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

被引：1

作者：

Koopmans, Suzanne M. ^{[1
]}

Schouten, Harry C. ^{[2
]}

van Marion, Arienne M. W. ^{[3
]}

机构：

[1] Univ Hosp Maastricht, Dept Pathol, NL-6202 AZ Maastricht, Netherlands

[2] Univ Hosp Maastricht, Dept Internal Med, Div Haematol, NL-6202 AZ Maastricht, Netherlands

[3] VieCuri Med Ctr, Dept Pathol, Venlo, Netherlands

来源：

HISTOLOGY AND HISTOPATHOLOGY | 2015年 / 30卷 / 02期

关键词：

Myeloproliferative neoplasia; Essential thrombocythemia; Polycythemia vera; Primary myelofibrosis; JAK2; mutation; GROWTH-FACTOR-BETA; CHRONIC MYELOCYTIC-LEUKEMIA; TYROSINE KINASE JAK2; BONE-MARROW FIBROSIS; ESSENTIAL THROMBOCYTHEMIA; POLYCYTHEMIA-VERA; PRIMARY MYELOFIBROSIS; MICROVESSEL DENSITY; MYELOID METAPLASIA; VEGF EXPRESSION;

D O I：

10.14670/HH-30.151

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

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.

引用

页码：151 / 161

页数：11

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