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      Improved outcomes after radiotherapy for prostate cancer: Anticoagulation, antiplatelet therapy, and platelet count as key factors in disease progression

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          Abstract

          Background

          Several studies have suggested that antiplatelet (AP) or anticoagulant (AC) therapy may improve outcome in men with prostate cancer. We evaluated the effects of AP/AC therapy and tested the hypothesis that platelet count may also be associated with outcomes.

          Methods

          A total of 482 patients received primary radiotherapy (median dose 72 Gy) for nonmetastatic prostate cancer; 49% received androgen deprivation therapy. NCCN risk was low/intermediate/high risk in 39%/39%/22%. AP/AC therapy and platelet counts were analyzed with respect to freedom from biochemical failure (FFBF, nadir+2), distant metastasis (FFDM), and cause specific survival (CSS).

          Results

          After a median follow‐up of 103 months, 10‐year FFBF, FFDM, and CSS were 77%, 92%, and 96%, respectively. The 10‐year cumulative incidence of BF and DM (with death as a competing event) was 19% and 7.0%, respectively. The 32% of men on AP/AC therapy had a lower incidence of 10‐year BF ( P = .016) and a trend toward a lower incidence of DM ( P = .084) and CSS ( P = .091). In the entire cohort, lowest platelet quartile (platelet count <187) was associated with higher 10‐year BF (31% vs 16%, P = .0042) but not DM (9.4% vs 5.2%, P = .22) nor CSS ( P = .76) compared with those patients with platelet count ≥187. AP/AC therapy was associated with a larger absolute reduction in BF for men with lowest platelet quartile (10‐year BF of 21% vs 38%, P = .092) vs platelet ≥187 (10‐year BF of 10% vs 18%, P = .053). Lowest platelet quartile remained associated with higher BF and DM on multivariable analysis controlling for risk category, WBC, and Hg.

          Conclusion

          AP/AC was associated with improved FFBF. Low platelet count was associated with inferior FFBF and FFDM after prostate radiotherapy. This association was tempered when antiplatelet and anticoagulant therapy was administered.

          Abstract

          482 men received primary radiotherapy for non‐metastatic prostate cancer and those men with pre‐treatment platelet count in the lowest quartile experienced worse 10‐year freedom from biochemical failure (61% vs 81%, P < .0001) and a trend towards worsened FFDM (88% vs 94%, P = .064). This negative effect was abrogated by antiplatelet therapy or anticoagulation, suggesting a connection between previously reported benefits of such therapy in prostate cancer outcomes and thrombocytopenia.

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          Most cited references27

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          Defining biochemical failure following radiotherapy with or without hormonal therapy in men with clinically localized prostate cancer: recommendations of the RTOG-ASTRO Phoenix Consensus Conference.

          In 1996 the American Society for Therapeutic Radiology and Oncology (ASTRO) sponsored a Consensus Conference to establish a definition of biochemical failure after external beam radiotherapy (EBRT). The ASTRO definition defined prostate specific antigen (PSA) failure as occurring after three consecutive PSA rises after a nadir with the date of failure as the point halfway between the nadir date and the first rise or any rise great enough to provoke initiation of therapy. This definition was not linked to clinical progression or survival; it performed poorly in patients undergoing hormonal therapy (HT), and backdating biased the Kaplan-Meier estimates of event-free survival. A second Consensus Conference was sponsored by ASTRO and the Radiation Therapy Oncology Group in Phoenix, Arizona, on January 21, 2005, to revise the ASTRO definition. The panel recommended: (1) a rise by 2 ng/mL or more above the nadir PSA be considered the standard definition for biochemical failure after EBRT with or without HT; (2) the date of failure be determined "at call" (not backdated). They recommended that investigators be allowed to use the ASTRO Consensus Definition after EBRT alone (no hormonal therapy) with strict adherence to guidelines as to "adequate follow-up." To avoid the artifacts resulting from short follow-up, the reported date of control should be listed as 2 years short of the median follow-up. For example, if the median follow-up is 5 years, control rates at 3 years should be cited. Retaining a strict version of the ASTRO definition would allow comparisons with a large existing body of literature.
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            NCCN Guidelines Updates: Prostate Cancer and Prostate Cancer Early Detection

            Peter H. Carroll, MD, MPH, and James L. Mohler, MD, updated attendees on what is new in the 2018 NCCN Guidelines for Prostate Cancer Early Detection and for Prostate Cancer, respectively. Their presentations touched on new screening recommendations, shared decision-making, risk stratification, the role of genomic and molecular testing, active surveillance, and newer systemic treatments.
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              Metastasis: new functional implications of platelets and megakaryocytes.

              Platelets are essential components of hemostasis. Due to a plethora of factors released on activation, platelet functions are also connected to tumor growth, notably by acting on angiogenesis. It is now well recognized that major roles of platelets in the poor outcome of cancer patients occurs during hematogenous dissemination of cancer cells. In this review, we describe recent insights into the molecular mechanisms supporting the prometastatic activity of platelets. Platelets have been shown to promote survival of circulating tumor cells (CTCs) in the bloodstream by conferring resistance to the shear stress and attack from natural killer cells. Recently, platelets were found to promote and/or maintain the state of epithelial to mesenchymal transition on CTCs through platelet secretion of transforming growth factor β in response to CTC activation. At a later stage in the metastatic process, platelets promote extravasation and establishment of metastatic cells in distant organs as observed in bone. This particular environment is also the site of hematopoiesis, megakaryocytopoiesis, and platelet production. Increasing the number of megakaryocytes (MKs) in the bone marrow results in a high bone mass phenotype and inhibits skeletal metastasis formation of prostate cancer cells. As a result of their specific location in vascular niches in the bone marrow, MK activity might contribute to the "seed and soil" suitability between CTCs and bone. In conclusion, recent findings have made a great advance in our knowledge on how platelets contribute to the metastatic dissemination of cancer cells and that may support the development of new antimetastasis therapies.
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                Author and article information

                Contributors
                sliauw@radonc.uchicago.edu
                Journal
                Cancer Med
                Cancer Med
                10.1002/(ISSN)2045-7634
                CAM4
                Cancer Medicine
                John Wiley and Sons Inc. (Hoboken )
                2045-7634
                13 May 2020
                July 2020
                : 9
                : 13 ( doiID: 10.1002/cam4.v9.13 )
                : 4667-4675
                Affiliations
                [ 1 ] Department of Radiation and Cellular Oncology University of Chicago Chicago IL USA
                [ 2 ] Radiation Oncology Associates Inova Hospital Fairfax VA USA
                [ 3 ] Department of Pathology University of Chicago Chicago IL USA
                Author notes
                [*] [* ] Correspondence

                Stanley L. Liauw, 5758 South Maryland Avenue, Chicago, IL 60637, USA.

                Email: sliauw@ 123456radonc.uchicago.edu

                Author information
                https://orcid.org/0000-0003-0300-1618
                https://orcid.org/0000-0002-4701-2469
                Article
                CAM43087
                10.1002/cam4.3087
                7333841
                32400122
                4204b5ec-7b91-4577-80f8-728fb8f3f8c7
                © 2020 The Authors. Cancer Medicine published by John Wiley & Sons Ltd.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                : 25 November 2019
                : 07 April 2020
                : 08 April 2020
                Page count
                Figures: 3, Tables: 3, Pages: 9, Words: 5677
                Categories
                Original Research
                Clinical Cancer Research
                Original Research
                Custom metadata
                2.0
                July 2020
                Converter:WILEY_ML3GV2_TO_JATSPMC version:5.8.5 mode:remove_FC converted:03.07.2020

                Oncology & Radiotherapy
                blood platelets,prostatic neoplasms,radiotherapy
                Oncology & Radiotherapy
                blood platelets, prostatic neoplasms, radiotherapy

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