TGFB1
Overview
TGFB1 (Transforming Growth Factor Beta 1) is a pleiotropic cytokine with dual roles in cancer: tumour suppressor in early-stage disease and promoter of invasion, immunosuppression, and fibrosis in advanced tumours. In the biliary/hepatic context it modulates the inflammatory microenvironment and is an important immunomodulatory readout in clinical trials involving microbiome-targeted interventions.
Alterations observed in the corpus
- Pro-inflammatory cytokine measured as a vancomycin-responsive immunomodulatory marker in the NCT03710122 trial context of cholangiocarcinoma/PSC; reviewed as part of gut-microbiota–bile-acid–immune signalling crosstalk PMID:25608663
- TGF-β-axis alteration in pancreatic ductal adenocarcinoma, part of broader TGF-β pathway disruption (alongside TGFBR1, TGFBR2, ACVR1B, ACVR1C, SMAD3, SMAD6) augmenting SMAD4 loss. PMID:25855536
- High TGF-beta1 (TGFB1) plasma levels correlate with poor outcomes in pancreatic cancer (PAAD); along with TGFBR2/SMAD4 expression and SMAD4 SNP rs11354983, TGFB1 is highlighted as a candidate biomarker for stratifying patients who may benefit from intensified local SBRT therapy. PMID:27826200
Cancer types (linked)
- CCA — implicated in the immunomodulatory landscape of cholangiocarcinoma via gut-microbiota–bile-acid axis signalling PMID:25608663
Co-occurrence and mutual exclusivity
- Functionally linked to TGR5/GPBAR1 pro-fibrotic signalling and NF-kB–mediated inflammation in cholestatic liver disease models PMID:25608663
Therapeutic relevance
- Measurement of TGFB1 as a pharmacodynamic biomarker of vancomycin-mediated immunomodulation in PSC patients; potential biomarker for microbiome-targeted therapies in CCA PMID:25608663
Open questions
- Whether TGFB1 levels are causally linked to CCA progression vs. being a secondary marker of inflammation remains unresolved PMID:25608663
Sources
This page was processed by entity-page-writer on 2026-05-15. - PMID:25855536
This page was processed by entity-page-writer on 2026-05-15. - PMID:27826200
This page was processed by entity-page-writer on 2026-05-15.