ReviewCurrent opinion in hematology2025
Hemostatic abnormalities in acute promyelocytic leukemia: clinical implications and mechanisms.
Review in Current opinion in hematology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Article
- Comparison of changes in blood cells and hemostatic biomarkers in mouse xenograft models of acute myeloid leukemia and acute promyelocytic leukemia.Research and practice in thrombosis and haemostasis · 2026Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
purpose of reviewAcute promyelocytic leukemia (APL) is a subtype of acute myeloid leukemia. The long-term prognosis for APL is generally more favorable than for other types of acute leukemia due to the use of differentiation therapies. However, early hemorrhagic death remains a significant clinical challenge in APL patients. RECENT
findingsReal-world studies reveal that the rate of early hemorrhagic death remains high (10-30%) in APL patients in the era of differentiation therapy. APL patients have systemic hemostatic changes including activation of coagulation followed by consumption of coagulation factors, hyperfibrinolysis, and severe thrombocytopenia. Our study found that tissue factor contributes to a bleeding phenotype in mouse models of APL. In-vitro studies suggest that there may be direct or indirect interaction between APL cells and brain endothelial cells. SUMMARY: Predictors of hemorrhagic death in APL are only partially understood. The associations between bleeding and hyperfibrinolysis or thrombocytopenia in APL need to be determined. The interaction between APL cells and brain endothelial cells need to be determined in vivo .
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