Revisiting thrombocytopenia in acute promyelocytic leukemia

Revisiting thrombocytopenia in acute promyelocytic leukemia Leukemia (2018) 32:1477–1478 https://doi.org/10.1038/s41375-018-0105-1 COMMENT Acute myeloid leukemia 1 2 Florian Kuchenbauer Christian Buske Received: 20 February 2018 / Accepted: 23 February 2018 / Published online: 23 March 2018 © Macmillan Publishers Limited, part of Springer Nature 2018 Acute promyelocytic leukemia (APL), which accounts for and the underlying molecular mechanisms of thrombocy- 10–15% of acute myeloid leukemia (AML) cases, is one of topenia, caused by APL cells are not fully understood. the true success stories in oncology, as targeted therapeutic In this issue of Leukemia, Lavallée et al. [8] reported approaches have converted this former lethal disease into a on intriguing findings, characterizing Podoplanin (PDPN), a disease from which the vast majority of patients is cured. gene involved in platelet aggregation, as a protein specifi- Historically, this unique and highly lethal leukemia subtype cally expressed in human APL and being able to cause was characterized by fatal bleeding events as documented thrombocytopenia and prolonged bleeding time in a xeno- by early studies in the 1950s with median survival rates graft model of human AML cell lines. often below 1 month [1]. This progress in the clinical How did they identify PDPN as a key gene in APL? management of http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Leukemia Springer Journals

Revisiting thrombocytopenia in acute promyelocytic leukemia

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Publisher
Nature Publishing Group UK
Copyright
Copyright © 2018 by Macmillan Publishers Limited, part of Springer Nature
Subject
Medicine & Public Health; Medicine/Public Health, general; Internal Medicine; Intensive / Critical Care Medicine; Cancer Research; Oncology; Hematology
ISSN
0887-6924
eISSN
1476-5551
D.O.I.
10.1038/s41375-018-0105-1
Publisher site
See Article on Publisher Site

Abstract

Leukemia (2018) 32:1477–1478 https://doi.org/10.1038/s41375-018-0105-1 COMMENT Acute myeloid leukemia 1 2 Florian Kuchenbauer Christian Buske Received: 20 February 2018 / Accepted: 23 February 2018 / Published online: 23 March 2018 © Macmillan Publishers Limited, part of Springer Nature 2018 Acute promyelocytic leukemia (APL), which accounts for and the underlying molecular mechanisms of thrombocy- 10–15% of acute myeloid leukemia (AML) cases, is one of topenia, caused by APL cells are not fully understood. the true success stories in oncology, as targeted therapeutic In this issue of Leukemia, Lavallée et al. [8] reported approaches have converted this former lethal disease into a on intriguing findings, characterizing Podoplanin (PDPN), a disease from which the vast majority of patients is cured. gene involved in platelet aggregation, as a protein specifi- Historically, this unique and highly lethal leukemia subtype cally expressed in human APL and being able to cause was characterized by fatal bleeding events as documented thrombocytopenia and prolonged bleeding time in a xeno- by early studies in the 1950s with median survival rates graft model of human AML cell lines. often below 1 month [1]. This progress in the clinical How did they identify PDPN as a key gene in APL? management of

Journal

LeukemiaSpringer Journals

Published: Mar 23, 2018

References

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