Red Blood Cell Biomechanics and Cancer-Associated Thrombosis

Area of Science:

• Hematology
• Oncology
• Biophysics

Background:

• Cancer-associated thrombosis (CAT) is a major cause of death in cancer patients.
• Current CAT models focus on procoagulant factors, platelets, and leukocytes, with limited attention to red blood cell (RBC) biomechanics.
• Malignancy and cancer therapies can impair RBC deformability and increase aggregation, influencing blood viscosity and flow.

Purpose of the Study:

• To review the mechanistic and clinical data linking altered RBC biomechanics to thrombosis in cancer.
• To explore the relationship between RBC biomechanical alterations and established cancer-related prothrombotic pathways.
• To assess current CAT risk assessment models and the potential of RBC biomechanical parameters as biomarkers.

Main Methods:

• Literature review synthesizing mechanistic and clinical data.
• Analysis of established cancer-related prothrombotic pathways.
• Critical assessment of current cancer-associated thrombosis risk assessment models.

Main Results:

• Emerging evidence suggests impaired RBC deformability and increased aggregation promote thrombosis in cancer.
• Altered RBC biomechanics interact with pathways like extracellular vesicle release, NETs, stasis, and oxidative stress.
• Current risk assessment models may not fully capture the contribution of RBC biomechanics.

Conclusions:

• Altered RBC biomechanics represent a significant, understudied factor in CAT pathogenesis.
• RBC biomechanical parameters show potential as dynamic biomarkers for improved thrombosis risk stratification in cancer patients.
• Advances in rheological technologies could facilitate clinical translation and enhance understanding of CAT.