Evidence map›Paper›PMID 29247345›Full record

ArticleStem cell reviews and reports2018

Bone Marrow Mesenchymal Stem Cells Carrying FANCD2 Mutation Differ from the Other Fanconi Anemia Complementation Groups in Terms of TGF-β1 Production.

Ilgin Cagnan, Aysen Gunel-Ozcan, Fatima Aerts-Kaya, Najim Ameziane, Baris Kuskonmaz, Josephine Dorsman, Fatma Gumruk, Duygu Uckan

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In one paragraph

Article in Stem cell reviews and reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.7field-weighted citation impact, top 26% 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

6 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Article
  3. Cancer in Children With Fanconi Anemia and Ataxia-Telangiectasia-A Nationwide Register-Based Cohort Study in Germany.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2022
    Article
  4. Article
  5. Review
  6. 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

8 authors at 2 institutions in 2 countries.

Ilgin CagnanDepartment of Stem Cell Sciences, Institute of Health Sciences, Center for Stem Cell Research and Development, Hacettepe University, 06100, Sıhhiye, Ankara, Turkey.
Aysen Gunel-OzcanDepartment of Stem Cell Sciences, Institute of Health Sciences, Center for Stem Cell Research and Development, Hacettepe University, 06100, Sıhhiye, Ankara, Turkey. agozcan@hacettepe.edu.tr.ORCID 0000-0003-3792-0823
Fatima Aerts-KayaDepartment of Stem Cell Sciences, Institute of Health Sciences, Center for Stem Cell Research and Development, Hacettepe University, 06100, Sıhhiye, Ankara, Turkey.
Najim AmezianeDepartment of Clinical Genetics, VU University Medical Center, Amsterdam, The Netherlands.
Baris KuskonmazDepartment of Pediatrics, Division of Bone Marrow Transplantation Unit, Faculty of Medicine, Hacettepe University, Ankara, Turkey.
Josephine DorsmanDepartment of Clinical Genetics, VU University Medical Center, Amsterdam, The Netherlands.
Fatma GumrukDepartment of Pediatric Hematology, Faculty of Medicine, Hacettepe University, Ankara, Turkey.
Duygu UckanDepartment of Stem Cell Sciences, Institute of Health Sciences, Center for Stem Cell Research and Development, Hacettepe University, 06100, Sıhhiye, Ankara, Turkey.
Hacettepe University · TRAmsterdam UMC Location Vrije Universiteit Amsterdam · NL

Funding

Türkiye Bilimsel ve Teknolojik Araştirma Kurumu 110S021Türkiye Bilimsel ve Teknolojik Araştirma Kurumu 214Z033
6 · The paper itself

Abstract

Transforming growth factor beta (TGF-β) secretion from cells in the bone marrow (BM) niche affects hematopoietic stem cell (HSC) fate and has a cardinal role in HSC quiescence. BM mesenchymal stem cells (BM-MSCs), a component of the BM niche, may produce abnormal levels of TGF-β in Fanconi anemia (FA) and may play a role in bone marrow failure. Here, we molecularly and cellularly characterized FA BM-MSCs by addressing their immunophenotype, proliferation- and differentiation- capacity, reactive oxygen species (ROS) production, senescence activity as well as expression and secretion levels of TGF-β isoforms. In ten FA patients, mutations were detected in FANCA (n = 7), FANCG (n = 1) and FANCD2 (n = 2) genes. The immunophenotype, with the exception of CD29, and differentiation capacity of FA BM-MSCs were similar to healthy donors. FA BM-MSCs showed decreased proliferation, increased ROS level and an arrest in G2 following DEB treatment. β-galactosidase staining indicated elevated senescence of FANCD2-deficient cells. FA BM-MSCs displayed TGF-β1 mRNA levels similar to donor BM-MSCs, and was not affected by DEB treatment. However, secretion of TGF-β was absent in FA-D2 BM-MSCs. Absence of TGF-β secretion may be related to early onset of senescence of the FANCD2-deficient BM-MSCs. The proliferative response of FA-D2 BM-MSCs to rTGF-β1 was not different from FANCA-deficient and donor cells and raises the possibility that rTGF-β1 may reverse the senescence of the FANCD2-deficient BM-MSCs which needs to be investigated further.

Indexed as

Bone Marrow CellsCell DifferentiationCells, CulturedDNA Mutational AnalysisFanconi AnemiaFanconi Anemia Complementation Group D2 ProteinFanconi Anemia Complementation Group G ProteinHumansMesenchymal Stem CellsMutationSignal TransductionTransforming Growth Factor beta1FANCG protein, humanFanconi Anemia Complementation Group D2 ProteinFanconi Anemia Complementation Group G ProteinTransforming Growth Factor beta1Bone marrowFANCD2Fanconi anemiaMesenchymal stem cellsTGF-BETA

Identifiers

PMID29247345
OpenAlexW2774413062

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.