The 39-year-old patient told the BBC that he was preparing for the end of his life when he learned about the experimental cancer drug.
Photo by Vladimir Smirnov\TASS via Getty Images
A new cancer therapy that uses a modified herpes virus to attack tumor cells showed promise in early clinical trials abroad.
The drug, called RP2, completely obliterated one patient's oral cancer. The 39-year-old told the BBC that he had cancer of the salivary glands, which continued to grow despite attempts at treatment.
He was preparing for the end of his life when he learned about the experimental drug, which was available through a phase one safety trial at the Institute of Cancer Research in the UK.
After a short course of the drug, the patient — Krzysztof Wojkowski of west London — has been cancer-free for two years and counting, he told the BBC.
Other patients in the trial saw their tumors shrink, although the majority did not have a significant change: three out of nine patients who were given the trial drug alone, and seven of 30 who received a combined treatment, appeared to benefit from the experimental therapy.
While more research needs to be done to see how RP2 compares to known therapies, the drug seemed to help some patients and only caused mild side effects, such as tiredness. These early results are promising, said Jonathan Zager of the Moffitt Cancer Center, who was not involved in the trial.
"We'll see some more studies done in the very near future, and I'm excited — certainly not disheartened or skeptical," Zager told Insider.
The experimental therapy involves a weakened form of herpes simplex — the virus that causes cold sores — that has been modified to only infect tumors.
According to results presented at a medical conference in Paris, the viral therapy is engineered to selectively enter cancer cells while leaving normal cells alone. It's injected directly into a tumor, while most other cancer drugs work systemically.
Once it has infiltrated, the virus replicates itself until the cancer cell explodes. What's unique about RP2 is that it delivers a "one-two punch" against tumors, not only destroying the cells but rallying the immune system to attack what's left, lead researcher Kevin Harrington said in a news release.
The drug works similarly to T-Vec, a viral therapy that was approved to treat advanced skin cancer in 2015. T-Vec was also engineered based on a herpes simplex virus and modified to include a gene that stimulates the production of immune cells, essentially preparing the immune system to attack.
These viral therapies hold great promise for treating multiple forms of cancer, with "truly impressive" treatment responses observed in patients with advanced esophageal cancer and a rare type of eye cancer, Harrington told the BBC.
The results are even more impressive considering that the patients recruited for clinical trials typically have tried several other treatments and surgeries to remove their cancers. Many, like Wojkowski, were out of options when they heard about RP2.
"When we have tumors that are heavily pretreated and they respond favorably — to RP2 or T-Vec — that's even more food for thought, in the sense that now we have tumors that were resistant to treatment and are responding," said Vager, who has treated hundreds of patients with T-Vec since it was approved.
According to Harrington, RP2 may work even better than T-Vec, if the early results are any indication.
"It's had other modifications to the virus so that when it gets into cancer cells it effectively signs their death warrant," Harrington told the BBC.
