Evidence map›Paper›PMID 19773435›Full record

ArticleCancer research2009

Rearrangements and amplification of IER3 (IEX-1) represent a novel and recurrent molecular abnormality in myelodysplastic syndromes.

David P Steensma, Jessemy D Neiger, Julie C Porcher, J Jonathan Keats, P Leif Bergsagel, Thomas R Dennis, Ryan A Knudson, Robert B Jenkins, Rafael Santana-Davila, Rajiv Kumar and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 19% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Pooled it
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  14. AMD Genetics in India: The Missing Links.Frontiers in aging neuroscience · 2016
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 4 institutions in 1 country.

David P SteensmaMayo Clinic, Rochester, MN 55905, USA. Steensma.david@mayo.edu
Jessemy D Neiger
Julie C Porcher
J Jonathan Keats
P Leif Bergsagel
Thomas R Dennis
Ryan A Knudson
Robert B Jenkins
Rafael Santana-Davila
Rajiv Kumar
Rhett P Ketterling
Mayo Clinic · USMayo Clinic in Arizona · USHypertension Institute · USTranslational Genomics Research Institute · US

Funding

Trageting the Multiple Myeloma EpigenomeP50CA100707 · NCI · DANA-FARBER CANCER INSTITUTE · PI ANDERSON, KENNETH C., MUNSHI, NIKHIL C. · 2003 to 2023
$45.0M
Paul Calabresi Program in Clinical/Translational Research at Mayo ClinicK12CA090628 · NCI · MAYO CLINIC ROCHESTER · PI WEROHA, SARAVUT · 2001 to 2025
$19.7M
REGULATIOIN OF RENAL PHOSPHATE EXCRETION AND VITAMIN D METABOLISM BY FGF 7R01DK076829 · NIDDK · MAYO CLINIC ROCHESTER · PI KUMAR, RAJIV · 2007 to 2010
$1.2M
Hyperoxaluria and Nephrolithiasis After Gastric Bypass Surgery for ObesityR21DK077669 · NIDDK · MAYO CLINIC ROCHESTER · PI KUMAR, RAJIV · 2007 to 2008
$412k
NCI NIH HHS 2 P50 CA100707-067285NCI NIH HHS K12 CA090628NCI NIH HHS K12 CA90628NCI NIH HHS P50 CA100707NIDDK NIH HHS R01 DK076829NIDDK NIH HHS R21 DK077669
6 · The paper itself

Abstract

IER3 (formerly IEX-1) encodes a 27-kDa glycoprotein that regulates death receptor-induced apoptosis, interacts with NF-kappaB pathways, and increases expression rapidly in response to cellular stresses such as irradiation. Animal models, gene expression microarray experiments, and functional studies in cell lines have suggested a potential role for IER3 in oncogenesis, but, to date, no abnormalities of IER3 at the DNA level have been reported in patients with neoplasia. Here, we describe breakpoint cloning of a t(6;9)(p21;q34) translocation from a patient with a myelodysplastic syndrome (MDS), facilitated by conversion technology and array-based comparative genomic hybridization, which revealed a rearrangement translocating the IER3 coding region away from critical flanking/regulatory elements and to a transcript-poor chromosomal region, markedly decreasing expression. Using split-signal and locus-specific fluorescence in situ hybridization (FISH) probes, we analyzed 204 patients with diverse hematological malignancies accompanied by clonal chromosome 6p21 abnormalities, and found 8 additional patients with MDS with IER3 rearrangements (translocations or amplification). Although FISH studies on 157 additional samples from patients with MDS and a normal-karyotype were unrevealing, and sequencing the IER3 coding and proximal promoter regions of 74 MDS patients disclosed no point mutations, reverse transcription-PCR results suggested that dysregulated expression of IER3 is common in MDS (61% >4-fold increase or decrease in expression with decreased expression primarily in early MDS and increased expression primarily in later MDS progressing toward leukemia), consistent with findings in previous microarray experiments. These data support involvement of IER3 in the pathobiology of MDS.

Indexed as

AgedAnimalsApoptosis Regulatory ProteinsBase SequenceChromosomes, Human, Pair 6Chromosomes, Human, Pair 9Comparative Genomic HybridizationGene AmplificationGene RearrangementHematopoietic Stem CellsHumansIn Situ Hybridization, FluorescenceMaleMembrane ProteinsMiceMolecular Sequence DataApoptosis Regulatory ProteinsIER3 protein, humanMembrane Proteins

Identifiers

PMID19773435
PMCPMC3157243
OpenAlexW2056892560

What OpenQuestion holds

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LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.