Making Cancer Immunotherapy Work with FMT– category –
-
PERFORM vs TACITO, the Segatella copri Problem, and the Commercial Frontier — Three Crossroads Facing FMT’s Clinical Translation | Making Cancer Immunotherapy Work with FMT, Vol. 3 (Final)
Series finale. Same metastatic RCC, contrasting designs: PERFORM (healthy donor, ipi/nivo) vs TACITO (ICI complete-responder donor, pembro+axitinib). The cross-trial Segatella copri context-dependent toxicity discovery (drives toxicity ONLY under dual ICI), the three-layer commercial map (Seres/Vedanta/Exeliom; Locus/Eligo; rational consortia), and structural implications for the global ecosystem. The clinical-translation year of FMT/LBP, synthesized. -
FMT Is Subtraction, Not Addition — How FMT-LUMINate Dissected the Real Mechanism Behind Microbiome-Empowered Cancer Immunotherapy | Making Cancer Immunotherapy Work with FMT, Vol. 2
Building on Volume 1, we dissect the convergent finding across the three April 2026 Nature Medicine trials: FMT works because patients lose their own deleterious bacteria, not because they acquire donor bacteria. FMT-LUMINate's mouse reverse-experiment proved causality. Mechanism: tryptophan/kynurenine pathway disturbance, IDO/AhR axis, regulatory T-cell expansion. Vol. 2 of the series. -
The Day Three Major FMT × Immunotherapy Trials Landed Together in Nature Medicine — Reshaping Cancer Immunotherapy with the Gut Microbiome | Making Cancer Immunotherapy Work with FMT, Vol. 1
In April 2026, Nature Medicine Vol. 32 No. 4 published three FMT-plus-immunotherapy trials in a single issue: 80% ORR in NSCLC, and a doubling of progression-free survival in metastatic RCC (24.0 vs 9.0 months, HR 0.50). But the deeper significance lies not in the numbers — it is the shared mechanistic finding that responders selectively lost their own deleterious bacteria, rather than acquiring beneficial bacteria from the donor. Volume 1 of our series surveys all three trials and what their simultaneous publication means.
1