Evidence map›Paper›PMID 25761935›Full record

ReviewLeukemia2015

Deregulation of innate immune and inflammatory signaling in myelodysplastic syndromes.

I Gañán-Gómez, Y Wei, D T Starczynowski, S Colla, H Yang, M Cabrero-Calvo, Z S Bohannan, A Verma, U Steidl, G Garcia-Manero

Open access · bronzeAbstract readReview
In one paragraph

Review in Leukemia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 151 papers.

0numbers the graph read from it
0cells of the map it votes in
151citing papers in PubMed
14.3field-weighted citation impact, top 1% 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

151 citing papers in PubMed, 232 citations in OpenAlex.

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  9. Stromal Gasdermin D-mediated Pyroptosis Drives Maladaptive CD4bioRxiv : the preprint server for biology · 2026
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91 more citing papers are in PubMed but not listed here.

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

10 authors at 1 institution in 1 country.

I Gañán-GómezDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Y WeiDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
D T Starczynowski1] Division of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA [2] Department of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
S CollaDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
H YangDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
M Cabrero-Calvo1] Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA [2] Department of Hematology, University Hospital of Salamanca, Salamanca, Spain.
Z S BohannanDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
A Verma1] Division of Hematologic Malignancies, Department of Medicine (Oncology), Einstein/Montefiore Medical Center, New York, NY, USA [2] Albert Einstein Cancer Center and Ruth L. and David S. Gottesman Institute for Stem Cell and Regenerative Medicine Research, Albert Einstein College of Medicine, New York, NY, USA [3] Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, New York, NY, USA.
U Steidl1] Division of Hematologic Malignancies, Department of Medicine (Oncology), Einstein/Montefiore Medical Center, New York, NY, USA [2] Albert Einstein Cancer Center and Ruth L. and David S. Gottesman Institute for Stem Cell and Regenerative Medicine Research, Albert Einstein College of Medicine, New York, NY, USA [3] Department of Cell Biology, Albert Einstein College of Medicine, New York, NY, USA.
G Garcia-ManeroDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Role of a Novel Homeobox Transcription Factor (HLX) in Acute Myeloid LeukemiaR01CA166429 · NCI · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI STEIDL, ULRICH · 2013 to 2017
$1.9M
Identification and characterization of genes in del(5q) myelodysplastic syndromeR01HL111103 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI STARCZYNOWSKI, DANIEL · 2012 to 2016
$1.9M
Role of TRAF6 in Myelodysplastic SyndromesR01HL114582 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI STARCZYNOWSKI, DANIEL · 2014 to 2016
$1.2M
Molecular Pathogenesis of MDSR01DK102759 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI STARCZYNOWSKI, DANIEL · 2014 to 2016
$701k
Communication Between Patients and their ProvidersR03CA110791 · NCI · UNIVERSITY OF TEXAS MD ANDERSON CAN CTR · PI PARKER, PATRICIA A · 2004 to 2005
$151k
NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA166429NCI NIH HHS R03 CA110791NHLBI NIH HHS R01 HL111103NHLBI NIH HHS R01HL111103NHLBI NIH HHS R01 HL114582NHLBI NIH HHS R01HL114582NIDDK NIH HHS R01 DK102759NIDDK NIH HHS R01DK102759
6 · The paper itself

Abstract

Myelodysplastic syndromes (MDSs) are a group of heterogeneous clonal hematologic malignancies that are characterized by defective bone marrow (BM) hematopoiesis and by the occurrence of intramedullary apoptosis. During the past decade, the identification of key genetic and epigenetic alterations in patients has improved our understanding of the pathophysiology of this disease. However, the specific molecular mechanisms leading to the pathogenesis of MDS have largely remained obscure. Recently, essential evidence supporting the direct role of innate immune abnormalities in MDS has been obtained, including the identification of multiple key regulators that are overexpressed or constitutively activated in BM hematopoietic stem and progenitor cells. Mounting experimental results indicate that the dysregulation of these molecules leads to abnormal hematopoiesis, unbalanced cell death and proliferation in patients' BM, and has an important role in the pathogenesis of MDS. Furthermore, there is compelling evidence that the deregulation of innate immune and inflammatory signaling also affects other cells from the immune system and the BM microenvironment, which establish aberrant associations with hematopoietic precursors and contribute to the MDS phenotype. Therefore, the deregulation of innate immune and inflammatory signaling should be considered as one of the driving forces in the pathogenesis of MDS. In this article, we review and update the advances in this field, summarizing the results from the most recent studies and discussing their clinical implications.

Indexed as

AnimalsHumansImmunity, InnateInflammationMyelodysplastic SyndromesSignal Transduction

Identifiers

PMID25761935
PMCPMC4857136
OpenAlexW2020719716

What OpenQuestion holds

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Registered trials

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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.