BCR-ABL negative myeloproliferative neoplasia: a review of involved molecular mechanisms

Suzanne M. Koopmans; Harry C. Schouten; Arienne M. W. van Marion

doi:10.14670/HH-30.151

BCR-ABL negative myeloproliferative neoplasia: a review of involved molecular mechanisms

Suzanne M. Koopmans^*, Harry C. Schouten, Arienne M. W. van Marion

^*Corresponding author for this work

Research output: Contribution to journal › Article › Academic › peer-review

Abstract

The clonal bone marrow stem cell disorders essential thrombocythemia (ET), polycythemia vera (PV) and primary myelofibrosis (PMF) belong to the group of Philadelphia chromosome negative myeloproliferative neoplasia (Ph- MPN). In 2005 the JAK2(V617F) mutation was discovered which has generated more insight in the pathogenetic mechanism of the MPNs. More mutations have been detected in MPN patients since. However, the underlying cause of MPN has not been discovered so far. The mechanism of increased angiogenesis in MPNs and the development of fibrosis in the bone marrow in PMF patients and in some ET and PV patients is still not known. This review will focus on the most important molecular pathogenetic mechanisms in MPN patients.

Original language	English
Pages (from-to)	151-161
Journal	Histology and Histopathology
Volume	30
Issue number	2
DOIs	https://doi.org/10.14670/HH-30.151
Publication status	Published - Feb 2015

Keywords

Myeloproliferative neoplasia
Essential thrombocythemia
Polycythemia vera
Primary myelofibrosis
JAK2 mutation

Access to Document

10.14670/HH-30.151

Cite this

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title = "BCR-ABL negative myeloproliferative neoplasia: a review of involved molecular mechanisms",

abstract = "The clonal bone marrow stem cell disorders essential thrombocythemia (ET), polycythemia vera (PV) and primary myelofibrosis (PMF) belong to the group of Philadelphia chromosome negative myeloproliferative neoplasia (Ph- MPN). In 2005 the JAK2(V617F) mutation was discovered which has generated more insight in the pathogenetic mechanism of the MPNs. More mutations have been detected in MPN patients since. However, the underlying cause of MPN has not been discovered so far. The mechanism of increased angiogenesis in MPNs and the development of fibrosis in the bone marrow in PMF patients and in some ET and PV patients is still not known. This review will focus on the most important molecular pathogenetic mechanisms in MPN patients.",

keywords = "Myeloproliferative neoplasia, Essential thrombocythemia, Polycythemia vera, Primary myelofibrosis, JAK2 mutation",

author = "Koopmans, {Suzanne M.} and Schouten, {Harry C.} and {van Marion}, {Arienne M. W.}",

year = "2015",

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doi = "10.14670/HH-30.151",

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journal = "Histology and Histopathology",

issn = "0213-3911",

publisher = "Universidad de Murcia",

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AU - Koopmans, Suzanne M.

AU - Schouten, Harry C.

AU - van Marion, Arienne M. W.

PY - 2015/2

Y1 - 2015/2

N2 - The clonal bone marrow stem cell disorders essential thrombocythemia (ET), polycythemia vera (PV) and primary myelofibrosis (PMF) belong to the group of Philadelphia chromosome negative myeloproliferative neoplasia (Ph- MPN). In 2005 the JAK2(V617F) mutation was discovered which has generated more insight in the pathogenetic mechanism of the MPNs. More mutations have been detected in MPN patients since. However, the underlying cause of MPN has not been discovered so far. The mechanism of increased angiogenesis in MPNs and the development of fibrosis in the bone marrow in PMF patients and in some ET and PV patients is still not known. This review will focus on the most important molecular pathogenetic mechanisms in MPN patients.

AB - The clonal bone marrow stem cell disorders essential thrombocythemia (ET), polycythemia vera (PV) and primary myelofibrosis (PMF) belong to the group of Philadelphia chromosome negative myeloproliferative neoplasia (Ph- MPN). In 2005 the JAK2(V617F) mutation was discovered which has generated more insight in the pathogenetic mechanism of the MPNs. More mutations have been detected in MPN patients since. However, the underlying cause of MPN has not been discovered so far. The mechanism of increased angiogenesis in MPNs and the development of fibrosis in the bone marrow in PMF patients and in some ET and PV patients is still not known. This review will focus on the most important molecular pathogenetic mechanisms in MPN patients.

KW - Myeloproliferative neoplasia

KW - Essential thrombocythemia

KW - Polycythemia vera

KW - Primary myelofibrosis

KW - JAK2 mutation

U2 - 10.14670/HH-30.151

DO - 10.14670/HH-30.151

M3 - Article

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SN - 0213-3911

VL - 30

SP - 151

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JO - Histology and Histopathology

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