Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2017 Jun;3(2):023001.
doi: 10.1088/2057-1739/aa6c05. Epub 2017 May 17.

Platelet count as a predictor of metastasis and venous thromboembolism in patients with cancer

Joanna L Sylman  1   2   3 , Annachiara Mitrugno  1 , Garth W Tormoen  4 , Todd H Wagner  2   5 , Parag Mallick  3 , Owen J T McCarty  1
Affiliations

Platelet count as a predictor of metastasis and venous thromboembolism in patients with cancer

Joanna L Sylman et al. Converg Sci Phys Oncol. 2017 Jun.

Abstract

Platelets are anucleate cells in the blood at concentrations of 150,000 to 400,000 cells/µL and play a key role in hemostasis. Several studies have suggested that platelets contribute to cancer progression and cancer-associated thrombosis. In this review, we provide an overview of the biochemical and biophysical mechanisms by which platelets interact with cancer cells and review the evidence supporting a role for platelet-enhanced metastasis of cancer, and venous thromboembolism (VTE) in patients with cancer. We discuss the potential for and limitations of platelet counts to discriminate cancer disease burden and prognosis. Lastly, we consider more advanced diagnostic approaches to improve studies on the interaction between the hemostatic system and cancer cells.

PubMed Disclaimer

Conflict of interest statement

Disclosures No conflicts of interest, financial or otherwise, are declared by the authors.

Figures

Figure 1
Figure 1
Platelets can support and encourage cancer cell metastasis by (A) shielding cancer cells from immune cells during vascular dissemination, (B) arresting cancer cells on the wall of a blood vessel, and (C) releasing growth factors that allow for extravasation of cancer cells through the endothelial cell and extracellular matrix barrier. (Key - TGFβ - transforming tumor growth factor β; MMP - matrix metalloproteases; VEGF - vascular endothelial growth factor; PDGF - platelet derived growth factor; ADP - adenosine diphosphate; ATP - adenosine triphosphate).
Figure 2
Figure 2
Cancer cells promote platelet activation and coagulation. Tissue factor is expressed on cancer cells and microparticles, which subsequently leads to the activation of FVII and FX via the extrinsic pathway. Inactive prothrombin is converted to thrombin, which then catalyzes the polymerization of fibrinogen to fibrin. Thrombin can also activate platelets through their PAR receptors (Key - PS - phosphatidylserine; MMP-2 - metalloproteases).
See this image and copyright information in PMC

References

    1. Ruggeri ZM. Von Willebrand factor, platelets and endothelial cell interactions. J. Thromb. Haemost. 2003;1:1335–42. - PubMed
    1. Brass L. Understanding and evaluating platelet function. Hematol. Educ. Program Am. Soc. Hematol. Am. Soc. Hematol. Educ. Program. 2010;2010:387–96. - PubMed
    1. Hoffman M, Monroe DM. Coagulation 2006: a modern view of hemostasis. Hematol. Oncol. Clin. North Am. 2007;21:1–11. - PubMed
    1. Auger JM, Kuijpers MJE, Senis YA, Watson SP, Heemskerk JWM. Adhesion of human and mouse platelets to collagen under shear: a unifying model. FASEB J. Off. Publ. Fed. Am. Soc. Exp. Biol. 2005;19:825–7. - PubMed
    1. Trousseau A, Hotel-Dieu . Clinique Médicale De L’hotel-dieu De Paris. Vol. 3. Nabu Press; 2011.

LinkOut - more resources