FLT3-ITD gets by with a little help from PRMT1

Kira Gritsman

doi:10.1182/blood.2019001876

FLT3-ITD gets by with a little help from PRMT1

Kira Gritsman

Medicine

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

Abstract

In this issue of Blood, He et al discuss their discovery that methylation of fms-like tyrosine kinase 3-internal tandem duplication (FLT3-ITD) at arginines 972 and 973 by protein arginine N-methyltransferase 1 (PRMT1) potentiates oncogenic signaling and that inhibition of PRMT1 can improve the efficacy of kinase inhibitors in FLT3-ITD acute myeloid leukemia (AML)

Original language	English (US)
Pages (from-to)	498-500
Number of pages	3
Journal	Blood
Volume	134
Issue number	6
DOIs	https://doi.org/10.1182/blood.2019001876
State	Published - Aug 8 2019

ASJC Scopus subject areas

Biochemistry
Immunology
Hematology
Cell Biology

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title = "FLT3-ITD gets by with a little help from PRMT1",

abstract = "In this issue of Blood, He et al discuss their discovery that methylation of fms-like tyrosine kinase 3-internal tandem duplication (FLT3-ITD) at arginines 972 and 973 by protein arginine N-methyltransferase 1 (PRMT1) potentiates oncogenic signaling and that inhibition of PRMT1 can improve the efficacy of kinase inhibitors in FLT3-ITD acute myeloid leukemia (AML)",

author = "Kira Gritsman",

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