Cancer and Metastasis Reviews

, Volume 33, Issue 1, pp 231–269

Platelets and cancer: a casual or causal relationship: revisited

  • David G. Menter
  • Stephanie C. Tucker
  • Scott Kopetz
  • Anil K. Sood
  • John D. Crissman
  • Kenneth V. Honn
NON-THEMATIC REVIEW

DOI: 10.1007/s10555-014-9498-0

Cite this article as:
Menter, D.G., Tucker, S.C., Kopetz, S. et al. Cancer Metastasis Rev (2014) 33: 231. doi:10.1007/s10555-014-9498-0

Abstract

Human platelets arise as subcellular fragments of megakaryocytes in bone marrow. The physiologic demand, presence of disease such as cancer, or drug effects can regulate the production circulating platelets. Platelet biology is essential to hemostasis, vascular integrity, angiogenesis, inflammation, innate immunity, wound healing, and cancer biology. The most critical biological platelet response is serving as “First Responders” during the wounding process. The exposure of extracellular matrix proteins and intracellular components occurs after wounding. Numerous platelet receptors recognize matrix proteins that trigger platelet activation, adhesion, aggregation, and stabilization. Once activated, platelets change shape and degranulate to release growth factors and bioactive lipids into the blood stream. This cyclic process recruits and aggregates platelets along with thrombogenesis. This process facilitates wound closure or can recognize circulating pathologic bodies. Cancer cell entry into the blood stream triggers platelet-mediated recognition and is amplified by cell surface receptors, cellular products, extracellular factors, and immune cells. In some cases, these interactions suppress immune recognition and elimination of cancer cells or promote arrest at the endothelium, or entrapment in the microvasculature, and survival. This supports survival and spread of cancer cells and the establishment of secondary lesions to serve as important targets for prevention and therapy.

Keywords

Platelet TCIPA Metastasis Thrombosis Extravasation CTC 

Copyright information

© Springer Science+Business Media New York 2014

Authors and Affiliations

  • David G. Menter
    • 1
    • 3
  • Stephanie C. Tucker
    • 5
  • Scott Kopetz
    • 1
  • Anil K. Sood
    • 2
    • 3
    • 4
  • John D. Crissman
    • 6
  • Kenneth V. Honn
    • 5
    • 6
  1. 1.Gastrointestinal Medical OncologyThe University of Texas MD Anderson Cancer CenterHoustonUSA
  2. 2.Gynecologic Oncology & Reproductive MedicineThe University of Texas MD Anderson Cancer CenterHoustonUSA
  3. 3.Department of Cancer BiologyThe University of Texas MD Anderson Cancer CenterHoustonUSA
  4. 4.Center for RNA Interference and Non-Coding RNAThe University of Texas MD Anderson Cancer CenterHoustonUSA
  5. 5.Bioactive Lipids Research Program, Department of PathologyWayne State UniversityDetroitUSA
  6. 6.Cancer Biology Division, Department of Pathology, School of MedicineWayne State University School of MedicineDetroitUSA

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