# Prothrombotic Tendency in the Shadow of Cancer: Hypercoagulability, Impaired Clot Contraction and Fibrinolysis in Colorectal Cancer and Gastric Cancer Patients Undergoing Chemotherapy

**Authors:** Karolina Aleksandrowicz, Tomasz Rusak, Elżbieta Bołtromiuk, Tomasz Misztal, Barbara Polityńska-Lewko, Anna M. Wojtukiewicz, Joanna Kruszewska, Marta Myśliwiec, Marek Z. Wojtukiewicz

PMC · DOI: 10.3390/ijms27042037 · International Journal of Molecular Sciences · 2026-02-21

## TL;DR

Cancer patients show abnormal blood clotting patterns that may increase their risk of thrombosis, with chemotherapy further affecting fibrinolysis.

## Contribution

This study is the first to reveal a significant inhibition of clot contraction in cancer patients using thromboelastometry and CCR measurements.

## Key findings

- Cancer patients showed hypercoagulability with shortened clotting time and enhanced clot strength.
- Clot contraction and fibrinolysis were significantly impaired in cancer patients compared to healthy controls.
- Chemotherapy prolonged fibrinolysis, particularly with platinum-based drugs.

## Abstract

Cancer is frequently accompanied by thrombotic complications, but conventional coagulation tests often fail to adequately detect cancer-associated hypercoagulability. In this study, blood from 34 patients with colorectal or gastric cancers (before, during and after 3 months of chemotherapy) and 21 healthy controls was analyzed to obtain a coagulation–fibrinolysis profile (by thromboelastometry) and determine the kinetics of clot contraction (CCR). Patients demonstrated hypercoagulable profiles characterized by shortened clotting time, enhanced clot strength, reduced CCR, and impaired fibrinolysis compared to healthy controls, which was more pronounced in colorectal cancer patients. Parameters related to increased clot formation, impaired CC and delayed fibrinolysis correlated with disease stage. Chemotherapy meaningfully prolonged fibrinolysis, which was further evident in vitro with platinum-based drugs. Our findings reveal, for the first time, a significant inhibition of CCR in cancer patients. Integrating thromboelastometry with CCR measurements may improve stratification of cancer-associated thrombotic risk, which appears to arise from the hemostatic disturbances identified in our study. These may extend the duration of clot presence due to reduced fibrinolysis, while decreasing clot stability through diminished CCR. Therefore, careful monitoring of the precarious balance between thrombotic and bleeding tendencies may hold important implications for the fate of cancer patients.

## Linked entities

- **Diseases:** colorectal cancer (MONDO:0005575), gastric cancer (MONDO:0001056)

## Full-text entities

- **Genes:** PLAT (plasminogen activator, tissue type) [NCBI Gene 5327] {aka T-PA, TPA}, F2 (coagulation factor II, thrombin) [NCBI Gene 2147] {aka PT, RPRGL2, THPH1}, PLG (plasminogen) [NCBI Gene 5340] {aka HAE4}, F3 (coagulation factor III, tissue factor) [NCBI Gene 2152] {aka CD142, TF, TFA}, FGB (fibrinogen beta chain) [NCBI Gene 2244] {aka HEL-S-78p}, SERPINC1 (serpin family C member 1) [NCBI Gene 462] {aka AT3, AT3D, ATIII, ATIII-R2, ATIII-T1, ATIII-T2}
- **Diseases:** Hypercoagulability (MESH:D019851), hyperfibrinolysis (MESH:C567640), gastrointestinal malignancies (MESH:D005770), Thromboembolic complications (MESH:D013923), Gastric Cancer (MESH:D013274), thrombocytosis (MESH:D013922), breast and prostate cancers (MESH:D001943), bleeding (MESH:D006470), embolization (MESH:D004617), chronic bleeding (MESH:D002908), hemophilia (MESH:D006467), hemostasis disorders (MESH:D009358), pulmonary embolism (MESH:D011655), Colorectal Cancer (MESH:D015179), CS (MESH:D006223), III (MESH:C537189), hemostatic disturbances (MESH:D020141), VTE (MESH:D054556), death (MESH:D003643), platelet dysfunction (MESH:D001791), Thrombus (MESH:D013927), injury to (MESH:D014947), pancreatic, ovarian, gastric, hematologic, gynecologic cancers (MESH:D010195), deep vein thrombosis (MESH:D020246), metastatic disease (MESH:D000092182), central nervous system tumors (MESH:D016543), thrombocytopenia (MESH:D013921), rupture (MESH:D012421), ischemic stroke (MESH:D002544), Cancers (MESH:D009369), coagulation (MESH:D001778)
- **Chemicals:** folinic acid (MESH:D002955), 5-FU (MESH:D005472), docetaxel (MESH:D000077143), oxaliplatin (MESH:D000077150), topotecan (MESH:D019772), calcium chloride (MESH:D002122), cisplatin (MESH:D002945), platinum (MESH:D010984), CV40 (-), trisodium citrate (MESH:C514290), irinotecan (MESH:D000077146)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

42 references — full list in the complete paper: https://tomesphere.com/paper/PMC12941335/full.md

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Source: https://tomesphere.com/paper/PMC12941335