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Two new drugs for melanoma were in the news earlier this week. These reports stemmed from research published at the world’s largest annual cancer conference, ASCO.

Dr Julie Sharp, Cancer Research UK’s Senior Science Information Manager, was there to hear the talks first hand:

A pile of newspapers

Skin cancer drug trials hit the headlines this week

At this years’ ASCO conference, Dr Antoni Ribas from the University of California in the US gave an uplifting overview of the latest progress in melanoma research.

He described 2011 as a year that has seen “major advances” in treatment for this disease after many years with limited options for patients.

In the USA, the FDA have already approved two new melanoma drugs this year, ipilimumab and peginterferon, the first new drugs for this disease for over 10 years. And at the conference this weekend the lecture theatre was buzzing with excitement as two international Phase III trials announced their latest results – which have been the subject of international media attention in the past couple of days.

Boosting the immune system

Dr Jedd Wolchok, of Memorial Sloan-Kettering Cancer Centre in New York, described a phase III trial comparing patients who were given ipilimumab in combination with dacarbazine with patients given the standard dacarbazine treatment alone. More than 500 patients from 24 countries took part in the study and all had melanoma that had spread.

Ipilimumab works by boosting the body’s immune system to fight the cancer. It interferes with the workings of a protein called CTLA-4, who’s normal function is to stop our immune system from attacking ourselves, but which also stops it from spotting and attacking cancer.

Results showed that the drug combination boosts survival – after a year 47.3 per cent of ipilimumab patients were still alive compared to 36 per cent for the standard treatment. And after three years 20.8 per cent of those given the combined treatment were still alive compared to 12.2 per cent for those on dacarbazine.

Targeting faults in BRAF

In the same session, Dr Paul Chapman also from Memorial Sloan-Kettering Cancer Centre presented results of a trial of second drug, which we’ve covered before on this blog: vemurafenib – also known as PLX4032. This is an example of a tailored (or personalised) treatment, as the drug only targets cancers which are driven by damage to a gene called BRAF.

At Cancer Research UK we’ve been following this drug’s development with keen interest, as the link between BRAF and cancer was discovered by our scientists. It’s now thought that BRAF is faulty in at least 50 per cent of melanomas, and a significant proportion of other cancers.

The latest trial to investigate vemurafenib involved 675 patients from 103 hospitals around the world. All had late-stage cancer driven by a specific fault in the BRAF gene.

Half of the patients received vemurafenib, while the other half were given the standard dacarbazine treatment. The results were striking – with 90 per cent of patients responding to vemurafenib . After three months this group had a 63 per cent reduction in the risk of death and a 74 per cent reduction in the risk of their cancer progressing.

Future hope

Both these trials offer hope for the future of melanoma treatment – set against a backdrop of soaring rates for this disease (caused by increased exposure to UV rays from the sun and sunbeds), which is extremely hard to treat once it has spread around the body.

Dr Chapman suggested that ipilimumab will be most useful in patients who have more stable, slow growing cancer, as it takes time to take effect. By contrast, vemurafenib shows quicker effects and might be the best approach for more advanced disease.

The fact that vemurafenib is used to treat patients with specific gene faults in their tumours also shows that the era of more tailored cancer treatments is dawning. The challenge now is for healthcare systems to improve and expand their genetic testing services so that, as drugs like these are approved for use, we have the resources to use them as intended.

Julie

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