Molecular markers in acute myeloid leukemia

	Approximate frequency in de-novo AML	Frequency in CN AML	Strong associations	Not recorded with	Outlook
NPM1	35 percent	50 percent	CN AML, FLT3-ITD, FLT3-TKD, DNMT3A, IDH1, IDH2	CEBPA double mutant	Favorable in patients with CN AML and in elderly patients
CEBPA	7 percent	8 to 19 percent	CN AML, FLT3-ITD	NPM1	Favorable in patients with CN AML (if biallelic)
FLT3-ITD	20 to 25 percent	30 to 35 percent	CN AML, APL, t(6;9), NPM1		Adverse in patients with CN AML; could vary with allelic burden; no clear effect in patients with APL
FLT3-TKD	5 percent	14 percent	CN AML, NPM1		Controversial
KIT		25 percent	Core binding factor leukemias	Most other karyotypes	Adverse in adult patients with core binding factor leukemias
TET2	8 to 12 percent	23 percent	Possibly CN AML	IDH1, IDH2	Controversial
DNMT3A	14 to 22 percent	20 to 33 percent	CN AML, NPM1, FLT3	Core binding factor leukemias, CEBPA, MLL translocations	Possibly adverse in patients with CN AML
**IDH1, IDH2**	8 to 16 percent	30 percent	CN AML, NPM1, FLT3	TET2, WT1	Controversial
ASXL1	5 to 30 percent	About 10 percent	Uncommon with NPM1 and FLT3	Possibly CEBPA	Adverse in patients with CN AML and older patients; more common in older patients

Changes of miRNAs 15, 16, 155, and 181 among others, have been reported. The prognostic effect varies and studies are needed to assess the individual miRNA families and their interactions with other mutations. Some studies have shown that overexpression of BAALC, MN1, and ERG genes is associated with poorer outcomes, but needs confirmation.

AML: acute myeloid leukemia; CN AML: cytogenetically normal acute myeloid leukemia; ITD: internal tandem duplication; TKD: tyrosine kinase domain; APL: acute promyelocytic leukemia.

Graphic 88091 Version 2.0

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Molecular markers in acute myeloid leukemia