A modified version of the herpes virus has been used to treat skin cancer patients, and one in four have responded positively to the treatment, remaining in remission at least six months afterwards.
The results come from a clinical trial in the UK involving more than 400 patients with aggressive melanoma, who signed up to be treated through virotherapy - a technique that uses altered viruses to attack specific pathogens such as cancer cells. "This is the big promise of this treatment. It’s the first time a virotherapy has been shown to be successful in a phase 3 trial," lead researcher Kevin Harrington, from the Institute of Cancer Research London, told Hannah Devlin at The Guardian.
The herpes-based drug, named Talimogene Laherparepvec (T-VEC), has proven so effective, Harrington and his team hope to see it on the market by 2016. A successful phase 3 trial means the only remaining hurdle for it to be sold commercially in the US and Europe by pharmaceuticals company, Amgen, is to get approval from the FDA and the European Medicines Agency.
The drug is administered once every two weeks for up to 18 months, and while participants in the trial received flu-like side effects after the first few injections, this was far preferable to the side effects that come with chemotherapy drugs.
According to the study, published in The Journal of Clinical Oncology, of the 436 patients with inoperable melanoma, 16.3 percent of them were still in remission six months after the treatment, compared to 2.1 percent in the control group, who were treated using immunotherapy, which boosts a patient’s immune response to the cancer.
Of those who took the T-VEC drug, 10 percent of the patients were in 'complete remission', having showed no signs of the cancer following the treatment, and during the trial, the T-VEC group lived an average of 41 months, while the control group lived an average of 21.5 months, showing a significant increase in the survival rate.
This is pretty incredible, because each of the patients, whether they’d had a relapsed or metastatic form of the cancer, were too far along to respond to conventional treatments, says Devlin at The Guardian. But the drug worked on a quarter of them, even if the cancer had spread to various other organs in the body. "They had disease that ranged from dozens to hundreds of deposits of melanoma on a limb all the way to patients where cancer had spread to the lungs and liver," Harrington told her.
Harrington, who has been developing the treatment for over 10 years, has been trying it out across a range of different cancer types, and found that melanoma responded the most positively to it. The team figured out how to harness its amazing capacity for replication by removing two genes that made it impossible for it to multiply inside healthy cells, but it still had its run of things inside the cancerous melanoma cells.
"Meanwhile, T-VEC has also been modified to produce a molecule called GM-CSF, which serves as a red flag waved at the immune system," Rachel Feltman reports for The Washington Post. "So in addition to the destructive power of the T-VEC cells themselves, the therapy summons the immune system right to where it's needed - the tumour."
The team will continue to test out the drug on other forms of cancer through clinical trials, and are keenly awaiting the decision of the European and American drug regulatory boards. If approved, they say the treatment will be made widely available to patients by 2016.