Cancer immunologist challenging conventional thinking on advanced cancer. Targeting #cancer cachexia to help patients survive.
Joined January 2021
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My book is out.
When the Body Turns Against Itself: A Patient's Guide to Cancer Cachexia.
Plain language. No jargon. Honest about what we know and what we don't.
For every family watching a loved one waste away.
amazon.com/dp/B0HKWZLF7P
The track record is sobering: appetite stimulants, ghrelin agonists, single cytokine blockers, anabolics. None delivered lasting functional or survival benefit. My read: they all aimed at one molecule while the disease is a whole-system disorder.
This review I wrote with a Stanford collaborator. Its question: why has decades of cachexia drug development failed — and what should the field do instead?
If a broad immune correction worked in the lab, the bigger question is why cachexia drugs have failed patients for decades. Next week's paper — written with a Stanford collaborator — is our answer.
Why R-ketorolac? It's one mirror-image half of the familiar painkiller ketorolac — the half our program developed as an immunomodulator. Same starting molecule, different job: correcting an immune disorder, not killing pain.
Keep it honest: this is mouse data from our lab, not a treatment for people. What exists now is a clinical trial (NCT05336266) testing whether the same logic holds in patients. Science moves from cages to clinics — slowly, and carefully.
A wife watched her husband disappear — not from the tumor, but from the wasting. Day by day, his body seemed to vanish before her eyes, despite all the care he was getting. This is a story about cancer cachexia, and what happened when she refused to stop searching.
The lower dose was decided by his wife and me. The drug had been stopped because of side effects, not because it stopped working. That told us he was likely a super responder to it. He was treated at a lower dose, and his tumor responded.
Most striking to me: the same cachectic mice also got standard chemo plus R-ketorolac, and survival again went from 10% to 100%. Four years ago I argued that correcting the immune disorder could reopen the door to treatment. The mice said maybe.
Two controls tell the real story. In mice without T cells, the drug did nothing — so the effect runs through immunity. And it worked independent of COX, meaning this isn't just an NSAID calming pain. A different mechanism entirely.
The wasting stopped too: body weight held, quadriceps muscle loss shrank from 28% to under 2%, and fat was protected. Circulating IL-6 dropped, and T cells — depleted in cachexia — recovered.