it accounts for more cancer deaths in the UK than any other form of cancer. About 20 per cent of lung cancers are small cell lung cancers. Most small cell lung cancer patients can only be treated with chemotherapy because most are undetected until the disease is at an advanced stage when it is too late for surgery.

Tumours with a protein called FGF-2 are known to be less likely to respond to treatment. The research team, led by Professor Michael Seckl and Dr Julian Downward, found that this is because FGF-2 is involved in the development of resistance to chemotherapy drugs.

Prof Seckl, of Cancer Research UK's Lung Cancer Biology Group at Imperial College London, said: "The main reason people die of lung cancer is drug resistance. We need to understand the precise mechanisms behind it or we will not be able to beat the disease."

Dr Downward, head of Cancer Research UK's Signal Transduction laboratory, said: "Looking at FGF-2 led us to other molecules required for drug resistance, particularly one called S6K2. We knew that S6K2 existed but no one knew exactly what it did before now. It seems to regulate a number of proteins that control whether cells live or die. It is also essential for the development of drug resistance in small cell lung cancer."

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