Evidence map›Paper›PMID 23315168›Full record

ArticleBlood2013

Fetal origins of hematopoietic failure in a murine model of Fanconi anemia.

Ashley N Kamimae-Lanning, Natalya A Goloviznina, Peter Kurre

Abstract read
In one paragraph

Article in Blood, 2013. 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
–field-weighted citation impact
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.

  1. Pooled it
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  3. Review
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  8. Article
  9. DNA repair fidelity in stem cell maintenance, health, and disease.Biochimica et biophysica acta. Molecular basis of disease · 2020
    Review
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  14. Loss of the homologous recombination geneProceedings of the National Academy of Sciences of the United States of America · 2017
    Article
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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

3 authors.

Ashley N Kamimae-LanningDepartments of Pediatrics, Oregon Health and Science University, Portland, OR 97239, USA.
Natalya A Goloviznina
Peter Kurre

Funding

NHLBI NIH HHS T32 HL778116
6 · The paper itself

Abstract

Hematopoietic failure is the predominant clinical manifestation of Fanconi anemia (FA), a rare, recessively inherited disorder. Mutations in 1 of 15 genes that coordinately function in a complex pathway to maintain DNA integrity also predispose patients to constitutional defects in growth and development. The hematologic manifestations have been considered to reflect the progressive loss of stem cells from the postnatal bone marrow microenvironment. Ethical concerns preclude the study of human hematopoiesis in utero. We report significant late gestational lethality and profound quantitative and qualitative deficiencies in the murine Fancc(-/-) fetal liver hematopoietic stem and progenitor cell pool. Fancc(-/-) fetal liver hematopoietic stem and progenitor cells revealed a significant loss of quiescence and decline in serial repopulating capacity, but no substantial difference in apoptosis or levels of reactive oxygen species. Our studies suggest that compromised hematopoiesis in Fancc(-/-) animals is developmentally programmed and does not arise de novo in bone marrow.

Indexed as

Disease Models, AnimalMice, TransgenicAnimalsBone Marrow CellsCells, CulturedEmbryo, MammalianFanconi AnemiaFanconi Anemia Complementation Group C ProteinFemaleHematopoiesisHematopoietic Stem CellsHematopoietic Stem Cell TransplantationMiceMice, Inbred C57BLModels, BiologicalPregnancyFanconi Anemia Complementation Group C Protein

Identifiers

PMID23315168
PMCPMC3645055

What OpenQuestion holds

Textmetadata
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.