https://www.wired.com/story/cancer-treatment-darwi

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To Gatenby's knowledge, no one had endeavored to exploit evolution against cancer in a clinical trial until he developed his prostate cancer experiment. He picked prostate cancer to test this approach partly because, unlike other cancers, a routine blood draw for a molecule called prostate-specific antigen (PSA) can offer an immediate proxy for the cancer’s progression.
To design a clinical trial, Gatenby and his Moffitt collaborators first needed to account for their idea that tumor cells vie against each other for resources. They turned to game theory to plot this dynamic and plugged the numbers into the Lotka-­Volterra equations. The computer simulations they ran with these equations estimated how quickly drug-resistant cells would outcompete other tumor cells when exposed to the continuous dosage of Zytiga typically given to advanced-stage prostate cancer patients.

In the simulations, the typical administration of the drug led to drug-resistant cancer cells rapidly running rampant. The treatment would ultimately fail each time. That bleak outcome matched up with the results seen in hospital records. In contrast, the computer simulations suggested that if Zytiga were administered only when the tumor seemed to be growing, then the drug-resistant cells would take much longer to gain enough advantage to overrun the cancer.

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“They published a report in 2017, far earlier than anticipated, to a generally positive reaction from prostate experts—particularly because it suggested a way that people with cancer might live longer with less medication. “If you can reduce side effects, I think that’s fantastic,” says Peter Nelson, an oncologist who studies prostate cancer at the Fred Hutchinson Cancer Research Center in Seattle. “Conceptually it’s a beautifully simple approach.” Jason Somarelli, a biologist at the Duke Cancer Institute, calls Gatenby a pioneer: “He’s turning cancer into a chronic disease.”

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