Evidence map›Paper›PMID 28631178›Full record

ReviewInternational journal of hematology2017

Recent insights into the molecular basis of Fanconi anemia: genes, modifiers, and drivers.

Ronald S Cheung, Toshiyasu Taniguchi

Open access · bronzeAbstract readReview
In one paragraph

Review in International journal of hematology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

32 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
  2. Review
  3. Further Evidence forMolecular syndromology · 2023
    Article
  4. Chromosomal instability in adult-type diffuse gliomas.Acta neuropathologica communications · 2022
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Cell and Gene Therapy for Anemia: Hematopoietic Stem Cells and Gene Editing.International journal of molecular sciences · 2021
    Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. sRNA/L1 retrotransposition: using siRNAs and miRNAs to expand the applications of the cell culture-based LINE-1 retrotransposition assay.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2020
    Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article
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

2 authors at 2 institutions in 2 countries.

Ronald S CheungDivision of Human Biology, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave. N., C1-015, Seattle, WA, 98109-1024, USA.
Toshiyasu TaniguchiDivision of Human Biology, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave. N., C1-015, Seattle, WA, 98109-1024, USA. ttanigu-tky@umin.ac.jp.ORCID http://orcid.org/0000-0002-7746-3658
Fred Hutch Cancer Center · USTokai University · JP

Funding

PEDIATRIC ONCOLOGY RESEARCH TRAINING PROGRAMT32CA009351 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI Elizabeth R Lawlor, SOHEIL MESHINCHI · 1985 to 2026
$7.0M
Cellular and Molecular Biology of Childhood DiseaseK12HD043376 · NICHD · UNIVERSITY OF WASHINGTON · PI STAPLETON, FIELDING BRUDER · 2003 to 2012
$3.3M
The Fanconi Anemia-BRCA Pathway And Chemosensitivity of Human CancerR01CA125636 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI TANIGUCHI, TOSHIYASU · 2007 to 2011
$1.6M
Japan Society for the Promotion of Science 15K21771National Cancer Institute R01 CA125636National Institute of Child Health and Human Development K12 HD043376National Institutes of Health T32 CA009351NCI NIH HHS R01 CA125636NCI NIH HHS T32 CA009351NICHD NIH HHS K12 HD043376
6 · The paper itself

Abstract

Fanconi anemia (FA), the most common form of inherited bone marrow failure, predisposes to leukemia and solid tumors. FA is caused by the genetic disruption of a cellular pathway that repairs DNA interstrand crosslinks. The impaired function of this pathway, and the genetic instability that results, is considered the main pathogenic mechanism behind this disease. The identification of breast cancer susceptibility genes (for example, BRCA1/FANCS and BRCA2/FANCD1) as being major players in the FA pathway has led to a surge in molecular studies, resulting in the concept of the FA-BRCA pathway. In this review, we discuss recent advances in the molecular pathogenesis of FA from three viewpoints: (a) new FA genes, (b) modifier pathways that influence the cellular and clinical phenotypes of FA and (c) non-canonical functions of FA genes that may drive disease progression independently of deficient DNA repair. Potential therapeutic approaches for FA that are relevant to each will also be proposed.

Indexed as

AldehydesAutophagyBRCA1 ProteinBRCA2 ProteinBreast NeoplasmsDisease ProgressionDNA RepairFanconi AnemiaFemaleGenetic Predisposition to DiseaseHumansMaleMolecular Targeted TherapyTransforming Growth Factor betaAldehydesBRCA1 ProteinBRCA1 protein, humanBRCA2 ProteinBRCA2 protein, humanTransforming Growth Factor betaAldehydesAutophagyBone marrow failureDNA interstrand crosslink repairTGFβ

Identifiers

PMID28631178
PMCPMC5904331
OpenAlexW2675278942

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.