{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,31]],"date-time":"2026-07-31T06:00:51Z","timestamp":1785477651532,"version":"3.56.0"},"reference-count":78,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,7,31]],"date-time":"2026-07-31T00:00:00Z","timestamp":1785456000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Pharmacol."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Anthracyclines are widely used antineoplastic agents with well-recognized cardiotoxicity; however, reports of hypercoagulable adverse events (HC-AEs) remain scattered and incompletely described. A systematic characterization of these events across large pharmacovigilance databases may help to clarify reporting patterns and generate hypotheses for further investigation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We performed a disproportionality analysis using the FDA Adverse Event Reporting System (FAERS) and the WHO Global Individual Case Safety Report Database (VigiBase) to identify HC-AEs reported in association with anthracyclines. Signals consistently observed in both databases were further explored descriptively with respect to reported drug-specific patterns and time-to-onset (TTO). To support hypothesis generation, exploratory analyses integrating transcriptomic data from The Cancer Genome Atlas (TCGA), retrospective clinical coagulation parameters, and\n                      <jats:italic>in vivo<\/jats:italic>\n                      observations from a tumor-bearing mouse model were conducted.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Across both pharmacovigilance platforms, 26 HC-AEs were consistently reported in association with anthracyclines. Doxorubicin was associated with the widest range of reported HC-AEs, whereas daunorubicin and aclarubicin showed more specific reporting patterns involving cerebral or intracardiac thrombosis and disseminated intravascular coagulation, respectively. The reported median TTO of HC-AEs following anthracycline exposure was 32.5 days (vs. 48.0 days in non-recipients,\n                      <jats:italic>P<\/jats:italic>\n                      &amp;lt; 0.001), with a predominance of early-onset events, particularly among younger patients (\u226439 years). Exploratory analyses suggested potential involvement of pathways related to cyclic adenosine monophosphate (cAMP) signaling and heparan sulfate biosynthesis, which were directionally consistent with observed alterations in coagulation-related parameters in clinical samples and experimental models.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>This multi-database pharmacovigilance analysis provides a systematic overview of HC-AEs reported in association with anthracyclines, highlighting drug-specific reporting patterns and variations in onset timing across age groups. While causal inference cannot be established, the concordant signals observed across independent data sources support heightened clinical awareness and hypothesis-driven surveillance of thrombotic complications during anthracycline therapy.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fphar.2026.1856410","type":"journal-article","created":{"date-parts":[[2026,7,31]],"date-time":"2026-07-31T05:38:45Z","timestamp":1785476325000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["From signal to significance: characterizing anthracycline-related hypercoagulable adverse events via pharmacovigilance, animal models, and clinical observation"],"prefix":"10.3389","volume":"17","author":[{"given":"Wen","family":"Huang","sequence":"first","affiliation":[{"name":"Department of Oncology, Zhujiang Hospital, Southern Medical University","place":["Guangzhou, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Junyi","family":"Shen","sequence":"additional","affiliation":[{"name":"Department of Oncology, Zhujiang Hospital, Southern Medical University","place":["Guangzhou, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jian","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Oncology, Zhujiang Hospital, Southern Medical University","place":["Guangzhou, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,7,31]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"380","DOI":"10.3390\/cancers10100380","article-title":"Cancer-associated thrombosis: an overview of mechanisms, risk factors, and treatment","volume":"10","author":"Abdol Razak","year":"2018","journal-title":"Cancers"},{"key":"B2","doi-asserted-by":"publisher","first-page":"23","DOI":"10.3390\/bloods1010006","article-title":"Doxorubicin enhances procoagulant activity of endothelial cells after exposure to tumour microparticles on microfluidic devices","volume":"1","author":"Algarni","year":"2020","journal-title":"Hemato"},{"key":"B3","doi-asserted-by":"publisher","first-page":"817977","DOI":"10.3389\/fcvm.2021.817977","article-title":"Novel mechanisms of anthracycline-induced cardiovascular toxicity: a focus on thrombosis, cardiac atrophy, and programmed cell death","volume":"8","author":"Antoniak","year":"2021","journal-title":"Front. 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