Allogeneic haematopoietic stem cell transplantation for primary myelofibrosis and myelofibrosis evolved from other myeloproliferative neoplasms. Review uri icon

Overview

abstract

  • PURPOSE OF REVIEW: Allogeneic haematopoietic stem cell transplantation (allo-HSCT) is the only curative treatment for myelofibrosis. Major improvements in the field, such as the introduction of reduced intensity conditioning regimens, have made transplant a better tolerated treatment that can be offered to older patients and those with comorbidities. However, treatment-related toxicities, graft-versus-host disease, infectious complications and relapse remain major problems posttransplant. We reviewed here the recent published data and outline the criteria to select patients with myelofibrosis who can benefit the most from this curative treatment. RECENT FINDINGS: Data regarding mutations in myelofibrosis have been useful to better define the prognosis of patients and have provided a tool to monitor minimal residual disease after transplantation. New data regarding the use of age and comorbidities has allowed a better selection of patients who can benefit from transplantation. Janus-activated kinase signal (JAK) 1/2 inhibitors pretransplant can improve patient's performance status and potentially improve transplant outcomes. SUMMARY: Improvements in the field of allo-HSCT, the ability to improve patient's performance status prior to transplant with JAK1/2 inhibitors and a more accurate disease risk stratification based on molecular mutations to select patients who can benefit from allo-HSCT should result in better transplant outcomes. Efforts should be made to transplant patients with myelofibrosis on prospective studies to answer some unresolved questions.

publication date

  • March 1, 2015

Research

keywords

  • Hematopoietic Stem Cell Transplantation
  • Myeloproliferative Disorders
  • Primary Myelofibrosis

Identity

Scopus Document Identifier

  • 84923225083

Digital Object Identifier (DOI)

  • 10.1097/MOH.0000000000000121

PubMed ID

  • 25635756

Additional Document Info

volume

  • 22

issue

  • 2