Clonal hematopoiesis and pre-leukemia -genetics, biology and clinical implications.

08:00 EDT 2nd April 2019 | BioPortfolio

Summary of "Clonal hematopoiesis and pre-leukemia -genetics, biology and clinical implications."

Myeloid neoplasms including myelodysplastic syndromes and acute myeloid leukemia originate from hematopoietic stem cells through sequential acquisition of genetic and epigenetic alterations that ultimately cause the disease-specific phenotype of impaired differentiation and increased proliferation. It has become clear that preleukemic clonal hematopoiesis, characterized by an expansion of stem and progenitor cells that carry somatic mutations but are still capable of normal differentiation, can precede the development of clinically overt myeloid neoplasia by many years. Clonal hematopoiesis commonly develops in the ageing hematopoietic system, yet progression to myelodysplasia or acute myeloid leukemia is rare. The discovery that myeloid neoplasms frequently develop from pre-malignant precursor conditions that are detectable in many healthy individuals has important consequences for the diagnosis, and potentially for the treatment of these disorders. In this review, we summarize the current knowledge on clonal hematopoiesis as a precursor of myeloid cancers and the implications of clonal hematopoiesis-related gene mutations in the diagnostic workup of patients with suspected myelodysplastic syndrome. We will discuss the risk of progression associated with clonal hematopoiesis in healthy persons and in patients undergoing chemotherapy for a non-hematologic cancer, and the significance of clonal hematopoiesis in autologous and allogeneic stem cell transplantation. Finally, we will review the significance of pre-leukemic clones in AML and their persistence in patients who achieve a remission after chemotherapeutic treatment. This article is protected by copyright. All rights reserved.


Journal Details

This article was published in the following journal.

Name: Genes, chromosomes & cancer
ISSN: 1098-2264


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