Platelet and Cancer-Cell Interactions Modulate Cancer-Associated Thrombosis Risk in Different Cancer Types

Simple Summary Cancer-associated thrombosis is the first cause of death in cancer after cancer-progression itself; however, thrombotic risk is not the same in all cancer types. Here, we exemplified cancer-cell interactions with platelets in tumor microenvironments and their effect on overall thrombotic risk. We chose three distinct cancer types with varying thrombotic risks: oral cancer (low risk), colorectal cancer (medium risk) and pancreatic cancer (high risk). Understanding these interactions and their consequences is crucial for deepening researcher's and clinician's knowledge of cancer-associated thrombosis and finding innovative biomarkers and therapeutic targets. The first cause of death in cancer patients, after tumoral progression itself, is thrombo-embolic disease. This cancer-associated hypercoagulability state is known as Trousseau's syndrome, and the risk for developing thrombotic events differs according to cancer type and stage, as well as within patients. Massive platelet activation by tumor cells is the key mediator of thrombus formation in Trousseau's syndrome. In this literature review, we aimed to compare the interactions between cancer cells and platelets in three different cancer types, with low, medium and high thrombotic risk. We chose oral squamous cell carcinoma for the low-thrombotic-risk, colorectal adenocarcinoma for the medium-thrombotic-risk, and pancreatic carcinoma for the high-thrombotic-risk cancer type. We showcase that understanding these interactions is of the highest importance to find new biomarkers and therapeutic targets for cancer-associated thrombosis.

Automated summary

This study compares the interactions between cancer cells and platelets in three different cancer types with varying thrombotic risks: oral cancer (low risk), colorectal cancer (medium risk), and pancreatic cancer (high risk). Understanding these interactions is crucial for finding new biomarkers and therapeutic targets for cancer-associated thrombosis.