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      Antiplatelet agents for cancer treatment: a real perspective or just an echo from the past?

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          Abstract

          The association between coagulation and cancer development has been observed for centuries. However, the connection between inflammation and malignancy is also well-recognized. The plethora of evidence indicates that among multiple hemostasis components, platelets play major roles in cancer progression by providing surface and granular contents for several interactions as well as behaving like immune cells. Therefore, the anticancer potential of anti-platelet therapy has been intensively investigated for many years. Anti-platelet agents may prevent cancer, decrease tumor growth, and metastatic potential, as well as improve survival of cancer patients. On the other hand, there are suggestions that antiplatelet treatment may promote solid tumor development in a phenomenon described as “cancers follow bleeding.” The controversies around antiplatelet agents justify insight into the subject to establish what, if any, role platelet-directed therapy has in the continuum of anticancer management.

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          The platelet contribution to cancer progression.

          N M Bambace, C. Holmes (2011)
          Traditionally viewed as major cellular components in hemostasis and thrombosis, the contribution of platelets to the progression of cancer is an emerging area of research interest. Complex interactions between tumor cells and circulating platelets play an important role in cancer growth and dissemination, and a growing body of evidence supports a role for physiologic platelet receptors and platelet agonists in cancer metastases and angiogenesis. Platelets provide a procoagulant surface facilitating amplification of cancer-related coagulation, and can be recruited to shroud tumor cells, thereby shielding them from immune responses, and facilitate cancer growth and dissemination. Experimental blockade of key platelet receptors, such as GP1b/IX/V, GPIIbIIIa and GPVI, has been shown to attenuate metastases. Platelets are also recognized as dynamic reservoirs of proangiogenic and anti-angiogenic proteins that can be manipulated pharmacologically. A bidirectional relationship between platelets and tumors is also seen, with evidence of 'tumor conditioning' of platelets. The platelet as a reporter of malignancy and a targeted delivery system for anticancer therapy has also been proposed. The development of platelet inhibitors that influence malignancy progression and clinical testing of currently available antiplatelet drugs represents a promising area of targeted cancer therapy. © 2011 International Society on Thrombosis and Haemostasis.
          Article 0 comments Cited 269 times – based on 0 reviews     Review now
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            Low-dose aspirin in the primary prevention of cancer: the Women's Health Study: a randomized controlled trial.

            Nancy Cook, I-Min Lee, J. Michael Gaziano … (2005)
            Basic research and observational evidence as well as results from trials of colon polyp recurrence suggest a role for aspirin in the chemoprevention of cancer. To examine the effect of aspirin on the risk of cancer among healthy women. In the Women's Health Study, a randomized 2 x 2 factorial trial of aspirin and vitamin E conducted between September 1992 and March 2004, 39 876 US women aged at least 45 years and initially without previous history of cancer, cardiovascular disease, or other major chronic illness were randomly assigned to receive either aspirin or aspirin placebo and followed up for an average of 10.1 years. A dose of 100 mg of aspirin (n=19 934) or aspirin placebo (n=19 942) administered every other day. Confirmed newly diagnosed invasive cancer at any site, except for nonmelanoma skin cancer. Incidence of breast, colorectal, and lung cancer were secondary end points. No effect of aspirin was observed on total cancer (n = 2865; relative risk [RR], 1.01; 95% confidence interval [CI], 0.94-1.08; P = .87), breast cancer (n = 1230; RR, 0.98; 95% CI, 0.87-1.09; P = .68), colorectal cancer (n = 269; RR, 0.97; 95% CI, 0.77-1.24; P = .83), or cancer of any other site, with the exception of lung cancer for which there was a trend toward reduction in risk (n = 205; RR, 0.78; 95% CI, 0.59-1.03; P = .08). There was also no reduction in cancer mortality either overall (n = 583; RR, 0.95; 95% CI, 0.81-1.11; P = .51) or by site, except for lung cancer mortality (n = 140; RR, 0.70; 95% CI, 0.50-0.99; P = .04). No evidence of differential effects of aspirin by follow-up time or interaction with vitamin E was found. Results from this large-scale, long-term trial suggest that alternate day use of low-dose aspirin (100 mg) for an average 10 years of treatment does not lower risk of total, breast, colorectal, or other site-specific cancers. A protective effect on lung cancer or a benefit of higher doses of aspirin cannot be ruled out.
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              Antimetastatic effects associated with platelet reduction.

              C. Stewart, T. Gasic, G. Gasic (1968)
              Article 0 comments Cited 139 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Marek Z. Wojtukiewicz: 48-85-6646734 , mzwojtukiewicz@gmail.com
                Journal
                Journal ID (nlm-ta): Cancer Metastasis Rev
                Journal ID (iso-abbrev): Cancer Metastasis Rev
                Title: Cancer Metastasis Reviews
                Publisher: Springer US (New York )
                ISSN (Print): 0167-7659
                ISSN (Electronic): 1573-7233
                Publication date (Electronic): 27 July 2017
                Publication date PMC-release: 27 July 2017
                Publication date (Print): 2017
                Volume: 36
                Issue: 2
                Pages: 305-329
                Affiliations
                [1 ]ISNI 0000000122482838, GRID grid.48324.39, Department of Oncology, , Medical University of Bialystok, ; 12 Ogrodowa St., 15-025, Bialystok, Poland
                [2 ]Department of Radiotherapy, Comprehensive Cancer Center in Bialystok, Bialystok, Poland
                [3 ]Department of Clinical Oncology, Comprehensive Cancer Center in Bialystok, Bialystok, Poland
                [4 ]Department of Pathology-School of Medicine, Bioactive Lipids Research Program, Detroit, MI 48202 USA
                [5 ]ISNI 0000 0001 1456 7807, GRID grid.254444.7, Departments of Chemistry, , Wayne State University, ; Detroit, MI 48202 USA
                [6 ]ISNI 0000 0001 1456 7807, GRID grid.254444.7, Department of Oncology, , Karmanos Cancer Institute, ; Detroit, MI 48202 USA
                Article
                Publisher ID: 9683
                DOI: 10.1007/s10555-017-9683-z
                PMC ID: 5557869
                PubMed ID: 28752248
                SO-VID: 770a08f9-e0de-4610-8b52-6c4df685a0cd
                Copyright © © The Author(s) 2017
                License:

                Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

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                Subject: Article
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                issue-copyright-statement © Springer Science+Business Media, LLC 2017

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: platelet,cancer,anti-platelet therapy
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: platelet, cancer, anti-platelet therapy

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