4.1 Article

Genetic Basis of MPN: Beyond JAK2-V617F

Journal

CURRENT HEMATOLOGIC MALIGNANCY REPORTS
Volume 8, Issue 4, Pages 299-306

Publisher

CURRENT MEDICINE GROUP
DOI: 10.1007/s11899-013-0184-z

Keywords

Myeloproliferative neoplasms; JAK2; Clonal evolution; Oncogene; Tumor suppressor; Hematologicmalignancy

Funding

  1. Austrian Science Fund [P23257-B12]
  2. MPN Research Foundation
  3. Austrian Science Fund (FWF) [P23257] Funding Source: Austrian Science Fund (FWF)
  4. Austrian Science Fund (FWF) [P 23257] Funding Source: researchfish

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The clonal blood disorders polycythemia vera, essential thrombocythemia and primary myelofibrosis belong to the BCR-ABL1-negative myeloproliferative neoplasms and are specified by increased production of terminally differentiated myeloid cells. Clonal evolution, disease initiation and progression are influenced by genetic alterations, often affecting cytokine signaling and gene expression. This review outlines somatic changes discovered in myeloproliferative neoplasms and how these genetic aberrations influence the pathogenesis of myeloproliferative neoplasms. Furthermore, genetic responses to drug treatments in myeloproliferative neoplasms are discussed.

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