A cure for cancer teems through our veins, but the trick is harnessing the immune system's tumour-destroying cells, say doctors.
Now, a US team has developed a new way to turn a patient's T-cells against a deadly, metastasised skin cancer. A 55-year old man who received the immune boost lives tumour-free, more than two years after treatment.
"He had a remarkable response," says Cassian Yee, an immunologist at Fred Hutchinson Cancer Research Center in Seattle, Washington, US, who developed the new treatment.
Yee's team treated eight other melanoma patients, but he says it is too early to tell whether their tumours have vanished as well.
Other cancer experts say the results could pave the road for a cancer vaccine, but more proof with additional patients is needed.
"They really showed what can be done when you get all the conditions right," says Louis Weiner, an oncologist at Georgetown University Medical Center in Washington, D.C., who was not involved in the study.
For a tumour to grow and spread, it must trick the immune system into thinking it is normal tissue. Immune cells that keep tumours in check remain oblivious to the malignancy or too low in number to make much of a difference.
But researchers have slowly learned how to unleash this response. The most common strategy is to collect a patient's white blood cells, grow the tumour-killing T-cells in a laboratory incubator and inject them back into the patient.
This approach, while sometimes successful, often requires doctors to kill off a patient's other T-cells and give them multiple cell treatments, as well as a toxic cocktail of immune chemicals.
In hopes of developing a simple regimen, Yee's team focused on a special kind of T-cell, called helper CD4 cells.
The researchers isolated a handful of these cells from the patient, whose melanoma had spread to his lung and groin. All the cells recognised a protein called NY-ESO-1 - this existed in his tumour, but not most healthy cells.
After the cells had been multiplying in the lab for two months, Yee's team injected about five billion of them into the patient in one dose.
The treatment annihilated the tumours within two months, and nearly two years later, there are no signs that the patient's cancer has crept back, Yee says.
The lab-grown cells remained at high levels for at least three months after treatment. However, Yee suspects that the injected CD4-cells also jolted other immune cells into action because tumour cells that didn't make NY-ESO-1 also disappeared.
"This is a case that really teaches us a huge amount," Weiner says. Ramping up CD4 cells that go after a tumour could be a goal for future cell therapies targeting other cancers and even a cell-free vaccine, he says.
And in the next five to 10 years, cancer immune therapy will expand from its status as a boutique treatment, he says. "What we see in front of us is no longer a mirage, but we still have a bit of distance to travel."
Steven Rosenberg, chief of surgery at the National Cancer Institute in Bethesda, Maryland, US, suspects that Yee's treatment conscripted another kind of T-cell - called a CD8 - to help destroy the tumour.
Rosenberg's team has developed a treatment that uses mostly this kind of cell to fight melanoma. At a recent conference, he reported a 72% success rate in a group of 93 patients.
Yet, while encouraging, the new treatment might work for only a fraction of melanoma patients, because many tumours do not contain NY-ESO-1 and not all patients have an immune system that recognises the protein, he says.