Abstract
Myeloproliferative neoplasms (MPNs) represent a group of diseases that affect the myeloid lineage, characterized by the presence of an excess of terminally differentiated myeloid cells. Defects causing clonal hematopoiesis are a key factor in the emergence of these diseases. Throughout the years, a number of causative defects have been identified, predominantly affecting cytokine signaling and gene expression regulation. This review aims to provide an update on the current status of the MPN field in relation to identification of molecular defects involved in the disease and its clonal evolution.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Clonal Evolution / genetics*
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Cytokines / biosynthesis
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Cytokines / genetics
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DNA-Binding Proteins / genetics
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DNA-Binding Proteins / metabolism
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Dioxygenases
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Epigenesis, Genetic
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Gene Expression Regulation, Neoplastic*
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Hematopoiesis
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Hematopoietic Stem Cells / metabolism
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Hematopoietic Stem Cells / pathology*
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Humans
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Janus Kinases / genetics
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Janus Kinases / metabolism
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Mutation
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Myeloproliferative Disorders / genetics*
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Myeloproliferative Disorders / metabolism
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Myeloproliferative Disorders / pathology
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Neoplasm Proteins / genetics*
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Neoplasm Proteins / metabolism
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Neoplasms / genetics*
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Neoplasms / metabolism
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Neoplasms / pathology
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Proto-Oncogene Proteins / genetics
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Proto-Oncogene Proteins / metabolism
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STAT Transcription Factors / genetics
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STAT Transcription Factors / metabolism
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Signal Transduction
Substances
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Cytokines
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DNA-Binding Proteins
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Neoplasm Proteins
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Proto-Oncogene Proteins
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STAT Transcription Factors
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Dioxygenases
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TET2 protein, human
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Janus Kinases