Evidence map›Paper›PMID 25762002›Full record

ArticleStem cells translational medicine2015

Pluripotent cell models of fanconi anemia identify the early pathological defect in human hemoangiogenic progenitors.

Naoya M Suzuki, Akira Niwa, Miharu Yabe, Asuka Hira, Chihiro Okada, Naoki Amano, Akira Watanabe, Ken-Ichiro Watanabe, Toshio Heike, Minoru Takata and 2 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Stem cells translational medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Frontiers in immunology · 2022
    Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. DNA repair fidelity in stem cell maintenance, health, and disease.Biochimica et biophysica acta. Molecular basis of disease · 2020
    Review
  8. Modeling Leukemia with Human Induced Pluripotent Stem Cells.Cold Spring Harbor perspectives in medicine · 2019
    Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Modeling Human Bone Marrow Failure Syndromes Using Pluripotent Stem Cells and Genome Engineering.Molecular therapy : the journal of the American Society of Gene Therapy · 2015
    Review
  17. Review
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

12 authors at 4 institutions in 1 country.

Naoya M SuzukiDepartments of Clinical Application and.
Akira NiwaDepartments of Clinical Application and.
Miharu YabeDepartment of Cell Transplantation and Regenerative Medicine, Tokai University School of Medicine, Isehara, Japan;
Asuka HiraLaboratory of DNA Damage Signaling, Department of Late Effects Studies, Radiation Biology Center, Kyoto University, Kyoto, Japan;
Chihiro OkadaReprogramming Science, Center for Induced Pluripotent Stem Cell Research and Application, and Mitsubishi Space Software Co., Ltd., Amagasaki, Japan;
Naoki AmanoReprogramming Science, Center for Induced Pluripotent Stem Cell Research and Application, and.
Akira WatanabeReprogramming Science, Center for Induced Pluripotent Stem Cell Research and Application, and.
Ken-Ichiro WatanabeDepartment of Pediatrics, Kyoto University Graduate School of Medicine, Kyoto, Japan; Department of Hematology and Oncology, Shizuoka Children's Hospital, Shizuoka, Japan.
Toshio HeikeDepartment of Pediatrics, Kyoto University Graduate School of Medicine, Kyoto, Japan;
Minoru TakataLaboratory of DNA Damage Signaling, Department of Late Effects Studies, Radiation Biology Center, Kyoto University, Kyoto, Japan;
Tatsutoshi NakahataDepartments of Clinical Application and.
Megumu K SaitoDepartments of Clinical Application and msaito@cira.kyoto-u.ac.jp.
Kyoto University · JPMitsubishi Space Software (Japan) · JPShizuoka Children's Hospital · JPTokai University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fanconi anemia (FA) is a disorder of genomic instability characterized by progressive bone marrow failure (BMF), developmental abnormalities, and an increased susceptibility to cancer. Although various consequences in hematopoietic stem/progenitor cells have been attributed to FA-BMF, the quest to identify the initial pathological event is still ongoing. To address this issue, we established induced pluripotent stem cells (iPSCs) from fibroblasts of six patients with FA and FANCA mutations. An improved reprogramming method yielded iPSC-like colonies from all patients, and iPSC clones were propagated from two patients. Quantitative evaluation of the differentiation ability demonstrated that the differentiation propensity toward the hematopoietic and endothelial lineages is already defective in early hemoangiogenic progenitors. The expression levels of critical transcription factors were significantly downregulated in these progenitors. These data indicate that the hematopoietic consequences in FA patients originate from the early hematopoietic stage and highlight the potential usefulness of iPSC technology for elucidating the pathogenesis of FA-BMF.

Indexed as

Bone MarrowCell DifferentiationCell LineageCellular ReprogrammingFanconi AnemiaFanconi Anemia Complementation Group A ProteinFibroblastsGenetic TherapyHematopoietic Stem CellsHumansInduced Pluripotent Stem CellsFanconi Anemia Complementation Group A ProteinDifferentiationFanconi anemiaHematopoietic progenitorsInduced pluripotent stem cellsTranscription factors

Identifiers

PMID25762002
PMCPMC4367500
OpenAlexW2170046742

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.