Special Issue "The Role of Thrombosis and Haemostasis in Cancer"
A special issue of Cancers (ISSN 2072-6694).
Deadline for manuscript submissions: 15 June 2018
Prof. Dr. Marco Falasca
Cancer-associated thrombosis is a lethal complication in cancer sufferers. The association between malignancy and thrombosis was first described over a century and half ago, by Jean-Baptiste Bouillard in 1823 and later in 1865 by Armand Trousseau. It is now well accepted that cancer patients are at an estimated four to seven-fold increased risk of developing venous thromboembolism (VTE) compared to non-cancer patients. The mechanisms by which cancer elicit thromboembolic events are not entirely understood. A significant role is attributed to the capability of cancer cells to activate the coagulation system, thus inducing a hypercoagulable or prothrombotic state in cancer patients. Cancer cells can activate the coagulation cascade through the expression of tissue factor, the release of proinflammatory cytokines, and interactions with endothelial and circulating blood cells. Platelets, a key regulator cell population of haemostasis and thrombosis, are known to be an important contributor of VTE, not only to through their involvement in thrombus formation but also in promoting cancer survival and spread. Recently, neutrophils are implicated as an important mediator of cancer-associated thrombosis. Neutrophil extracellular traps (NETs), released from activated neutrophils, have been reported in tumour samples and their presence in vivo is associated with metastasis.
This Special Issue will cover the current research of thrombosis and haemostasis in cancer development. Both basic mechanisms underlying the processes, clinical observations and therapeutic implications of targeting key regulators of thrombosis and haemostasis will be discussedProf. Dr. Marco Falasca
Dr. Pat Metharom
Manuscript Submission Information
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access monthly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1000 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.
- cancer biology
- cancer-associated thrombosis
The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.
Title: Bone Marrow Defects and Platelet Function
Authors: Robert K. Andrews1 et al. (TBA)
Affiliation: Australian Centre for Blood Diseases, Monash University, Melbourne, Australia
Abstract: The bloodstream typically contains >500 billion anucleate circulating platelets, derived from megakaryocytes in the bone marrow or in other tissue(s) in the body. 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, erythrocytes and platelets, recent evidence has shown that lymphoid lineage defects in cell lines leading to B cells, T cells and natural killer (NK) cells surprisingly also lead to abnormal circulating platelets. Current evidence is limited regarding whether this latter phenomenon might potentially result 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.
Title: Cancer-associated thrombosis: mechanisms, treatment and implications for cancer metastasis
Authors: Norbaini Abdol Razak and Pat Metharom
Abstract: Cancer-associated thrombosis is a major cause of mortality in cancer patients, the most common type being venous thromboembolism (VTE). Several risk factors for developing VTE coexist with cancer patients, such as chemotherapy and immobilisation, contributing to the increased risk cancer patients have of developing VTE compared to non-cancer patients. Cancer cells are capable of activating the coagulation cascade and other pro-thrombotic properties of host cells, and many anti-cancer treatments themselves are being described as additional mechanisms for promoting VTE. Furthermore, studies have reported that coagulation and haemostatic activation in cancer may also contribute to tumour progression and metastasis. This review will discuss the multiple mechanisms involved in cancer-associated thrombosis including the role of anti-cancer drugs, the current treatment strategies available for VTE in cancer patients, and the existing associations of thrombosis and tumour progression in cancer patients.