A few years back, we learned that a dear friend of ours had been diagnosed with pancreatic cancer. She was a vibrant woman in her mid-40s, with a husband who loved her beyond words, and a young daughter just spreading her wings to enter her adult life. When our friend was diagnosed, they told her to plan on no more than three months.
She lasted five.
Pancreatic cancer is one of the worst cancers. It’s too often not diagnosed until it has spread. It’s a death sentence. But now, a new drug is offering patients some hope for at least a few more weeks or months, and it may well have an impact on other cancers, as well.
Enthusiasm around daraxonrasib is reaching a fever pitch. In the phase 3 trial of 500 patients, the drug was shown to double the survival time of patients with advanced pancreatic cancer, a notoriously deadly cancer: 13.2 months, on average, compared to 6.7 months for people who got chemo. On Sunday, Wainberg and his colleagues presented those results at the American Society of Clinical Oncology’s annual meeting in Chicago. The full study was simultaneously published in the New England Journal of Medicine.
When Revolution Medicines, which makes the drug, released the trial’s preliminary findings in April, Dr. Rachna Shroff, chief of the division of hematology and oncology at the University of Arizona Cancer Center in Tucson, said she “started crying tears of joy.”
“It’s that big of a game-changer for those of us who treat pancreatic cancer,” she said. “It’s unprecedented.”
Here’s how the new drug works:
Daraxonrasib targets a mutation in a gene called KRAS, which works like an on/off switch controlling how cells grow in the body. The mutation, which is found in more than 90% of pancreatic cancers, causes the switch to get stuck in an “on” position, allowing cancer cells to grow wildly out of control.
Scientists have known for years that if they could target the KRAS mutation, they could wrench that switch from its “on” position.
“It’s been incredibly hard to drug that mutation,” Wolpin said. “That mutated protein is like a round ball, and you just can’t get the drug to stick to it, to block the effect.” It’s only “through some really amazing chemistry work,” he said, that scientists have been able to develop a drug to work on the mutation.
Daraxonrasib is that first drug. It works by pairing up with a protein called cyclophilin A inside cells, acting like a “molecular glue,” Wolpin said, glomming onto the mutated protein.
Daraxonrasib may well have applications in other cancers, as well. Cancers that result from the KRAS mutation include not only pancreatic cancer for also colorectal cancer, non-small cell lung cancer, bile tract cancers, uterine cancers, ovarian cancers, cervical cancers, and testicular germ cell cancers.
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Medical science has made amazing inroads into cancer treatment in recent years, but it’s still one of the worst diagnoses anyone can get. It’s hit my family as well as my circle of friends; a few years ago, my dear sister died after months of horrendous chemotherapy for what started as breast cancer and which turned into everything cancer. She finally refused any further treatment and ended up dying a few weeks later, with both of her sisters at her side. She was later found to have had five separate kinds of cancer in her body.
Cancer has plagued humanity forever. This new drug isn’t a panacea, but if it shows these kinds of results for pancreatic cancer patients, people who literally have nothing to lose, then this drug or similar ones may well be a powerful new tool in the oncologist’s toolkit for quite a variety of cancers.
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