Evidence map›Paper›PMID 23889587›Full record

ArticleBritish journal of haematology2013

Cytokine production by bone marrow mononuclear cells in inherited bone marrow failure syndromes.

Ken Matsui, Neelam Giri, Blanche P Alter, Ligia A Pinto

Open access · greenAbstract read
In one paragraph

Article in British journal of haematology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

14 citing papers in PubMed, 19 citations in OpenAlex.

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  9. Loss of the homologous recombination geneProceedings of the National Academy of Sciences of the United States of America · 2017
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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

4 authors at 3 institutions in 1 country.

Ken MatsuiHuman Papillomavirus Immunology Laboratory, Science Applications International Corporation (SAIC)-Frederick, Incorporated, Frederick National Laboratory for Cancer Research, Frederick, MD, USA.
Neelam Giri
Blanche P Alter
Ligia A Pinto
Frederick National Laboratory for Cancer Research · USNational Cancer Institute · USNational Institutes of Health · US

Funding

Clinical Genetic Studies of Familial and Hereditary Cancer SyndromesZIACP010144 · NCI · DIVISION OF CANCER EPIDEMIOLOGY AND GENETICS · PI SAVAGE, SHARON A. · 2009 to 2025
$111.8M
CASE-CONTROL STUDY OF BRAIN CANCER AND OCCUPATIONN01CP011019 · CP · ABT ASSOCIATES, INC. · PI STONER, DIANE · 1985 to 1986
–
CCR NIH HHS HHSN261200800001CIntramural NIH HHS ZIA CP010144NCI NIH HHS HHSN261200800001ENCI NIH HHS N02 CP011019NCI NIH HHS N02-CP-91026PHS HHS HHSN261200655001C
6 · The paper itself

Abstract

Fanconi anaemia (FA), dyskeratosis congenita (DC), Diamond-Blackfan anaemia (DBA), and Shwachman-Diamond syndrome (SDS) are characterized by the progressive development of bone marrow failure. Overproduction of tumour necrosis factor-α (TNF-α) from activated bone marrow T-cells has been proposed as a mechanism of FA-related aplasia. Whether such overproduction occurs in the other syndromes is unknown. We conducted a comparative study on bone marrow mononuclear cells to examine the cellular subset composition and cytokine production. We found lower proportions of haematopoietic stem cells in FA, DC, and SDS, and a lower proportion of monocytes in FA, DC, and DBA compared with controls. The T- and B-lymphocyte proportions were similar to controls, except for low B-cells in DC. We did not observe overproduction of TNF-α or IFN-γ by T-cells in any patients. Induction levels of TNF-α, interleukin (IL)-6, IL-1β, IL-10, granulocyte colony-stimulating factor, and granulocyte-macrophage colony-stimulating factor in monocytes stimulated with high-dose lipopolysaccharide (LPS) were similar at 4 h but lower at 24 h when compared to controls. Unexpectedly, patient samples showed a trend toward higher cytokine level in response to low-dose (0·001 μg/ml) LPS. Increased sensitivity to LPS may have clinical implications and could contribute to the development of pancytopenia by creating a chronic subclinical inflammatory micro-environment in the bone marrow.

Indexed as

AdolescentAdultAgedAnemia, AplasticBone Marrow CellsBone Marrow DiseasesBone Marrow Failure DisordersChildChild, PreschoolCytokinesHemoglobinuria, ParoxysmalHumansIntracellular SpaceLipopolysaccharidesMiddle AgedMonocytesCytokinesLipopolysaccharidesbone marrowcytokinesimmunologyinherited bone marrow failure syndromesmonocytes

Identifiers

PMID23889587
PMCPMC3930339
OpenAlexW2049355496

What OpenQuestion holds

Textmetadata
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.