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Review
. 2021 Jun 10;137(23):3174-3180.
doi: 10.1182/blood.2019003976.

Lessons to learn from tumor-educated platelets

Harvey G Roweth  1   2 , Elisabeth M Battinelli  1   2
Affiliations
Review

Lessons to learn from tumor-educated platelets

Harvey G Roweth et al. Blood. .

Abstract

Platelets have long been known to play important roles beyond hemostasis and thrombosis. Now recognized as a bona fide mediator of malignant disease, platelets influence various aspects of cancer progression, most notably tumor cell metastasis. Interestingly, platelets isolated from cancer patients often display distinct RNA and protein profiles, with no clear alterations in hemostatic activity. This phenotypically distinct population, termed tumor-educated platelets, now receive significant attention for their potential use as a readily available liquid biopsy for early cancer detection. Although the mechanisms underpinning platelet education are still being defined, direct uptake and storage of tumor-derived factors, signal-dependent changes in platelet RNA processing, and differential platelet production by tumor-educated megakaryocytes are the most prominent scenarios. This article aims to cover the various modalities of platelet education by tumors, in addition to assessing their diagnostic potential.

Keywords: Adhesion and adhesion receptors; CHEMOKINES; Chemokines; Circulating tumor cells; HEMATOPOIESIS; Megakaryocytes; PLATELETS; Platelet aggregation; Platelets; Tumor educated platelet; Tumor microenvironment; secretion and procoagulant activity.

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Figures

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Graphical abstract
Figure 1.
Figure 1.
Mechanisms underpinning the generation of TEPs. Tumor-derived factors can educate mature platelets within blood circulation through several modalities. Direct mechanisms include the transfer of RNA or protein cargo via exosomes, or receptor-mediated endocytosis of soluble factors within circulation. Indirect education largely encompasses signal-dependent changes in RNA processing, most notably though alternative RNA splicing, but potentially through additional regulation of mature RNA transcripts. Tumor-derived factors may also alter the development and function of MKs within the bone marrow, resulting in a distinct platelet population that enters circulation.
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