ArticleGastroenterology2026
Depletion of Fibrinogen Suppresses Growth of Primary Tumors and Metastasis of Pancreatic Ductal Adenocarcinoma.
Article in Gastroenterology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
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Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Prognostic value of peripheral blood fibrinogen-to-albumin ratio in pancreatic cancer patients: a systematic review and meta-analysis.BMC cancer · 2026Pooled it
- Immune-inflammatory-fibrinogen score as a novel prognostic biomarker in patients with gastric cancer undergoing radical gastrectomy: a multicenter study.World journal of surgical oncology · 2026Trial
- Multi-omics-driven precision medicine.iMeta · 2026Review
- Targeting APE1 endonuclease activity impairs metastasis and enhances genotoxic therapy response in pancreatic cancer.Journal of experimental & clinical cancer research : CR · 2026Article
Corrections and comments
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Authors and funding
23 authors.
Funding
Abstract
BACKGROUND &
aimsPancreatic ductal adenocarcinoma (PDAC) is an aggressive, highly metastatic disease that provokes dysregulation of the coagulation system. Patients exhibit significantly elevated circulating levels of blood clotting protein fibrin(ogen). Extravascular fibrin deposits contribute to the complex tumor microenvironment in PDAC.
methodsWe depleted fibrinogen in 3 PDAC patient-derived xenograft models using technology platforms that are currently being tested clinically (antisense oligonucleotide or lipid nanoparticles containing small interfering RNAs) and monitored tumor growth and metastasis. Proteomics and spatial transcriptomics were used to interrogate the mechanisms behind the in vivo work.
resultsThe role of fibrin on tumor progression was evaluated in vitro and in vivo and reduction of fibrin led to decreased tumor cell proliferation in vitro and significantly suppressed primary orthotopic tumor growth. Fibrin depletion provoked a significant shift in extracellular matrix-associated proteins and serine protease inhibitors, suggesting a decrease in the activity of serine proteases known to be responsible for extracellular matrix remodeling and metastatic dissemination. Spatial transcriptomics revealed that tumors from fibrinogen-depleted mice exhibit significantly increased presence of stromal components, including tumor-restraining cancer-associated fibroblasts. Congruently, fibrinogen knockdown in a metastatic orthotopic model markedly impaired spontaneous metastasis to the liver. However, fibrinogen knockdown did not affect liver colonization in an intrasplenic injection model, which recapitulates the late stages of metastasis.
conclusionsThese data suggest that fibrin(ogen) reprograms the primary tumor microenvironment to support growth and promote early, but not late, metastatic steps. Our findings support prospective evaluation of a novel clinical approach involving the integration of fibrin(ogen)-targeting or depleting agents into chemotherapy regimens to control the spread of pancreatic cancer.
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