title: Platelets at the interface of thrombosis, inflammation, and cancer.
abstract: Although once primarily recognized for its roles in hemostasis and thrombosis, the platelet has been increasingly recognized as a multipurpose cell. Indeed, circulating platelets have the ability to influence a wide range of seemingly unrelated pathophysiologic events. Here, we highlight some of the notable observations that link platelets to inflammation, reinforcing the platelet's origin from a lower vertebrate cell type with both hemostatic and immunologic roles. In addition, we consider the relevance of platelets in cancer biology by focusing on the hallmarks of cancer and the ways platelets can influence multistep development of tumors. Beyond its traditional role in hemostasis and thrombosis, the platelet's involvement in the interplay between hemostasis, thrombosis, inflammation, and cancer is likely complex, yet extremely important in each disease process. The existence of animal models of platelet dysfunction and currently used antiplatelet therapies provide a framework for understanding mechanistic insights into a wide range of pathophysiologic events. Thus, the basic scientist studying platelet function can think beyond the traditional hemostasis and thrombosis paradigms, while the practicing hematologist must appreciate platelet relevance in a wide range of disease processes.
authors.affiliation: Department of Physiology & Biophysics, University of Arkansas for Medical Sciences, Little Rock, AR.
authors.forename: Aime T
authors.identifier: http://orcid.org/0000-0002-1677-5228
authors.initials: AT
authors.lastname: Franco
authors.affiliation: Department of Physiology & Biophysics, University of Arkansas for Medical Sciences, Little Rock, AR.
authors.forename: Adam
authors.initials: A
authors.lastname: Corken
authors.affiliation: Department of Physiology & Biophysics, University of Arkansas for Medical Sciences, Little Rock, AR.
authors.forename: Jerry
authors.identifier: http://orcid.org/0000-0001-8860-6338
authors.initials: J
authors.lastname: Ware
mesh_terms: D000818:Animals; D016588:Anticarcinogenic Agents / Q000494:pharmacology; D001241:Aspirin / Q000494:pharmacology; D001792:Blood Platelets / Q000276:immunology / Q000502:physiology*; D016923:Cell Death; D049109:Cell Proliferation; D055252:Cell-Derived Microparticles / Q000276:immunology / Q000502:physiology; D006801:Humans; D007249:Inflammation / Q000097:blood* / Q000150:complications / Q000276:immunology; D008954:Models, Biological; D009361:Neoplasm Invasiveness; D009362:Neoplasm Metastasis; D009369:Neoplasms / Q000097:blood* / Q000209:etiology / Q000276:immunology; D014411:Neoplastic Stem Cells / Q000473:pathology / Q000502:physiology; D009389:Neovascularization, Pathologic; D009504:Neutrophils / Q000502:physiology; D015398:Signal Transduction; D013927:Thrombosis / Q000097:blood* / Q000209:etiology / Q000276:immunology; D019139:Tumor Escape
chemical_list: D016588:Anticarcinogenic Agents; D001241:Aspirin