Bone marrow morphological features and therapy in patients with Philadelphia-negative neoplasms

Expert Rev Hematol. 2021 Sep;14(9):841-850. doi: 10.1080/17474086.2021.1967138. Epub 2021 Aug 20.

Abstract

Introduction Chronic myeloproliferative neoplasm (MPNs) are clonal malignant bone marrow (BM) diseases, arising from a hematopoietic stem cell. All therapies for these neoplasms have peculiar effects on the bone marrow, but little evidence has been described in the literature.Areas covered This review examines BM morphological changes following the main treatments in Philadelphia-negative MPNs. Hydroxyurea can reduce the cellularity of the erythroid and megakaryocyte lineages but has minimal impact on fibrotic evolution. There is general agreement on its dysplastic effects, with a high incidence of acute myeloid leukemia and myelodysplastic syndrome. Interferon treatment can reduce or normalize BM cellularity, improve erythropoiesis, and reduce the number and atypicality of megakaryocytes. Most data describe reduction or complete resolution of marrow fibrosis; dysplastic effects are not reported. Anagrelide may induce an increase in the number of BM megakaryocytes, especially immature megakaryocytes or precursors, and a worsening of marrow fibrosis or increased transformation of essential thrombocythemia into myelofibrosis. Ruxolitinib can improve or stabilize BM fibrosis and reduces the frequency and dense clustering of megakaryocytes.Expert opinion Since previous therapy can modify BM features, it is essential to obtain information on previous or current therapies and to collect complete clinical information.

Keywords: Chronic myeloproliferative neoplasm; anagrelide; bone marrow; hydroxyurea; interferon; ruxolitinib.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Bone Marrow / pathology
  • Humans
  • Myeloproliferative Disorders* / diagnosis
  • Myeloproliferative Disorders* / etiology
  • Myeloproliferative Disorders* / therapy
  • Neoplasms* / complications
  • Primary Myelofibrosis* / drug therapy
  • Primary Myelofibrosis* / etiology
  • Thrombocythemia, Essential* / pathology