In a new experiment, a woman with advanced pancreatic cancer saw her tumors shrink dramatically after Oregon researchers turbocharged her own immune cells, highlighting a possible new way to treat various cancers.
Katie Wilkes has not been cured, but said what is left of her cancer shows no signs of growth after a single treatment last June.
“I knew that regular chemotherapy would not save my life, and I would have,” said Wilkes of Ormond Beach, Florida, who followed the scientist thousands of miles and asked him to try the experiment.
The study, published Wednesday in the New England Journal of Medicine, examines a new method of controlling the immune system to create “living drugs” capable of searching for and destroying tumors.
“It’s really exciting. This is the first time this type of treatment has worked on a very difficult-to-treat type of cancer, ”said Dr. Josh Witch of the Fred Hutchinson Cancer Research Center in Seattle, who was not involved in the experiment.
This is only the first step and much more research is needed, he warned, noting that Wilkes is one of only two people known to have tried this approach and failed in the other patient.
However, Weich said the findings were “principled evidence that this is possible” and that other researchers were also testing this type of immunotherapy.
T-cells are key immune soldiers capable of killing diseased cells – but too often cancer avoids them. Doctors have already learned how to strengthen T cells to fight certain types of leukemia and lymphoma. They add an artificial receptor to patients’ T cells so that immune fighters can recognize a marker on the outside of blood cancer cells and attack.
But this CAR-T therapy does not work against the more common solid tumors that do not carry the same risk marker.
The new twist: At the Providence Cancer Institute in Oregon, researcher Eric Tran genetically engineered Wilkes’ T cells so they could spot a mutant protein hidden in her tumor cells – and only there, not in healthy cells.
How? Some molecules sit on the surface of cells and give the immune system a brief look at what proteins are inside. If a complex T-cell receptor recognizes both the genetically engineered human HLA molecule and one of the protein fragments embedded in it, the target mutant, that immune fighter can be trapped.
This is an approach known as T-cell receptor or TCR therapy. Tran stressed that the study remains highly experimental, but said Wilkes’s remarkable response “gives me optimism that we are on the right track.”
Dr Eric Rubin, editor-in-chief of the New England Journal, said the study raised the possibility of possibly targeting a number of mutations that cause cancer.
“We are talking about the possibility of distinguishing tumor cells from non-tumor cells in a way we have never been able to before,” he said.
Wilkes underwent chemotherapy, radiation and surgery for pancreatic cancer. Doctors later discovered new tumors in her lungs – pancreatic cancer has spread, a stage when there is no good treatment.
Wilkes knew that researchers were testing immunotherapy to fight various difficult-to-treat tumors, and a biopsy showed that a specific mutation was feeding her cancer. Her search led to Tran, who in 2016 co-authored a study on a subset of T cells that naturally contain receptors capable of detecting the same so-called KRAS mutation.
Wilkes also had the right type of HLA molecule. So Tran and his colleague, Dr. Rom Leidner, an oncologist, received permission from the Food and Drug Administration to reprogram her T cells to carry a special receptor to fight mutants.
They extracted T cells from Wilkes’ blood, genetically modified them in the laboratory, and then raised billions of copies. Six months after the transfusion of the altered cells, her tumors have shrunk by 72% – and Wilkes said recent tests show her disease remains stable.
Tran said it was unclear why the experiment had failed in another patient, although lessons from the case led to some changes in Wilkes’ treatment.
The Oregon team found little research to further test TCR therapy for patients with incurable cancers fueled by what Tran calls “hot spots” mutations.
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This Associated Press series was created in partnership with the scientific education department of Howard Hughes Medical Institute. AP is solely responsible for all content.
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