A drug that could stop cancer cells repairing themselves has shown early signs of working.
More than half of the 40 patients given berzosertib had the growth of their tumours halted.
Berzosertib was even more effective when given alongside chemotherapy, the trial run by the Institute of Cancer Research (ICR) and the Royal Marsden NHS Trust suggested.
The trial was designed to test the safety of the drug.
The drug is the first to be trialled of a new family of treatments, which block a protein involved in DNA repair.
Blocking this protein prevents cancers from mending damage to their cells.
It’s part of a branch of treatment known as “precision medicine”, which targets specific genes or genetic changes.
The study involved patients with very advanced tumours, for whom no other treatment had worked.
This was what is known as a “phase one” trial, which is only designed to test the safety of a treatment.
But the ICR said the researchers did find some early indications that berzosertib could stop tumours growing.
One of the study’s authors, Prof Chris Lord, a professor of cancer genomics at the ICR, said these early signs were “very promising”, adding that it was unusual in phase one trials to see a clinical response.
Further trials will be needed to demonstrate the drug’s effectiveness, though.
“This study involved only small numbers of patients…Therefore, it is too early to consider berzosertib a game changer in cancer treatment,” said Dr Darius Widera at the University of Reading.
“Nevertheless, the unusually strong effects of berzosertib, especially in combination with conventional chemotherapy, give reasons to be optimistic regarding the outcomes of follow-up studies.”
Philip Malling, a 62-year-old who was diagnosed with bowel cancer in 2012, was enrolled on the trial after two years of unsuccessful chemotherapy.
“I was told ‘there’s nothing more we can do for you’,” he said. “In April 2014, I was told ‘you’ll probably be dead by Christmas'”.
He has now been receiving berzosertib treatment for six years, his tumours have shrunk and his condition is stable.
“It means everything,” Mr Malling told the BBC.
Another patient, whose ovarian cancer returned following a different course of treatment, saw her tumours shrink after combination treatment with the drug and chemotherapy.
Chemotherapy works by damaging cancer cells’ DNA, so using it in conjunction with this new treatment, which stops the cells from repairing themselves, appears to give an even greater benefit.
And berzosertib is able to target tumour cells without affecting other healthy cells, Prof Lord said.
“Our new clinical trial is the first to test the safety of a brand-new family of targeted cancer drugs in people, and it’s encouraging to see some clinical responses even in at this early stage,” said Professor Johann de Bono, head of drug development at the ICR and the Royal Marsden.
In the future, these drugs could be used to “boost the effect of treatments like chemotherapy” and tackle resistance that could develop to other targeted treatments, he added.
Whereas the traditional approach to cancer treatment has been to categorise it by tumour site – breast cancer, lung cancer and so on – the precision-medicine approach targets the genetic abnormality in the tumour, regardless of where it is.
Precision approaches are already used, for example in prostate cancers to block the effect of the testosterone hormone involved in the tumour’s growth.
If used alone this could provide a less aggressive option than chemotherapy, which attacks cells indiscriminately.
The next phase of trialling berzosertib is already under way.
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