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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.
This article was published in the following journal.
Name: Genes, chromosomes & cancer
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The development and formation of various types of BLOOD CELLS. Hematopoiesis can take place in the BONE MARROW (medullary) or outside the bone marrow (HEMATOPOIESIS, EXTRAMEDULLARY).
A basic helix-loop-helix transcription factor that plays a critical role in HEMATOPOIESIS and as a positive regulator in the differentiation of ERYTHROID CELLS. Chromosome translocations involving the TAL-1 gene are associated with T-CELL ACUTE LYMPHOCYTIC LEUKEMIA.
Clonal hematopoetic disorder caused by an acquired genetic defect in PLURIPOTENT STEM CELLS. It starts in MYELOID CELLS of the bone marrow, invades the blood and then other organs. The condition progresses from a stable, more indolent, chronic phase (LEUKEMIA, MYELOID, CHRONIC PHASE) lasting up to 7 years, to an advanced phase composed of an accelerated phase (LEUKEMIA, MYELOID, ACCELERATED PHASE) and BLAST CRISIS.
A spectrum of disorders characterized by clonal expansions of the peripheral blood LYMPHOCYTE populations known as large granular lymphocytes which contain abundant cytoplasm and azurophilic granules. Subtypes develop from either CD3-negative NATURAL KILLER CELLS or CD3-positive T-CELLS. The clinical course of both subtypes can vary from spontaneous regression to progressive, malignant disease.
A receptor tyrosine kinase that is involved in HEMATOPOIESIS. It is closely related to FMS PROTO-ONCOGENE PROTEIN and is commonly mutated in acute MYELOID LEUKEMIA.
Leukemia is a type of cancer of the blood or bone marrow characterized by an abnormal increase of immature white blood cells called "blasts". Leukemia is a broad term covering a spectrum of diseases. In turn, it is part of the even broader grou...
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