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Clinical features and prognostic impact of PRDM16 expression in adult acute myeloid leukemia.

Authors :
Yamato G
Yamaguchi H
Handa H
Shiba N
Kawamura M
Wakita S
Inokuchi K
Hara Y
Ohki K
Okubo J
Park MJ
Sotomatsu M
Arakawa H
Hayashi Y
Source :
Genes, chromosomes & cancer [Genes Chromosomes Cancer] 2017 Nov; Vol. 56 (11), pp. 800-809. Date of Electronic Publication: 2017 Aug 11.
Publication Year :
2017

Abstract

High PRDM16 (also known as MEL1) expression is a representative marker of acute myeloid leukemia (AML) with NUP98-NSD1 and is a significant predictive marker for poor prognosis in pediatric AML. However, the clinical features of adult AML with PRDM16 expression remain unclear. PRDM16 is highly homologous to MDS1/EVI1, which is an alternatively spliced transcript of MECOM (also known as EVI1). We investigated PRDM16 expression in 151 AML patients, with 47 (31%) exhibiting high PRDM16 expression (PRDM16/ABL1 ratio ≥ 0.010). High PRDM16 expression significantly correlated with DNMT3A (43% vs. 15%, P < 0.001) and NPM1 (43% vs. 21%, P = 0.010) mutations and partial tandem duplication of KMT2A (22% vs. 1%, P < 0.001). Remarkably, high-PRDM16-expression patients were frequent in the noncomplete remission group (48% vs. 21%, P = 0.002). Overall survival (OS) was significantly worse in high-PRDM16-expression patients than in low-PRDM16-expression patients (5-year OS, 18% vs. 34%; P = 0.002). This trend was observed more clearly among patients aged <65 years (5-year OS, 21% vs. 50%; P = 0.001), particularly in FLT3-ITD-negative patients in the intermediate cytogenetic risk group (5-year OS, 25% vs. 59%; P = 0.009). These results suggest that high PRDM16 expression is a significant predictive marker for poor prognosis in adult AML patients, similar to pediatric AML patients.<br /> (© 2017 Wiley Periodicals, Inc.)

Details

Language :
English
ISSN :
1098-2264
Volume :
56
Issue :
11
Database :
MEDLINE
Journal :
Genes, chromosomes & cancer
Publication Type :
Academic Journal
Accession number :
28710806
Full Text :
https://doi.org/10.1002/gcc.22483