The 'Achilles heel' of breast cancer cells has been identified, according to scientists.
A study has shed light on why the disease can return years after women appear to be free of it.
Many invasive forms of breast cancer have too much of the protein HER2 on the surface of the cancerous cells, which leads to uncontrolled growth.
HER2 is present in all human cells, but unusually high levels are found in about one in five breast and stomach cancers, known as HER2-positive types.
The cancer drugs Herceptin and Perjeta – the brand names for trastuzumab and pertuzumab, respectively – recognise HER2 but they do not kill off the cancerous cells. Instead, they only render the cells dormant, which means they can become active again at any time.
This means many women can appear to be 'cured', only for their cancer to re-awaken years later.
In a study published in Nature Communications, researchers from Zurich University aimed to find out why these drugs merely slow the growth of tumours, rather than destroy them.
HER2 uses several signalling pathways at the same time to inform a cell that it should grow and divide. Currently available drugs block only one of those signalling pathways, while others remain active.
But now scientists believe they have developed a method to switch off all the signals, using a protein compound that binds to HER2 and changes its structure.
This prevents any growth signals being transmitted to the cell's interior, causing the cancer cell to die.
Crucially, the technique targets only cancer cells, leaving healthy ones unharmed.
Professor Dr Andreas Pluckthun, of Zurich University, said: 'Now that we have identified the Achilles heel of HER2-positive cancer cells, new opportunities are opening up for treating invasive tumour types like breast cancer more effectively in the future.'
Meanwhile, separate research has shown that up to 1,200 patients with one of the deadliest types of cancer could survive for at least five years using a different method of treatment.
It reveals that offering a combination of two chemotherapy drugs for pancreatic cancer is far more effective than one on its own.
Scientists from Liverpool University studied 732 patients who underwent surgery followed by chemotherapy at hospitals in the UK, Germany, Sweden and France.
About half were offered the standard chemotherapy of gemcitabine alone and half were offered a combination of gemcitabine and capecitabine.
The study – which will be presented at the American Society for Clinical Oncology cancer conference – shows 29 per cent of patients given the combined drugs lived at least five years, compared with only 16 per cent of patients given just gemcitabine. It suggests about 1,200 patients a year could benefit from the technique.
The findings were so compelling they have prompted experts to change the treatment guidelines for pancreatic cancer. From now on, doctors will be told to offer both chemotherapy drugs.
Pancreatic cancer is one of the deadliest forms and there are 9,400 new cases and 8,800 deaths in the UK each year.
Professor John Neoptolemos of Liverpool University said: 'This important trial shows that this drug combination could give pancreatic patients valuable extra months and even years and so will become the new treatment for patients with this disease.
'The difference in short-term survival may seem modest, but improvement in long-term survival is substantial for this cancer.
'Although pancreatic cancer is difficult to treat, finding drugs that will shrink the tumour enough to make it suitable for surgery will help in the fight against this disease.
'We've learnt a lot about pancreatic cancer from our clinical trials and now this drug combination will become the new standard of care for patients with the disease.'
Cancer Research UK's Professor Peter Johnson said: 'Nearly 10,000 people are diagnosed with pancreatic cancer each year in the UK and it remains a very difficult disease to find and treat. Despite this we are making steady progress through trials like this one, where the use of better chemotherapy after surgery was able to increase the number of people surviving the disease.'
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