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Cold sore virus could treat cancer

27th May 2015


Scientists have the first proof that a new way of combating cancer, using genetically modified viruses to attack tumour cells, can benefit patients.

Specialists at the NHS Royal Marsden Hospital and the Institute of Cancer Research (ICR) confirmed that melanoma skin cancer patients treated with a modified herpes virus (the virus that causes cold sores) had improved survival – a world first.

In some patients, the improvements were striking. Although all had aggressive, inoperable malignant melanoma, those treated with the virus therapy – known as T-VEC – at an earlier stage survived on average 20 months longer than patients given an alternative.

In other patients results were more modest, but the study represents a landmark: it is the first, large, randomised trial of a so-called oncolytic virus to show success. Cancer scientists predict it will be the first of many in the coming years.

The method – known as viral immunotherapy – works by launching a two-pronged attack on cancer cells. The virus is genetically modified so that it can’t replicate in healthy cells – meaning it homes in on cancer cells.

It multiplies inside the cancer cells, bursting them from within. At the same time, other genetic modifications to the virus mean it stimulates the body’s own immune response to attack and destroy tumours.

Other forms of immunotherapy – the stimulation of the body’s own immune system to fight cancer – using antibodies rather viruses, have been developed into successful drugs. It is hoped that T-VEC could be used in combination with these.

Findings from trials of T-VEC, which is manufactured by the American pharmaceutical company Amgen, have already been submitted to drugs regulators in Europe and the USA. Viral immunotherapies are also being investigated for use against advanced head and neck cancers, bladder cancers and liver cancers.

Kevin Harrington, UK trial leader and professor of biological cancer therapies at the ICR and an honorary consultant at the Royal Marsden, said he hoped the treatment could be available for routine use within a year in many countries, although it would need to pass the UK’s own regulatory approval before it could be prescribed here. “I hope, having worked for two decades in this field, that it really is the start of something really exciting,” said Professor Harrington. “We hope this is the first of a wave of indications for these sorts of [cancer fighting] agents that we will see coming through in the next decade or so.”

Professor Paul Workman, chief executive of the ICR said: “We may normally think of viruses as the enemies of mankind, but it’s their very ability to specifically infect and kill human cells that can make them such promising cancer treatments.”

The study, which is published in the Journal of Clinical Oncology, included 436 patients, all of whom had aggressive, inoperable malignant melanoma. More than 16 per cent of patients were responding to treatment after six months, compared to 2.1 per cent who were given a control treatment. Some patients were still responding to treatment after three years.





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