Down for the count in acute myeloid leukemia

Aaron D. Goldberg, Martin S. Tallman

Research output: Contribution to journalComment/debatepeer-review

1 Scopus citations


In this issue of Blood, Rauch et al provide evidence for a novel mechanism to explain a fundamental yet enigmatic observation that has plagued hematologists for decades: the decline in nonleukemic hematopoiesis in the bone marrow of patients with acute myeloid leukemia (AML). The authors found that high expression of the thrombopoietin (TPO) receptor MPL on AML blasts predicts neutropenia and thrombocytopenia, and that AML blasts expressing high levels of MPL deplete TPO in cell culture and in mouse models.

Original languageEnglish (US)
Pages (from-to)2195-2197
Number of pages3
Issue number18
StatePublished - Nov 3 2016

ASJC Scopus subject areas

  • Biochemistry
  • Immunology
  • Hematology
  • Cell Biology


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