Research progress on molecular pathogenesis of myeloproliferative neoplasms.
- Author:
Liu LIU
1
;
Zhi-Jian XIAO
Author Information
1. Institute of Hematology & Blood Diseases Hospital, Chinese Academy of Medical Sciences, Tianjin 300020, China.
- Publication Type:Journal Article
- MeSH:
Bone Marrow Neoplasms;
genetics;
Genetic Predisposition to Disease;
Humans;
Janus Kinase 2;
genetics;
Mutation;
Myeloproliferative Disorders;
genetics;
Polycythemia Vera;
genetics;
Primary Myelofibrosis;
genetics;
Thrombocythemia, Essential;
genetics
- From:
Journal of Experimental Hematology
2011;19(1):239-243
- CountryChina
- Language:Chinese
-
Abstract:
Classical BCR/ABL fusion gene negative myeloproliferative neoplasms (MPN), including polycythemia vera (PV), essential thrombocythemia (ET) and primary myelofibrosis (PMF), are clonal hematopoietic malignancies sharing in common origin in a multipotential hematopoietic stem cell. The phenotypic variability of the three entities can not be elucidated by JAK2V617F mutation only. Recent discoveries indicated that JAK2V617F allele burden, other mutated genes (such as TET2, ASXL1) and inherited predisposition can play roles in the complicated pathogenesis of MPN, which are summarized in this review.
