thyroid-cancer

Gut bacterium Terrisporobacter causally linked to papillary thyroid cancer progression.

Mendelian randomization showed a causal association between higher Terrisporobacter abundance and increased PTC risk (OR 2.06). In TCGA validation, higher Terrisporobacter correlated with immunosuppressive TME (more M2 macrophages, fewer CD8+ T cells) and NTRK1 upregulation (HR 2.15 for poor OS). In vitro experiments confirmed Terrisporobacter culture supernatant upregulated NTRK1, promoted PTC cell proliferation, invasion, and de-differentiation. TRK inhibition reversed these effects.

Key Findings

Mendelian randomization: Terrisporobacter abundance causally associated with PTC risk (OR 2.06)
Higher Terrisporobacter correlated with M2 macrophage infiltration and fewer CD8+ T cells
Terrisporobacter abundance strongly correlated with NTRK1 upregulation
NTRK1 independently predicted poorer OS (HR 2.15)
TRK inhibition reversed bacteria-induced aggressive phenotype

Implications

Terrisporobacter defines a novel gut-thyroid axis promoting PTC via NTRK1 upregulation and immunosuppression. TRK inhibitors may have therapeutic value in Terrisporobacter-high PTC.

Caveats

Multi-stage design using GWAS and TCGA data; abstract-only. Causal mechanisms need further experimental validation. Terrisporobacter measurement and clinical application are in early development.

Source: Frontiers in immunology — 2026-01-01

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