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Persistent altered fusion transcript splicing identifies RUNX1-RUNX1T1+ AML patients likely to relapse.

Abstract：

:In acute myeloid leukemia (AML) mouse models, the RUNX1-RUNX1T1 fusion protein has failed to produce leukemia by itself, but alternative splicing of exon 9a of the RUNX1-RUNX1T1 fusion transcript (FT) has recently been shown to enhance the leukemogenic potential. We have analyzed 138 diagnosis and follow-up samples from 13 RUNX1-RUNX1T1+ patients as well as diagnosis samples from 13 RUNX1-RUNX1T1- AML patients and 26 healthy donors. Levels of native RUNX1T1 mRNA were low in both healthy and RUNX1-RUNX1T1-negative AML samples. Likewise, the ratio between RUNX1T1 mRNA harboring exon 9a and lacking exon 9a was low and tightly regulated (0.017-0.11). In contrast, 11/13 RUNX1-RUNX1T1-positive AML patients displayed high and variable ratios of FT ranging from 0.05 to 0.46 (P < 0.001, Wilcoxon rank-sum test), indicating altered exon 9a splicing in these patients. Importantly, patients who remained in continuous complete remission displayed a faster disappearance of the RUNX1-RUNX1T1 exon 9a splice variant compared to patients bound to relapse (P = 0.02). In conclusion, alternative splicing seems to be part of the leukemogenic process in the majority of RUNX1-RUNX1T1-positive AML patients, and splice variant kinetics under cytoreduction may be a predictor for patients prone to relapse.

journal_name

Eur J Haematol

journal_title

European journal of haematology

authors

Ommen HB,Ostergaard M,Yan M,Braendstrup K,Zhang DE,Hokland P

doi

10.1111/j.1600-0609.2009.01371.x

subject

Has Abstract

pub_date

2010-02-01 00:00:00

pages

128-32

issue

2

eissn

0902-4441

issn

1600-0609

pii

EJH1371

journal_volume

84

pub_type

杂志文章

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