Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz

Logo MUG-Forschungsportal

Gewählte Publikation:

Vinatzer, U; Mannhalter, C; Mitterbauer, M; Gruener, H; Greinix, H; Schmidt, HH; Fonatsch, C; Wieser, R.
Quantitative comparison of the expression of EVI1 and its presumptive antagonist, MDS1/EVI1, in patients with myeloid leukemia.
Genes Chromosomes Cancer. 2003; 36(1):80-89
Web of Science PubMed FullText FullText_MUG

 

Autor/innen der Med Uni Graz:
Greinix Hildegard
Schmidt Helmut
Altmetrics:

Dimensions Citations:

Plum Analytics:

Scite (citation analytics):

Abstract:
The EVI1 gene in chromosome band 3q26 exhibits a number of properties consistent with a role as an oncogene, and its expression is activated in most myeloid leukemia patients with, as well as in a minority of patients without, 3q26 rearrangements. A splice variant of this gene, MDS1/EVI1, acts as its antagonist at least in some tissue culture assays. We established real-time quantitative reverse transcriptase polymerase chain reaction (RTQ-RT-PCR) assays for these mRNA variants to compare their expression levels in a quantitatively reliable manner. EVI1 was overexpressed to highly variable extents in all patients with, as well as in 14% of patients without, 3q26 rearrangements. In some of these samples, MDS1/EVI1 was also transcribed at elevated levels compared to those of healthy controls. However, although the induction of MDS1/EVI1 was comparable to, or higher than, that of EVI1 in three of five samples with a normal EVI1 locus, this was true for only two of 13 patients with a 3q26 aberration. We further provide preliminary evidence that the RTQ-RT-PCR assay may be useful for disease monitoring in patients overexpressing EVI1. Copyright 2002 Wiley-Liss, Inc.
Find related publications in this database (using NLM MeSH Indexing)
Adult -
Aged -
Alternative Splicing - genetics
Child -
Chromosome Aberrations -
Chromosome Banding -
Chromosomes, Human, Pair 3 - genetics
Cyclophilins - genetics
DNA-Binding Proteins - antagonists & inhibitors DNA-Binding Proteins - biosynthesis DNA-Binding Proteins - genetics
Disease Progression -
Female -
Humans -
K562 Cells -
Leukemia, Myeloid - genetics Leukemia, Myeloid - metabolism Leukemia, Myeloid - pathology
Male -
Middle Aged -
Molecular Sequence Data -
Oncogene Proteins, Fusion -
Proto-Oncogenes -
Recombinant Fusion Proteins - biosynthesis Recombinant Fusion Proteins - genetics Recombinant Fusion Proteins - physiology
Reverse Transcriptase Polymerase Chain Reaction - methods
Transcription Factors - antagonists & inhibitors Transcription Factors - biosynthesis Transcription Factors - genetics
Tumor Cells, Cultured -
U937 Cells -

© Med Uni Graz Impressum