# Anticoagulant outcomes in managing tumor thrombus: a systematic review

**Authors:** Lama Alfehaid, Samaher Alatmi, Bishier Alfadhel, Razan Alqahtani, Shooa bin Nafisah, Yara Alotaibi, Mohammed AlSheef, Nada Alsuhebany

PMC · DOI: 10.3389/fonc.2026.1773327 · Frontiers in Oncology · 2026-02-23

## TL;DR

This review finds that anticoagulants alone do not effectively treat tumor thrombus and may increase bleeding risks, suggesting tumor-directed therapies are more critical.

## Contribution

The study provides a systematic synthesis of anticoagulant outcomes in tumor thrombus, highlighting the lack of evidence for routine use.

## Key findings

- Anticoagulation alone did not lead to radiographic regression of tumor thrombus.
- Thrombus resolution occurred only with tumor-directed or mechanical interventions.
- Anticoagulation was linked to a clinically meaningful risk of major bleeding.

## Abstract

Tumor thrombus (TT), defined as intravascular extension of malignant tissue, is a distinct manifestation of cancer-associated thrombosis driven by malignant vascular invasion rather than fibrin-rich clot. Despite limited evidence, anticoagulant therapy is frequently prescribed empirically. This systematic review synthesized available data on the effectiveness and safety of anticoagulation in adults with solid tumor–associated TT.

A PRISMA (2020) compliant systematic review (PROSPERO-registered) was conducted using PubMed/MEDLINE, Embase, and CENTRAL through September 2025. Eligible studies included adults with solid tumor–associated TT who received anticoagulation and reported thrombus response, thromboembolic recurrence, survival, or bleeding outcomes. Results were synthesized narratively in accordance with SWiM guidance. Risk of bias was assessed using the Newcastle–Ottawa Scale and the Joanna Briggs Institute tools, and the certainty of evidence was assessed using the GRADE approach.

Eight studies met the inclusion criteria, comprising three retrospective cohort studies and five case reports. Anticoagulants evaluated included low-molecular-weight heparin, vitamin K antagonists, direct oral anticoagulants, unfractionated heparin, and parenteral direct thrombin inhibitors. Across all studies, anticoagulation alone was not associated with radiographic regression of TT. Apparent thrombus resolution occurred exclusively following tumor-directed or mechanical interventions, such as surgical thrombectomy or percutaneous aspiration, and could not be attributed to anticoagulation alone. Evidence for a reduction in thromboembolic recurrence was limited, heterogeneous, and inconsistently adjudicated as bland thrombosis versus malignant embolic disease. No survival benefit attributable to anticoagulation was demonstrated. In contrast, anticoagulant therapy was associated with a clinically meaningful risk of major bleeding, particularly among patients with renal cell carcinoma–associated TT. Overall certainty of evidence ranged from very low to moderate.

Current evidence does not demonstrate a consistent benefit of routine anticoagulation for isolated TT. Anticoagulation may be appropriate when conventional indications are present (e.g., pulmonary embolism, proximal deep-vein thrombosis, atrial fibrillation, catheter-associated thrombosis). Tumor-directed therapy remains the primary determinant of outcomes. Prospective studies are needed to define optimal management strategies.

https://www.crd.york.ac.uk/PROSPERO/view/CRD420251111117, identifier CRD420251111117.

## Linked entities

- **Diseases:** pulmonary embolism (MONDO:0005279), atrial fibrillation (MONDO:0004981), renal cell carcinoma (MONDO:0005086)

## Full-text entities

- **Genes:** F3 (coagulation factor III, tissue factor) [NCBI Gene 2152] {aka CD142, TF, TFA}, TXK (TXK tyrosine kinase) [NCBI Gene 7294] {aka BTKL, PSCTK5, PTK4, RLK, TKL}, VEGFA (vascular endothelial growth factor A) [NCBI Gene 7422] {aka L-VEGF, MVCD1, VEGF, VPF}
- **Diseases:** urothelial carcinoma (MESH:D014523), hypertension (MESH:D006973), death (MESH:D003643), VTE (MESH:D054556), TT (MESH:D013927), portal hypertension (MESH:D006975), Ewing sarcoma (MESH:D012512), DVT (MESH:D020246), antiphospholipid syndrome (MESH:D016736), toxicity (MESH:D064420), Pulmonary tumor embolism (MESH:D009360), atrial fibrillation (MESH:D001281), thromboembolic (MESH:D013923), IVC (MESH:C567679), embolic (MESH:D004617), solid (MESH:D018250), gastrointestinal bleeding (MESH:D006471), endothelial (MESH:D005642), RCC (MESH:D002292), oncologic (MESH:D000072716), HCC (MESH:D006528), cirrhosis (MESH:D005355), melanoma (MESH:D008545), variceal (MESH:D014648), liver disease (MESH:D008107), leiomyosarcoma (MESH:D007890), Tumor (MESH:D009369), inferior vena cava (MESH:C563013), hypercoagulability (MESH:D019851), Bleeding (MESH:D006470), APS (MESH:D016884), sarcoma (MESH:D012509), PE (MESH:D011655)
- **Chemicals:** DOAC (-), etoposide (MESH:D005047), rivaroxaban (MESH:D000069552), ifosfamide (MESH:D007069), LMWH (MESH:D006495), UFH (MESH:D006493), cabozantinib (MESH:C558660), danaparoid (MESH:C035838), apixaban (MESH:C522181), sunitinib (MESH:D000077210), bevacizumab (MESH:D000068258)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12967944/full.md

## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC12967944/full.md

## References

29 references — full list in the complete paper: https://tomesphere.com/paper/PMC12967944/full.md

---
Source: https://tomesphere.com/paper/PMC12967944