WHAT YOU NEED TO KNOW:
- A promising new cancer treatment uses a weakened herpes virus to destroy cancer cells.
- RP2 was engineered to selectively infect cancer cells, causing them to explode and alert the immune system.
- The drug is still in early trial stages but has already helped a patient become cancer-free for over two years.
A weakened herpes virus modified to attack cancer cells has shown potential to be a new cancer therapy. A 39-year-old patient who had tried other treatments to no avail saw his oral cancer disappear after the treatment.
Krzysztof Wojkowski of west London told BBC that he had cancer of the salivary glands. Even after several treatments, it still continued to grow. He was running out of options until he learned about the experimental drug, which was available through a phase one safety trial in the UK’s Institute of Cancer Research.
Thanks to the RP2 drug, Wojkowski has been cancer-free for two years and counting.
The therapy modified a weakened form of herpes simplex, a virus that causes cold sores, to leave normal cells alone while selectively infecting cancer cells. Unlike most cancer drugs that work systemically, RP2 is injected directly into a tumor.
After the virus has infiltrated the tumor, it replicates itself until the cancer cell explodes, alerting the immune system to attack what remains.
There is still more research needed to determine how RP2 holds up to other therapies.
The drug seemed to help some patients, with some tumors shrinking. However, it did not cause a significant change in the majority of the participants. The therapy only benefited three out of nine patients who received the therapy alone, and seven out of 30 who received the therapy in combination with another treatment. The therapy also only caused mild side effects, such as fatigue.
A similar therapy based on a herpes simplex virus, called T-Vec, was approved in 2015 as a treatment for advanced skin cancer. This therapy was engineered to include a gene that stimulates the production of immune cells to bolster the immune system.
Jonathan Zager of the Moffitt Cancer Center, who was not involved in the trial but had treated hundreds of patients since T-Vec’s approval, expressed optimism about RP2 and how it could inspire other similar treatments in the future. He also noted that tumors that were once resistant to treatment now respond favorably to T-Vec or RP2.
Like Wojkowski, many patients who participated in the clinical trials had already tried other treatments or surgeries and were out of options until they heard about RP2.
Lead researcher Kevin Harrington said that the early findings suggest that RP2 may even work better than T-Vec. He noted that since RP2 has other modifications, “when it gets into cancer cells it effectively signs their death warrant.”
Harrington added that RP2 showed “truly impressive” treatment responses for different kinds of cancer, such as esophageal cancer and even a rare type of eye cancer.