Transcription factor RUNX1 promotes survival of acute myeloid leukemia cells

Abstract

The accession numbers for the antibody nucleotide sequences were incorrectly noted in Methods. The correct sentence appears below.Antibody nucleotide sequences have been deposited in GenBank (JX458933-52); antibody X-ray structure has been deposited in the Protein Data Bank (4GSD).The authors regret the error.

Expression levels of the runt-related transcription factor�1 and�3 genes in the development of acute myeloid leukemia

“…By contrast, deactivating the RUNX1 gene may cause amplification of myeloid progenitors and the subsequent development of AML. A previous study undertaken by Silva et al (25) suggested that the RUNX1 gene acts as a classical tumor suppressor gene; however, other studies have suggested that RUNX1 functions as an oncogene and that it may cause AML development due to its pro-survival role in leukemia cell proliferation (27)(28)(29)(30). The results of these studies also suggested that the prognostic impact in CN-AML depends on the RUNX1 expression level.…”

“…The results of these studies also suggested that the prognostic impact in CN-AML depends on the RUNX1 expression level. A study undertaken by Goyama et al (28) reported that overexpression of the RUNX1 gene inhibited the growth of regular cord blood cells by inducing myeloid differentiation. It was suggested that the RUNX1 gene may be a valuable novel marker for risk stratification in patients with AML and that it is an excellent candidate for anticancer-targeted therapy due to the modulation of its post-translational modifications (29).…”

Myeloid neoplasms with germ line RUNX1 mutation

“…In general, RUNX1 mutations are considered to result in the loss of RUNX1 functions. On the other hand, recent several reports indicate that wild-type RUNX1 is also important for growth and survival of leukemia cells [16].…”

The RUNX1–PU.1 axis in the control of hematopoiesis

“…These data show that RUNX1-ETO and 1 3 RUNX1 are in balance with each other, and additional studies have shown that each regulate distinct sets of genes which are both required to keep AML cells alive [127]. This dependency on the wild-type copy of RUNX1 has also been demonstrated for other RUNX1 and CBF translocations [127,128]. Genome-wide binding studies have shown that RUNX1-ETO binds to thousands of genes in chromatin [122,125].…”