Next Article in Journal
p53-Autophagy-Metastasis Link
Next Article in Special Issue
Antithrombotic Agents and Cancer
Previous Article in Journal
The Long Non-Coding RNA RP5-1024C24.1 and Its Associated-Gene MPPED2 Are Down-Regulated in Human Thyroid Neoplasias and Act as Tumour Suppressors
Article Menu
Issue 5 (May) cover image

Export Article

Open AccessReview
Cancers 2018, 10(5), 147;

Bone Marrow Defects and Platelet Function: A Focus on MDS and CLL

Australian Centre for Blood Diseases, Monash University, Melbourne, VIC 3004, Australia
ACRF Department of Cancer Biology and Therapeutics, The John Curtin School of Medical Research, The Australian National University, Canberra, ACT 2600, Australia
Author to whom correspondence should be addressed.
Received: 20 April 2018 / Revised: 11 May 2018 / Accepted: 16 May 2018 / Published: 18 May 2018
(This article belongs to the Special Issue The Role of Thrombosis and Haemostasis in Cancer)
Full-Text   |   PDF [521 KB, uploaded 18 May 2018]   |  


The bloodstream typically contains >500 billion anucleate circulating platelets, derived from megakaryocytes in the bone marrow. This review will focus on two interesting aspects of bone marrow dysfunction and how this impacts on the quality of circulating platelets. In this regard, although megakaryocytes are from the myeloid lineage leading to granulocytes (including neutrophils), erythrocytes, and megakaryocytes/platelets, recent evidence has shown that defects in the lymphoid lineage leading to B cells, T cells, and natural killer (NK) cells also result in abnormal circulating platelets. Current evidence is limited regarding whether this latter phenomenon might potentially arise from (a) some form of as-yet-undetected defect common to both lineages; (b) adverse interactions occurring between cells of different lineages within the bone marrow environment; and/or (c) unknown disease-related factor(s) affecting circulating platelet receptor expression/function after their release from megakaryocytes. Understanding the mechanisms underlying how both myeloid and lymphoid lineage bone marrow defects lead to dysfunction of circulating platelets is significant because of the potential diagnostic and predictive value of peripheral platelet analysis for bone marrow disease progression, the additional potential effects of new anti-cancer drugs on platelet function, and the critical role platelets play in regulation of bleeding risk, inflammation, and innate immunity. View Full-Text
Keywords: platelets; bone marrow defects; glycoprotein Ibα; glycoprotein VI platelets; bone marrow defects; glycoprotein Ibα; glycoprotein VI

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

Share & Cite This Article

MDPI and ACS Style

Luu, S.; Gardiner, E.E.; Andrews, R.K. Bone Marrow Defects and Platelet Function: A Focus on MDS and CLL. Cancers 2018, 10, 147.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Cancers EISSN 2072-6694 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top