JAK2 and JMJD1C activate NFE2 in MPNs

John D. Crispino

doi:10.1182/blood-2018-03-839779

JAK2 and JMJD1C activate NFE2 in MPNs

John D. Crispino

Medicine, Hematology Oncology Division

Research output: Contribution to journal › Review article › peer-review

Abstract

Overexpression of nuclear factor erythroid 2 (NFE2) is commonly observed in the myeloproliferative neoplasms (MPNs), especially polycythemia vera (PV) and primary myelofibrosis,^1,2 but the mechanism that drives this feature has been unclear. In this issue of Blood, Peeken et al reveal a 2-pronged epigenetic pathway that promotes NFE2 overexpression and disease³

Original language	English (US)
Pages (from-to)	1998-1999
Number of pages	2
Journal	Blood
Volume	131
Issue number	18
DOIs	https://doi.org/10.1182/blood-2018-03-839779
State	Published - May 3 2018

ASJC Scopus subject areas

Biochemistry
Immunology
Hematology
Cell Biology

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abstract = "Overexpression of nuclear factor erythroid 2 (NFE2) is commonly observed in the myeloproliferative neoplasms (MPNs), especially polycythemia vera (PV) and primary myelofibrosis,1,2 but the mechanism that drives this feature has been unclear. In this issue of Blood, Peeken et al reveal a 2-pronged epigenetic pathway that promotes NFE2 overexpression and disease3",

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AB - Overexpression of nuclear factor erythroid 2 (NFE2) is commonly observed in the myeloproliferative neoplasms (MPNs), especially polycythemia vera (PV) and primary myelofibrosis,1,2 but the mechanism that drives this feature has been unclear. In this issue of Blood, Peeken et al reveal a 2-pronged epigenetic pathway that promotes NFE2 overexpression and disease3

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JAK2 and JMJD1C activate NFE2 in MPNs

Abstract

ASJC Scopus subject areas

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