Last week, the former senator from Nebraska Ben Sasse announced that his Stage 4 pancreatic cancer had developed resistance to a cutting edge treatment. Cancer specialists were not surprised: Nearly every pancreatic cancer patient taking that drug, called daraxonrasib, eventually develops resistance, said Dr. Andrew Aguirre, a pancreatic cancer specialist at the Dana-Farber Cancer Institute in Boston.
The drug, which was approved in August, electrified patients and doctors by doubling the median survival of patients with advanced pancreatic cancer. And yet like other targeted cancer drugs, it is not a cure: Even for patients in which the treatment is effective, it can suddenly stop working after about seven months. But now researchers are finding ways that resistance forms, hoping to extend life further.
They are focusing on the big questions: Why would pancreatic cancer stop responding to daraxonrasib? And how was resistance even developing? After all, the drug strangles a protein the cancer cells need to survive.
So how do the cells escape it and grow? Some were found in a preliminary study presented on Friday at the American Association for Cancer Research Conference on Pancreatic Cancer in San Diego, by Dr. Aguirre, who is a principal investigator for the study.
The work involved an unusual effort by three groups: Break Through Cancer, a nonprofit that brings researchers together to tackle challenging problems in cancer treatment; the Lustgarten Foundation, which supports research on pancreatic cancer; and Revolution Medicines, which makes daraxonrasib. Although developing resistance is common for all types of cancer treatments — which is why patients may have to try one therapy after another — each type of resistance looks different. To figure out how this particular resistance was emerging, researchers at leading medical centers recruited 66 patients with advanced pancreatic cancer who were already enrolled in an early stage study of the drug.
They were then asked to have their tumors biopsied in order to advance science. For each participant, one biopsy was done before treatment began, the next about two weeks later and the third when the drug stopped working. The first thing the investigators noticed was that daraxonrasib was killing cancer cells so quickly that by two weeks after treatment began, their number was cut in half.
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