Rebound Thrombocytosis after Induction Chemotherapy is a Strong Biomarker for Favorable Outcome in AML Patients
Supplemental Digital Content is available in the text Whereas the molecular events underlying acute myeloid leukemia (AML) are increasingly identified, dynamics of hematologic recovery following induction chemotherapy remain mysterious. Platelet recovery may vary between incomplete and excess recove...
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Published in | HemaSphere Vol. 3; no. 2; pp. e180 - n/a |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Wolters Kluwer Health
01.04.2019
Wiley |
Online Access | Get full text |
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Summary: | Supplemental Digital Content is available in the text
Whereas the molecular events underlying acute myeloid leukemia (AML) are increasingly identified, dynamics of hematologic recovery following induction chemotherapy remain mysterious. Platelet recovery may vary between incomplete and excess recovery among patients achieving remission. We analyzed platelet recovery after the first induction cycle in 291 consecutive AML patients. We defined excess platelet rebound (EPR) as platelet increase above 500 G/L. We observed EPR in 120 (41.2%) patients. EPR+ patients had lower platelets at diagnosis, higher marrow infiltration, more frequently NPM1 mutations, and were associated with ELN favorable risk. Absence of EPR correlated with complex karyotypes, ELN intermediate‐I and adverse risk, and therapy‐related AML. Overall survival was better in EPR+ patients than EPR‐ (median 125 vs 41 months; p = 0.04), as was disease‐free survival. By multivariate analysis, EPR+ was an independent parameter associated with favorable survival. Plasma thrombopoietin (TPO) levels at diagnosis indicated EPR+ (p < 0.0001), while GATA‐1, GATA‐2, and MPL mRNA expression did not differ between EPR+ and EPR‐ patients. Finally, transcription factors blocking early megakaryopoiesis were upregulated in EPR‐ patients, while NFE2 involved in late megakaryocyte differentiation was increased in EPR+ patients. Our work identifies mechanisms involved in platelet recovery after induction chemotherapy. |
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Bibliography: | www.hemaspherejournal.com The authors have indicated they have no potential conflicts of interest to disclose. Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal's Website Bianca R. Schnell and Katja Seipel contributed equally. . ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 2572-9241 2572-9241 |
DOI: | 10.1097/HS9.0000000000000180 |